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ATP + 1-phosphatidyl-1D-myo-inositol
ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
additional information
?
-
ATP + 1-phosphatidyl-1D-myo-inositol
ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol
ADP + 1-phosphatidyl-1D-myo-inositol 5-phosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
the main function of PPK-3 is to mediate membrane retrieval from matured lysosomes through regulation of PtdIns(3,5)P2. Complete loss of ppk-3 function induces developmental defects characterized by embryonic lethality, whereas partial loss of function leads to growth retardation. At the cellular level, ppk-3 mutants display a striking enlargement of vacuoles positive for lysosome-associated membrane protein 1 in different tissues
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
Drosophila sp. (in: flies)
-
Fab1 phosphatidylinositol 3-phosphate 5-kinase controls trafficking but not silencing of endocytosed receptors. Drosophila fab1 mutants contain undetectable phosphatidylinositol 3,5-bisphosphate levels, show profound increases in cell and organ size, and die at the pupal stage
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, interleukins, UV radiation, and autophosphorylation, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
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?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
preferred substrate
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
stress-activated enzyme
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
essential for vacuole function
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
generation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is regulated by Vac7 protein, whereas turnover of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is mediated in part by the Sac1 polyphosphoinositide phosphatase family member Fig4
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview, enzymes hydrolyzing the product are counteracting, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
Fab1p and AP-1 are required for trafficking of endogenously ubiquitylated cargoes to the vacuole lumen
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
phosphatidylinositol(3,5)bisphosphate is essential for cellular responses to various stresses and for the mating pheromone signalling under starvation conditions
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
-
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
recombinant enzyme
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate
-
recombinant enzyme
-
-
?
additional information
?
-
TLC measurement of phospholipids in wild-type and FAB1A-GFP-expressing plants, overview
-
-
?
additional information
?
-
-
PIKfyve participates in the SGK1-dependent regulation of the Na+, glucose cotransporter SGLT1 (SLC5A1)
-
-
?
additional information
?
-
-
substrate specificity in descending order: 1-phosphatidyl-1D-myo-inositol 3-phosphate, 1-phosphatidyl-1D-myo-inositol 4-phosphate, and 1-phosphatidyl-1D-myo-inositol, the enzyme also shows lipid kinase activity
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?
additional information
?
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
substrate specificity, the enzyme also shows lipid kinase activity
-
-
?
additional information
?
-
-
Fab1p activators, Vac7p and Vac14p, independently regulate Fab1p activity. A maximal increase in the levels of PI3,5P2 requires both Vac7p and the Vac14pFig4p complex
-
-
?
additional information
?
-
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
-
substrate specificity in descending order: 1-phosphatidyl-1D-myo-inositol 3-phosphate, 1-phosphatidyl-1D-myo-inositol 4-phosphate, and 1-phosphatidyl-1D-myo-inositol
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
additional information
?
-
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
the main function of PPK-3 is to mediate membrane retrieval from matured lysosomes through regulation of PtdIns(3,5)P2. Complete loss of ppk-3 function induces developmental defects characterized by embryonic lethality, whereas partial loss of function leads to growth retardation. At the cellular level, ppk-3 mutants display a striking enlargement of vacuoles positive for lysosome-associated membrane protein 1 in different tissues
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
Drosophila sp. (in: flies)
-
Fab1 phosphatidylinositol 3-phosphate 5-kinase controls trafficking but not silencing of endocytosed receptors. Drosophila fab1 mutants contain undetectable phosphatidylinositol 3,5-bisphosphate levels, show profound increases in cell and organ size, and die at the pupal stage
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, interleukins, UV radiation, and autophosphorylation, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
stress-activated enzyme
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
essential for vacuole function
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
generation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is regulated by Vac7 protein, whereas turnover of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate is mediated in part by the Sac1 polyphosphoinositide phosphatase family member Fig4
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview, enzymes hydrolyzing the product are counteracting, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
Fab1p and AP-1 are required for trafficking of endogenously ubiquitylated cargoes to the vacuole lumen
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
phosphatidylinositol(3,5)bisphosphate is essential for cellular responses to various stresses and for the mating pheromone signalling under starvation conditions
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
reaction is essential for retrograde trafficking between the vacuole/lysosome and the late endosome and also for trafficking of some proteins into the vacuole via multivesicular bodies, enzyme synthesis is regulated by vac14 and vac7, 2 upstream activators, physiological roles of the enzyme and regulation mechnaism, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
regulation of 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate synthesis involving osmotic stress, overview
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
?
ATP + 1-phosphatidyl-1D-myo-inositol 3-phosphate
ADP + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate
-
-
-
-
?
additional information
?
-
TLC measurement of phospholipids in wild-type and FAB1A-GFP-expressing plants, overview
-
-
?
additional information
?
-
-
PIKfyve participates in the SGK1-dependent regulation of the Na+, glucose cotransporter SGLT1 (SLC5A1)
-
-
?
additional information
?
-
physiological roles of the catalyzed reaction, overview
-
-
?
additional information
?
