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metabolism
the enzyme methylates pri-miRNAs, marking them for recognition and processing by the RNA binding protein DGCR8. The enzyme is required for basal expression of the vast majority of miRNAs in these cancerous and non-cancerous cells
drug target
activators of METTL3-14-WTAP can be potential anticancer agents against glioblastoma
drug target
-
m6A modification may be a target for antivirals of enterovirus 71 (EV71)
drug target
METTL3 is probably involved in pancreatic carcinogenesis. It could eventually be a prognostic marker or a therapeutic target for pancreatic cancer
drug target
METTL3 may be an effective therapeutic target for bone tissue repair and regeneration
drug target
targeting m6A through its writer enzyme METTL3 may represent a therapeutic strategy for managing maladaptive cardiac hypertrophy and remodeling during the progression of heart failure
drug target
the enzyme (METTL3) contributes to transforming growth factor-beta-induced epithelial-mesenchymal transition of lung cancer cells through the regulation of JUNB. The significance of the regulation for m6A RNA modification in the important step of cancer progression provides the possibility to develop therapeutic strategies for the treatment of cancer metastasis
drug target
the enzyme (METTL3) may be a therapeutic target which is potential to be used for the treatment of human osteosarcoma
malfunction
-
depletion of isoforms METTL3 and METTL14 leads to apoptosis in cancer cells
malfunction
conditional knockout of the m6A methyltransferase Mettl3 in bone marrow mesenchymal stem cells induces pathological features of osteoporosis in mice. Mettl3 loss-of-function results in impaired bone formation, incompetent osteogenic differentiation potential and increased marrow adiposity. Knockout of Mettl3 reduces the translation efficiency of mesenchymal stem cell lineage allocator Pth1r, and disrupts the PTH-induced osteogenic and adipogenic responses in vivo
malfunction
deleting the enzyme (Mettl3) from the adult haematopoietic system leads to an accumulation of haematopoietic stem cell in the bone marrow and marked reduction of reconstitution potential due to a blockage of haematopoietic stem cell differentiation. Deleting Mettl3 from myeloid cells using Lysm-cre does not impact myeloid cell number or function. m6A sequencing reveals 2073 genes with significant m6A modification in haematopoietic stem cells
malfunction
depleting METTL3 in mouse hippocampus reduces memory consolidation ability, yet unimpaired learning outcomes can be achieved if adequate training is given or the m6A methyltransferase function of METTL3 is restored
malfunction
enzyme depletion reduces the binding of DGCR8 to pri-miRNAs and results in the global reduction of mature miRNAs and concomitant accumulation of unprocessed pri-miRNAs
malfunction
-
enzyme knockdown drastically reduces hepatocellular carcinoma cell proliferation, migration, and colony formation in vitro. Enzyme knockout remarkably suppresses hepatocellular carcinoma tumorigenicity and lung metastasis in vivo
malfunction
-
enzyme knockdown results in decreased enterovirus 71 replication
malfunction
-
enzyme knockdown results in early degeneration of microspores at the vacuolated pollen stage and simultaneously causes abnormal meiosis in prophase I. Loss of enzyme function disrupts the m6A modifications of threonine protease and NTPase genes during sporogenesis by directly binding to them and leads to microspores being degenerate at the early microspore stage
malfunction
hepatocyte-specific knockout of the enzyme (METTL3) in mice fed a high-fat diet improves insulin sensitivity and decreases fatty acid synthesis. Furthermore, mechanism analysis demonstrates that METTL3 silence decreases the m6A methylated and total mRNA level of fatty acid synthase (Fasn), subsequently inhibits fatty acid metabolism
malfunction
METTL3 knockdown in MIA PaCa-2 and BxPC-3 cells decreases RNA m6A modifications. Cell proliferation, invasion, and migration are decreased by METTL3 knockdown in cancerous cell lines
malfunction
METTL3 knockdown induces maladaptive eccentric remodeling and leads to morphological and functional signs of heart failure
malfunction
METTL3 knockdown significantly changes HSP70, HSP60, and HSP27 mRNA expression in HepG2 cells using siRNA. mRNA lifetime is not impacted. Knockdown of METTL3 changes the methylation patterns of heat shock proteins transcript
malfunction
specific depletion of Mettl3 in dendritic cell results in impaired phenotypic and functional maturation of dendritic cells, with decreased expression of costimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo
malfunction
the accumulation of phenotypic hematopoietic stem cells in Mettl3-deficient mice is most likely due to a loss of hematopoietic stem cell quiescence
physiological function
-
isoforms METTL3 and METTL4 are required for normal embryogenesis
physiological function
-
isoforms METTL3 and METTL4 regulate stem cell differentiation and reprogramming. Isoform METTL3 regulates circadian periods
physiological function
-
the enzyme is essential for viability and required for Notch signaling during oogenesis
physiological function
-
the enzyme is required for embryonic development , normal growth patterns, apical dominance, and plant development
physiological function
-
the enzyme is required for meiosis and sporulation
physiological function