-
-
Fab1p activators, Vac7p and Vac14p, independently regulate Fab1p activity. A maximal increase in the levels of PI3,5P2 requires both Vac7p and the Vac14pFig4p complex
-
-
?
additional information
?
-
-
physiological roles of the catalyzed reaction, overview
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
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1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Cell-Wall-Degrading Enzymes Required for Virulence in the Host Selective Toxin-Producing Necrotroph Alternaria alternata of Citrus.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Class III PI 3-kinase is the main source of PtdIns3P substrate and membrane recruitment signal for PIKfyve constitutive function in podocyte endomembrane homeostasis.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Deletion of PIKfyve alters alveolar macrophage populations and exacerbates allergic inflammation in mice.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
PIKfyve deficiency in myeloid cells impairs lysosomal homeostasis in macrophages and promotes systemic inflammation in mice.
1-phosphatidylinositol-3-phosphate 5-kinase deficiency
Transcription factor STE12alpha has distinct roles in morphogenesis, virulence, and ecological fitness of the primary pathogenic yeast Cryptococcus gattii.
Acquired Immunodeficiency Syndrome
Trehalose limits opportunistic mycobacterial survival during HIV co-infection by reversing HIV-mediated autophagy block.
Adenocarcinoma
Combined Inhibition of p38MAPK and PIKfyve Synergistically Disrupts Autophagy to Selectively Target Cancer Cells.
Albuminuria
Nephron specific knockin of the PIKfyve binding deficient Vac14L156R mutant results in albuminuria and mesangial expansion.
Alzheimer Disease
A cell-permeable tool for analysing APP intracellular domain function and manipulation of PIKfyve activity.
Alzheimer Disease
APP controls the formation of PI(3,5)P(2) vesicles through its binding of the PIKfyve complex.
Alzheimer Disease
The amyloid precursor protein (APP) binds the PIKfyve complex and modulates its function.
Arthritis
Inhibition of c-Rel DNA binding is critical for the anti-inflammatory effects of novel PIKfyve inhibitor.
Autoimmune Diseases
Structure-activity relationship study, target identification, and pharmacological characterization of a small molecular IL-12/23 inhibitor, APY0201.
Autoimmune Diseases
The Phosphoinositide Kinase PIKfyve Promotes Cathepsin-S-Mediated Major Histocompatibility Complex Class II Antigen Presentation.
Breast Neoplasms
The PIKfyve-ArPIKfyve-Sac3 triad in human breast cancer: Functional link between elevated Sac3 phosphatase and enhanced proliferation of triple negative cell lines.
Carcinogenesis
Elevated levels of PtdIns5P in NPM-ALK transformed cells: implication of PIKfyve.
Carcinogenesis
The phosphoinositide kinase PIKfyve mediates epidermal growth factor receptor trafficking to the nucleus.
Carcinoma
The phosphoinositide kinase PIKfyve mediates epidermal growth factor receptor trafficking to the nucleus.
Carcinoma, Hepatocellular
Akebia saponin E, as a novel PIKfyve inhibitor, induces lysosome-associated cytoplasmic vacuolation to inhibit proliferation of hepatocellular carcinoma cells.
Carcinoma, Non-Small-Cell Lung
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Cardiomyopathies
Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice.
Corneal Dystrophies, Hereditary
A novel mutation (p.Glu1389AspfsX16) of the phosphoinositide kinase, FYVE finger containing gene found in a Japanese patient with fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
A novel PIKFYVE mutation in fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
Characterization of pip5k3 fleck corneal dystrophy-linked gene in zebrafish.
Corneal Dystrophies, Hereditary
Corneal dystrophies.
Corneal Dystrophies, Hereditary
Endosomal phosphoinositides and human diseases.
Corneal Dystrophies, Hereditary
Identification of novel PIKFYVE gene mutations associated with Fleck corneal dystrophy.
Corneal Dystrophies, Hereditary
Mutations in PIP5K3 are associated with François-Neetens mouchetée fleck corneal dystrophy.
COVID-19
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
COVID-19
Synergistic block of SARS-CoV-2 infection by combined drug inhibition of the host entry factors PIKfyve kinase and TMPRSS2 protease.
COVID-19
The Global Phosphorylation Landscape of SARS-CoV-2 Infection.
COVID-19
The PIKfyve Inhibitor Apilimod: A Double-Edged Sword against COVID-19.
Dystonia
Altered homodimer formation and increased iron accumulation in VAC14-related disease: Case report and review of the literature.
Endometrial Hyperplasia
Autophagy in the physiological endometrium and cancer.
Endometrial Neoplasms
Autophagy in the physiological endometrium and cancer.
Glucose Intolerance
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Glucose Intolerance
Unexpected severe consequences of Pikfyve deletion by aP2- or Aq-promoter-driven Cre expression for glucose homeostasis and mammary gland development.
Hyperinsulinism
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Hypopigmentation
PIKfyve complex regulates early melanosome homeostasis required for physiological amyloid formation.
Infections
An STE12 gene identified in the mycorrhizal fungus Glomus intraradices restores infectivity of a hemibiotrophic plant pathogen.
Infections
fost12, the Fusarium oxysporum homolog of the transcription factor Ste12, is upregulated during plant infection and required for virulence.
Infections
Inhibition of PIKfyve kinase prevents infection by EBOV and SARS-CoV-2.
Infections
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2.
Infections
Loss of PIKfyve drives the spongiform degeneration in prion diseases.
Infections
PIKfyve/Fab1 is required for efficient V-ATPase and hydrolase delivery to phagosomes, phagosomal killing, and restriction of Legionella infection.
Infections
Proteoglycan-Dependent Endo-Lysosomal Fusion Affects Intracellular Survival of Salmonella Typhimurium in Epithelial Cells.
Infections
Relevance of the transcription factor PdSte12 in Penicillium digitatum conidiation and virulence during citrus fruit infection.
Infections
Ste12 transcription factor homologue CpST12 is down-regulated by hypovirus infection and required for virulence and female fertility of the chestnut blight fungus Cryphonectria parasitica.
Infections
Synergistic block of SARS-CoV-2 infection by combined drug inhibition of the host entry factors PIKfyve kinase and TMPRSS2 protease.
Infections
The phosphatidylinositol-3-phosphate 5-kinase inhibitor apilimod blocks filoviral entry and infection.
Infections
The role of mitogen-activated protein (MAP) kinase signalling components and the Ste12 transcription factor in germination and pathogenicity of Botrytis cinerea.
Infections
Transcription Factor CfSte12 of Colletotrichum fructicola Is a Key Regulator of Early Apple Glomerella Leaf Spot Pathogenesis.
Infections
Vaccinia Virus Infection Requires Maturation of Macropinosomes.
Infertility
A dominant truncation allele identifies a gene, STE20, that encodes a putative protein kinase necessary for mating in Saccharomyces cerevisiae.
Infertility
Isolation of suppressor mutants of phosphatidylinositol 3-phosphate 5-kinase deficient cells in Schizosaccharomyces pombe.
Infertility
Role of STE genes in the mating factor signaling pathway mediated by GPA1 in Saccharomyces cerevisiae.
Infertility
Rst1 and Rst2 are required for the a/alpha diploid cell type in yeast.
Insulin Resistance
Muscle-specific Pikfyve gene disruption causes glucose intolerance, insulin resistance, adiposity, and hyperinsulinemia but not muscle fiber-type switching.
Insulin Resistance
Unexpected severe consequences of Pikfyve deletion by aP2- or Aq-promoter-driven Cre expression for glucose homeostasis and mammary gland development.
Liver Neoplasms
Inhibition of PIKfyve using YM201636 suppresses the growth of liver cancer via the induction of autophagy.
Lung Neoplasms
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Lymphoma, Non-Hodgkin
B-cell non-Hodgkin lymphoma: Selective vulnerability to PIKFYVE inhibition.
Lymphoma, Non-Hodgkin
Identification of apilimod as a first-in-class PIKfyve kinase inhibitor for treatment of B-cell non-Hodgkin lymphoma.
Multiple Myeloma
Identification of PIKfyve kinase as a target in multiple myeloma.
Neoplasms
A Family of PIKFYVE Inhibitors with Therapeutic Potential Against Autophagy-Dependent Cancer Cells Disrupt Multiple Events in Lysosome Homeostasis.
Neoplasms
Autophagy in the physiological endometrium and cancer.
Neoplasms
B-cell non-Hodgkin lymphoma: Selective vulnerability to PIKFYVE inhibition.
Neoplasms
Combined Inhibition of p38MAPK and PIKfyve Synergistically Disrupts Autophagy to Selectively Target Cancer Cells.
Neoplasms
Elevated levels of PtdIns5P in NPM-ALK transformed cells: implication of PIKfyve.
Neoplasms
Inhibition of PIKfyve using YM201636 suppresses the growth of liver cancer via the induction of autophagy.
Neoplasms
PIKfyve inhibitor cytotoxicity requires AKT suppression and excessive cytoplasmic vacuolation.
Neoplasms
PIKfyve, MTMR3 and their product PtdIns5P regulate cancer cell migration and invasion through activation of Rac1.
Neoplasms
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
Neoplasms
Small molecule PIKfyve inhibitors as cancer therapeutics: Translational promises and limitations.
Neoplasms
The effects of PIKfyve inhibitor YM201636 on claudins and malignancy potential of nonsmall cell cancer cells.
Neoplasms
The Phosphoinositide Kinase PIKfyve Promotes Cathepsin-S-Mediated Major Histocompatibility Complex Class II Antigen Presentation.
Neurodegenerative Diseases
PIKfyve: a lipid kinase target for COVID-19, cancer and neurodegenerative disorders.
Obesity
Inhibition of PIKfyve prevents myocardial apoptosis and hypertrophy through activation of SIRT3 in obese mice.
Osteosarcoma
TRIM68, PIKFYVE, and DYNLL2: The Possible Novel Autophagy- and Immunity-Associated Gene Biomarkers for Osteosarcoma Prognosis.
Pancreatitis
Early to Late Endosome Trafficking Controls Secretion and Zymogen Activation in Rodent and Human Pancreatic Acinar Cells.
phosphatidylinositol 3-kinase deficiency
Active vacuolar H+ ATPase and functional cycle of Rab5 are required for the vacuolation defect triggered by PtdIns(3,5)P2 loss under PIKfyve or Vps34 deficiency.
Pneumonia
Deletion of PIKfyve alters alveolar macrophage populations and exacerbates allergic inflammation in mice.
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2.
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Transcriptional Regulation of PIK3CD and PIKFYVE in T-Cell Acute Lymphoblastic Leukemia by IKAROS and Protein Kinase CK2.
Prion Diseases
Loss of PIKfyve drives the spongiform degeneration in prion diseases.
Severe Acute Respiratory Syndrome
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2.
Starvation
AMPK-activated ULK1 phosphorylates PIKFYVE to drive formation of PtdIns5P-containing autophagosomes during glucose starvation.
Starvation
An AMPK-ULK1-PIKFYVE signaling axis for PtdIns5P-dependent autophagy regulation upon glucose starvation.
Starvation
Candida glabrata STE12 is required for wild-type levels of virulence and nitrogen starvation induced filamentation.
Starvation
Genomewide mechanisms of chronological longevity by dietary restriction in budding yeast.
Starvation
Glucose starvation induces autophagy via ULK1-mediated activation of PIKfyve in an AMPK-dependent manner.
Starvation
Phosphatidylinositol 3-phosphate 5-kinase is required for the cellular response to nutritional starvation and mating pheromone signals in Schizosaccharomyces pombe.
Starvation
Regulation of mating and mating-type-specific genes in Zygosaccharomyces sp. yeast.
Starvation
The STE12alpha homolog is required for haploid filamentation but largely dispensable for mating and virulence in Cryptococcus neoformans.
Thrombosis
Loss of PIKfyve in platelets causes a lysosomal disease leading to inflammation and thrombosis in mice.
Thrombosis
Phosphatidylinositol 3 monophosphate metabolizing enzymes in blood platelet production and in thrombosis.
Tuberculosis
Trehalose limits opportunistic mycobacterial survival during HIV co-infection by reversing HIV-mediated autophagy block.
Vesicular Stomatitis
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2.
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metabolism
amino acid transporter SLC-36.1 and PPK-3 function in the same genetic pathway, and they directly interact with one another. The SLC-36.1-PPK-3 axis is essential for autophagic lysosome reformation (ALR)
additional information
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Gly867 and Gly1870 are required for the functioning of CgFab1
malfunction
a loss of enzyme function causes the release of late endosomal proteins, Ara7, and SNX1 from the endosome membrane. Downregulation of FAB1A/B or YM201636 inhibitor treatment affects the auxin distribution and and alteration of PIN2 localization in root cells. FAB1 knockdown causes relocation of the basal polarity of PIN2 in young root cortical cells
malfunction
enzyme inhibition reduces contraction- and AICAriboside (5-amino-4-imidazolecarboxamide riboside)-stimulated glucose uptake. PIKfyve knockdown in C2C12 myotubes reduced AICAriboside-stimulated glucose transport
malfunction
the vacuolation phenotype in cultured Vps34 (EC 2.7.1.137)-deficient podocytes is caused by the absence of a substrate for the Vps34 downstream effector PtdIns 3-phosphate 5-kinase, which phosphorylates Vps34-generated 1-phosphatidyl-1D-myo-inositol 3-phosphate to produce + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate. PtdIns 3-phosphate 5-kinase perturbation and 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate reduction result in massive membrane vacuolation along the endosomal system. Genetic deletion of the enzyme in endocytically active proximal tubular cells results in the development of large cytoplasmic vacuoles caused by arrested endocytic traffic progression at a late-endosome stage, while deletion of the enzyme in glomerular podocytes does not significantly alter the endosomal morphology, even in age 18-month-old mice
malfunction
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CgFAB1 disruption impaires vacuole homeostasis and actin organization, and the F-actin stabilizing compound jasplakinolide rescues azole toxicity in cytoskeleton defective-mutants including the Cgfab1DELTA mutant. The actin depolymerization factor CgCof1 binds to multiple lipids including phosphatidylinositol 3,5-bisphosphate. CgCof1 distribution along with the actin filament-capping protein CgCap2 is altered upon both CgFAB1 disruption and fluconazole exposure. Actin polymerization inhibition renders fluconazole fully and partially fungicidal in azole-susceptible and azole-resistant Candida glabrata clinical isolates, respectively, thereby, underscoring the role of fluconazole-effectuated actin remodeling in azole resistance. MDR genes are activated in the Cgfab1DELTA mutant upon fluconazole exposure. Fluconazole-treated wild-type and Cgfab1DELTA cells display a 1.5fold increased efflux of the MDR pump substrate rhodamine 6G
malfunction
loss of PPK-3, the Caenorhabditis elegans homologue of the PtdIns3P 5-kinase PIKfyve, causes accumulation of phagolysosomal vacuoles that are defective in phagocytic lysosome reformation (PLR). Loss of slc-36.1 and ppk-3 causes strong defects in autophagic lysosome reformation in adult animals. Ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutants of slc-36.1(yq110) with ppk-3(n2668) contain enlarged autolysosomes similar to ppk-3(n2668) single mutants
malfunction
Ste12PIKFYVE-deficient mutants are unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles has any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE-deficient mutants reduces cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. Ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. No major impact on TORC1 or TORC2 activity is observed in the ste12-deficient mutants. Advancement of cell division is markedly compromised in ste12PIKFYVE.W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE-W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. ste12PIKFYVE-W1037STOP autophagy defect is unlikely to account for the inability to control size after nitrogen stress
malfunction
the intracellular trafficking of pathogens, Zaire EBOV GP (VSV-MeGFPZEBOV) and SARS-CoV-2 S Wuhan-Hu-1 strain (VSV-eGFP-SARS-CoV-2), is elicited by inhibition of PIKfyve kinase via apilimod and vacuolin-1, small-molecule inhibitors of the main endosomal phosphatidylinositol-3-phosphate/phosphatidylinositol 5-kinase, PIKfyve
malfunction
-
Ste12PIKFYVE-deficient mutants are unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles has any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE-deficient mutants reduces cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. Ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. No major impact on TORC1 or TORC2 activity is observed in the ste12-deficient mutants. Advancement of cell division is markedly compromised in ste12PIKFYVE.W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE-W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. ste12PIKFYVE-W1037STOP autophagy defect is unlikely to account for the inability to control size after nitrogen stress
-
malfunction
-
Ste12PIKFYVE-deficient mutants are unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles has any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE-deficient mutants reduces cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. Ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. No major impact on TORC1 or TORC2 activity is observed in the ste12-deficient mutants. Advancement of cell division is markedly compromised in ste12PIKFYVE.W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE-W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. ste12PIKFYVE-W1037STOP autophagy defect is unlikely to account for the inability to control size after nitrogen stress
-
physiological function
in Xenopus oocytes expressing mammalian excitatory amino acid transporter EAAT4, glutamate induces a current which is significantly enhanced by coexpression of isoform PIKfyve and glucocorticoid inducible kinase SGK1. This glutamate-induced current is significantly larger than the current in Xenopus oocytes expressing EAAT4 together with either kinase alone. Coexpression of the inactive SGK1 mutant K127N does not significantly alter glutamate-induced current in EAAT4-expressing Xenopus oocytes and abolishes the stimulation of glutamate-induced current by coexpression of isoform PIKfyve. The stimulating effect of PIKfyve is abrogated by mutation S318A in the SGK consensus sequence of PIKfyve. Coexpression of PIKfyve S318A mutant significantly blunts the stimulating effect of SGK1 on EAAT4 activity
physiological function
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PIKFYVE knockdown produces a 36% reduction in phosphatidylinositol 3,5-bisphosphate and a 13% increase in phosphatidylinositol 3-phosphate. PIKFYVE and class II phosphatidylinositol 3-kinase PI3K-C2alpha are necessary for activation of the kinase complex mechanistic target of rapamycin mTORC1 and its translocation to the plasma membrane in 3T3-L1 adipocytes. The mTORC1 component Raptor directly interacts with phosphatidylinositol 3,5-bisphosphate
physiological function
the enzyme activity is implicated in be involved in contraction/AMPK (AMP-activated protein kinase)-stimulated glucose uptake in skeletal muscle rather than insulin-stimulated glucose uptake. The enzyme is an AMPK substrate whose phosphorylation at Ser307 promotes PIKfyve translocation to endosomes for PtdIns(3,5)P2 synthesis to facilitate GLUT4 (glucose transporter 4) translocation
physiological function
-
the enzyme activity is required for the stimulation of skeletal muscle glucose uptake by contraction/AMPK activation. In opossum kidney cells, wild-type, but not S307A mutant, PIKfyve is recruited to endosomal vesicles in response to AMPK activation
physiological function
the enzyme mediates endosome maturation to establish endosome-cortical microtubule interaction in Arabidopsis thaliana. The enzyme and its product, 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate, are essential for the maturation process of endosomes to mediate cortical microtubule association of endosomes, thereby controlling proper PIN-FORMED protein trafficking in young cortical and stele cells of root. The enzyme and its product mediate the late endosome maturation by recruiting endosomal effector molecules, Ara7 and SNX1, onto endosomes to establish endosome-cortical microtubule interaction
physiological function
analysis of the intracellular trafficking of pathogens elicited by inhibition of PIKfyve kinase
physiological function
-
enzyme CgFab1 is implicated in azole tolerance through actin network remodeling. CgFab1 is required for vacuole homeostasis. Fluconazole induces actin cytoskeletal depolarization in a CgFab1-dependent manner, in part, through the PI 3,5-bisphosphate [PI(3,5)P2]-binding protein, CgCof1. CgFab1 is involved in response to azole, cell membrane and cell wall stress. Fluconazole-treated wild-type and Cgfab1DELTA cells display a 1.5fold increased efflux of the MDR pump substrate rhodamine 6G
physiological function
PIKFYVE is a 1-phosphatidylinositol-3-phosphate 5-kinase that is required for the production of a signalling phospholipid required for vacuole functions and endosome dynamics, phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2). PI(3,5)P2 is reported to be a positive regulator of TORC1 activity on the yeast vacuole, that is required for TORC1 inhibition of autophagy under nutrient-rich conditions. PIKFYVE also regulates cell type-specific activation and localization of mTORC1 in 3T3-L1 adipocytes. In humans, mutations predicted to lead to minor changes in PI(3,5)P2 levels are associated with severe neurological diseases and are implicated in the invasive behaviour of cancer cells. Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control. Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division
physiological function
the phosphatidylinositol 3-phosphate (PtdIns3P) 5-kinase PIKfyve and the lysosomal calcium channel TRPML1 are required for endocytic lysosome reformation. PIKfyve generates phosphatidylinositol 3,5-bisphosphate, which activates TRPML1 to control lysosomal Ca2+ efflux. The SLC-36.1-PPK-3 axis is essential for ALR
physiological function
-
PIKFYVE is a 1-phosphatidylinositol-3-phosphate 5-kinase that is required for the production of a signalling phospholipid required for vacuole functions and endosome dynamics, phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2). PI(3,5)P2 is reported to be a positive regulator of TORC1 activity on the yeast vacuole, that is required for TORC1 inhibition of autophagy under nutrient-rich conditions. PIKFYVE also regulates cell type-specific activation and localization of mTORC1 in 3T3-L1 adipocytes. In humans, mutations predicted to lead to minor changes in PI(3,5)P2 levels are associated with severe neurological diseases and are implicated in the invasive behaviour of cancer cells. Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control. Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division
-
physiological function
-
PIKFYVE is a 1-phosphatidylinositol-3-phosphate 5-kinase that is required for the production of a signalling phospholipid required for vacuole functions and endosome dynamics, phosphatidylinositol-3,5-bisphosphate (PI(3,5)P2). PI(3,5)P2 is reported to be a positive regulator of TORC1 activity on the yeast vacuole, that is required for TORC1 inhibition of autophagy under nutrient-rich conditions. PIKFYVE also regulates cell type-specific activation and localization of mTORC1 in 3T3-L1 adipocytes. In humans, mutations predicted to lead to minor changes in PI(3,5)P2 levels are associated with severe neurological diseases and are implicated in the invasive behaviour of cancer cells. Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control. Ste12PIKFYVE is required for nitrogen-stress mediated advancement of mitosis to reduce cell size at division
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S1448L
naturally occuring mutation yq24, yq24 mutants exhibit embryonic vacuoles similar to slc-36.1 mutants. Double mutants of yq24 with ced-4(n1162) show neither button-like apoptotic cell corpses nor vacuolar structures. The yq24 embryonic vacuoles are enriched for both LAAT-1::GFP and HIS-24::mCh. Mutant yq24 embryonic vacuoles are phagolysosomes arising from apoptosis
S318A
in Xenopus oocytes expressing mammalian excitatory amino acid transporter EAAT4, glutamate induces a current which is significantly enhanced by coexpression of isoform PIKfyve and glucocorticoid inducible kinase SGK1. The stimulating effect of PIKfyve is abrogated by mutation S318A in the SGK consensus sequence of PIKfyve. Coexpression of PIKfyve S318A mutant significantly blunts the stimulating effect of SGK1 on EAAT4 activity
D2134R
site-directed mutagenesis, in vivo abrogation of lipid kinase activity of the enzyme
K2059M
site-directed mutagenesis, in vitro abrogation of lipid kinase activity of the enzyme
G1867/1870V
-
site-directed mutagenesis, the Cgfab1DELTA mutant carrying CgFab1G1867/1870V is sensitive to both azole and metal ion stress
W1037stop
gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
W1037stop
-
gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
-
W1037stop
-
gene ste12 next generation sequencing reveals a truncating, premature stop codon at position W1037 of the Ste12PIKFYVE-phosphatidylinositol-3-phosphate 5-kinase. The advancement of cell division is markedly compromised in ste12PIKFYVE. Mutant W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE.W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. No significant changes in TORC1 and TORC2 activities are observed in ste12PIKFYVE-W1037STOP mutants. Phenotype, overview
-
additional information
knockdown of FAB1A/B expression
additional information
ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutant of slc-36.1(yq110) with ppk-3(n2668) contains enlarged autolysosomes similar to ppk-3(n2668) single mutants
additional information
-
ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutant of slc-36.1(yq110) with ppk-3(n2668) contains enlarged autolysosomes similar to ppk-3(n2668) single mutants
additional information
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enzyme defect leads to enlarged vacuoles that do not acidify correctly, the defect can be complemented by enzyme overexpression, mutants grow poorly at elevated temperature
additional information
FAB1 null mutants possess no phosphatidylinositol 3,5-bisphosphate and shows vacuolar defects, expression of murine enzyme PIKfyve, but of the enzyme from Schizosaccharomyces pombe, can revert the vacuolar defects in vivo, while the enzyme from Schizosaccharomyces pombe can restore catalytic activity in response to hyperosmotic stress
additional information
-
enzyme defect leads to enlarged vacuoles that do not acidify correctly, the defect can be complemented by enzyme overexpression, mutants grow poorly at elevated temperature
additional information
identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
additional information
-
identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
additional information
-
identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
-
additional information
-
identification of a non-functional ste12PIKFYVE mutant that is unable to invoke the normal advancement of mitotic onset and adjust cell size at division in response to nitrogen stress
-
additional information
-
generation of a deletion strain for the CgFAB1 gene, using the homologous recombination-based strategy. The mutant is sensitive to azoles (fluconazole, clotrimazole and ketoconazole), and cell membrane (SDS) and cell wall (caffeine) stressors. The growth of the Cgfab1DELTA mutant is also slightly impaired in the presence of the oxidative stressor, hydrogen peroxide, and at high temperature. MDR genes are activated in the Cgfab1DELTA mutant upon fluconazole exposure
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Cooke, F.T.; Dove, S.K.; McEwen, R.K.; Painter, G.; Holmes, A.B.; Hall, M.N.; Michell, R.H.; Parker, P.J.
The stress-activated phosphatidylinositol 3-phosphate 5-kinase Fab1p is essential for vacuole function in S. cerevisiae
Curr. Biol.
8
1219-1222
1998
Saccharomyces cerevisiae
brenda
Gary, J.D.; Sato, T.K.; Stefan, C.J.; Bonangelino, C.J.; Weisman, L.S.; Emr, S.D.
Regulation of fab1 phosphatidylinositol 3-phosphate 5-kinase pathway by vac7 protein and fig4, a polyphosphoinositide phosphatase family member
Mol. Biol. Cell
13
1238-1251
2002
Saccharomyces cerevisiae
brenda
Morishita, M.; Morimoto, F.; Kitamura, K.; Koga, T.; Fukui, Y.; Maekawa, H.; Yamashita, I.; Shimoda, C.
Phosphatidylinositol 3-phosphate 5-kinase is required for the cellular response to nutritional starvation and mating pheromone signals in Schizosaccharomyces pombe
Genes Cells
7
199-215
2002
Schizosaccharomyces pombe
brenda
Cooke, F.T.
Phosphatidylinositol 3,5-bisphosphate: metabolism and function
Arch. Biochem. Biophys.
407
143-151
2002
Arabidopsis thaliana, Caenorhabditis elegans, Candida albicans, Drosophila melanogaster, Homo sapiens, Mus musculus, Oryza sativa, Schizosaccharomyces pombe, Saccharomyces cerevisiae (P34756)
brenda
Dove, S.K.; McEwen, R.K.; Mayes, A.; Hughes, D.C.; Beggs, J.D.; Michell, R.H.
Vac14 controls PtdIns(3,5)P2 synthesis and Fab1-dependent protein trafficking to the multivesicular body
Curr. Biol.
12
885-893
2002
Saccharomyces cerevisiae, Schizosaccharomyces pombe
brenda
Shojaiefard, M.; Strutz-Seebohm, N.; Tavare, J.M.; Seebohm, G.; Lang, F.
Regulation of the Na(+), glucose cotransporter by PIKfyve and the serum and glucocorticoid inducible kinase SGK1
Biochem. Biophys. Res. Commun.
359
843-847
2007
Homo sapiens
brenda
Cabezas, A.; Pattni, K.; Stenmark, H.
Cloning and subcellular localization of a human phosphatidylinositol 3-phosphate 5-kinase, PIKfyve/Fab1
Gene
371
34-41
2006
Homo sapiens (Q9Y2I7), Homo sapiens
brenda
Duex, J.E.; Tang, F.; Weisman, L.S.
The Vac14p-Fig4p complex acts independently of Vac7p and couples PI3,5P2 synthesis and turnover
J. Cell Biol.
172
693-704
2006
Saccharomyces cerevisiae
brenda
Rutherford, A.C.; Traer, C.; Wassmer, T.; Pattni, K.; Bujny, M.V.; Carlton, J.G.; Stenmark, H.; Cullen, P.J.
The mammalian phosphatidylinositol 3-phosphate 5-kinase (PIKfyve) regulates endosome-to-TGN retrograde transport
J. Cell Sci.
119
3944-3957
2006
Homo sapiens
brenda
Phelan, J.P.; Millson, S.H.; Parker, P.J.; Piper, P.W.; Cooke, F.T.
Fab1p and AP-1 are required for trafficking of endogenously ubiquitylated cargoes to the vacuole lumen in S. cerevisiae
J. Cell Sci.
119
4225-4234
2006
Saccharomyces cerevisiae
brenda
Nicot, A.S.; Fares, H.; Payrastre, B.; Chisholm, A.D.; Labouesse, M.; Laporte, J.
The phosphoinositide kinase PIKfyve/Fab1p regulates terminal lysosome maturation in Caenorhabditis elegans
Mol. Biol. Cell
17
3062-3074
2006
Caenorhabditis elegans
brenda
Rusten, T.E.; Rodahl, L.M.; Pattni, K.; Englund, C.; Samakovlis, C.; Dove, S.; Brech, A.; Stenmark, H.
Fab1 phosphatidylinositol 3-phosphate 5-kinase controls trafficking but not silencing of endocytosed receptors
Mol. Biol. Cell
17
3989-4001
2006
Drosophila sp. (in: flies)
brenda
Alesutan, I.S.; Ureche, O.N.; Laufer, J.; Klaus, F.; Zuern, A.; Lindner, R.; Strutz-Seebohm, N.; Tavare, J.M.; Boehmer, C.; Palmada, M.; Lang, U.E.; Seebohm, G.; Lang, F.
Regulation of the glutamate transporter EAAT4 by PIKfyve
Cell. Physiol. Biochem.
25
187-194
2010
Mus musculus (Q9Z1T6)
brenda
Bridges, D.; Ma, J.T.; Park, S.; Inoki, K.; Weisman, L.S.; Saltiel, A.R.
Phosphatidylinositol 3,5-bisphosphate plays a role in the activation and subcellular localization of mechanistic target of rapamycin 1
Mol. Biol. Cell
23
2955-2962
2012
Mus musculus
brenda
Liu, Y.; Lai, Y.C.; Hill, E.V.; Tyteca, D.; Carpentier, S.; Ingvaldsen, A.; Vertommen, D.; Lantier, L.; Foretz, M.; Dequiedt, F.; Courtoy, P.J.; Erneux, C.; Viollet, B.; Shepherd, P.R.; Tavare, J.M.; Jensen, J.; Rider, M.H.
Phosphatidylinositol 3-phosphate 5-kinase (PIKfyve) is an AMPK target participating in contraction-stimulated glucose uptake in skeletal muscle
Biochem. J.
455
195-206
2013
Didelphis sp., Rattus norvegicus (D3ZYT8)
brenda
Venkatareddy, M.; Verma, R.; Kalinowski, A.; Patel, S.R.; Shisheva, A.; Garg, P.
Distinct requirements for vacuolar protein sorting 34 downstream effector phosphatidylinositol 3-phosphate 5-kinase in podocytes versus proximal tubular cells
J. Am. Soc. Nephrol.
27
2702-2719
2016
Mus musculus (Q9Z1T6)
brenda
Hirano, T.; Munnik, T.; Sato, M.H.
Phosphatidylinositol 3-phosphate 5-kinase, FAB1/PIKfyve kinase mediates endosome maturation to establish endosome-cortical microtubule interaction in Arabidopsis
Plant Physiol.
169
1961-1974
2015
Arabidopsis thaliana (Q9LUM0)
brenda
Gan, Q.; Wang, X.; Zhang, Q.; Yin, Q.; Jian, Y.; Liu, Y.; Xuan, N.; Li, J.; Zhou, J.; Liu, K.; Jing, Y.; Wang, X.; Yang, C.
The amino acid transporter SLC-36.1 cooperates with PtdIns3P 5-kinase to control phagocytic lysosome reformation
J. Cell Biol.
218
2619-2637
2019
Caenorhabditis elegans (G5ED98), Caenorhabditis elegans
brenda
Bhakt, P.; Shivarathri, R.; Choudhary, D.K.; Borah, S.; Kaur, R.
Fluconazole-induced actin cytoskeleton remodeling requires phosphatidylinositol 3-phosphate 5-kinase in the pathogenic yeast Candida glabrata
Mol. Microbiol.
110
425-443
2018
[Candida] glabrata
brenda
Cobley, D.; Halova, L.; Schauries, M.; Kaczmarek, A.; Franz-Wachtel, M.; Du, W.; Krug, K.; Macek, B.; Petersen, J.
Ste12/Fab1 phosphatidylinositol-3-phosphate 5-kinase is required for nitrogen-regulated mitotic commitment and cell size control
PLoS ONE
12
e0172740
2017
Schizosaccharomyces pombe (O59722), Schizosaccharomyces pombe, Schizosaccharomyces pombe ATCC 24843 (O59722), Schizosaccharomyces pombe 972 (O59722)
brenda
Kang, Y.L.; Chou, Y.Y.; Rothlauf, P.W.; Liu, Z.; Soh, T.K.; Cureton, D.; Case, J.B.; Chen, R.E.; Diamond, M.S.; Whelan, S.P.J.; Kirchhausen, T.
Inhibition of PIKfyve kinase prevents infection by Zaire ebolavirus and SARS-CoV-2
Proc. Natl. Acad. Sci. USA
117
20803-20813
2020
Homo sapiens (Q9Y2I7)
brenda