catalytic subunit METTL3 interacts in a dense network of proteins. Presence of WTAP (Wilms' tumor associated protein), METTL14 and protein KIAA1429 are required for methylation. WTAP-dependent methylation sites are located at internal positions in transcripts, are topologically static across a variety of systems, and are inversely correlated with mRNA stability. WTAP-independent sites form at the first transcribed base as part of the cap structure, and are present at thousands of sites, forming a layer of transcriptome complexity
physiological function
in the m6A methyltransferase complex, METTL3 primarily functions as the catalytic core, while METTL14 serves as an RNA-binding platform
physiological function
knockdown of methyltransferase like 3 (METTL3) impairs X-inactive specific transcript-mediated gene silencing. X-inactive specific transcript XIST mediates the transcriptional silencing of genes on the X chromosome. YTH domain containing 1 (YTHDC1) preferentially recognizes m6A residues on XIST and is required for XIST function
physiological function
methylation at m6A by METTL3/METTL14 facilitates the methylation of m5C by NSUN2, and vice versa. NSUN2-mediated m5C and METTL3/METTL14-mediated m6A methylation synergistically enhance p21 expression at the translational level, leading to elevated expression of p21 in oxidative stress-induced cellular senescence
physiological function
METTL14 and m6A methyltransferase METTL3 form a stable heterodimer core complex of METTL3-14 that functions in cellular m6A deposition on mammalian nuclear RNAs. WTAP, a mammalian splicing factor, can interact with this complex and affect this methylation. Knockdown of cellular METTL3, METTL14, and WTAP decreases the m6A level in polyadenylated RNA by about 30%, 40%, and 50% in HeLa cells, respectively, and about 20%, 35%, and 42% in HEK-293FT cells, respectively
physiological function
METTL3 associates with ribosomes and promotes translation in the cytoplasm. METTL3 depletion inhibits translation, and both wild-type and catalytically inactive METTL3 promote translation when tethered to a reporter mRNA. METTL3 enhances mRNA translation through an interaction with the translation initiation machinery
physiological function
-
METTL3 knockdown leads to a significant downregulation of 3' terminal exons. Demethylase FTO and METTL3 act reciprocally in the regulation of alternative splicing and 3' untranslated region expression
physiological function
morpholino-mediated knockdown targeting Wilms' tumor 1-associating protein WTAP and/or METTL3 in zebrafish embryos causes tissue differentiation defects and increases apoptosis
physiological function
N6-methyladenosine (m6A) transferase METTL3 is as a regulator for terminating murine naive pluripotency. Mettl3 knockout preimplantation epiblasts and naive embryonic stem cells are depleted for N6-methyladenosine in mRNAs, yet are viable. They fail to adequately terminate their naive state and undergo aberrant and restricted lineage priming at the postimplantation stage, which leads to early embryonic lethality. N6-methyladenosine predominantly and directly reduces mRNA stability
physiological function
the levels of m6A and METTL3 are up-regulated in human dental pulp cells stimulated by lipopolysaccharide. METTL3 depletion decreases the expression of inflammatory cytokines and the phosphorylation of IKKalpha/beta, p65 and IkappaBalpha in the NF-kappaB signalling pathway as well as p38, ERK and JNK in the MAPK signalling pathway in lipopolysaccharide-induced dental pulp cells. The vast number of genes affected by METTL3 depletion is associated with the inflammatory response. METTL3 knockdown facilitates the expression of MyD88S, a splice variant of MyD88 that inhibits inflammatory cytokine production
physiological function
Wilms' tumor 1-associating protein (WTAP) interacts with METTL3 and METTL14, and is required for their localization into nuclear speckles enriched with pre-mRNA processing factors and for catalytic activity of the m6A methyltransferase in vivo. In the absence of WTAP, the RNA-binding capability of METTL3 is strongly reduced. In addition, WTAP and METTL3 regulate expression and alternative splicing of genes involved in transcription and RNA processing
physiological function
m6A RNA methylation by METTL3 regulates heat shock protein gene expression
physiological function
methylation of adenosine at the N6 position by methyltransferase like 3 (METTL3)-METTL14 complex post-transcriptionally regulates hepatic P450s expression
physiological function
Mettl3-mediated m6A RNA methylation regulates the fate of bone marrow mesenchymal stem cells and osteoporosis. Mettl3 overexpression in mesenchymal stem cells protects the mice from estrogen deficiency-induced osteoporosis. Parathyroid hormone/Pth1r (parathyroid hormone receptor-1) signaling axis is an important downstream pathway for m6A regulation in mesenchymal stem cells
physiological function
Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation and function. Role for Mettl3-mediated m6A modification in increasing translation of certain immune transcripts for physiological promotion of dendritic cell activation and dendritic cell-based T cell response. Mettl3-mediated m6A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhances their translation in dendritic cells for stimulating T cell activation, and strengthening TLR4/NF-kappaB signaling-induced cytokine production
physiological function
METTL3-mediated N6-methyladenosine mRNA modification enhances long-term memory consolidation
physiological function
Mettl3-Mettl14 methyltransferase complex regulates the quiescence of adult hematopoietic stem cells. It functions through promoting the expression of genes that maintain hematopoietic stem cell quiescence
physiological function
-
overexpression of the enzyme significantly promotes hepatocellular carcinoma growth both in vitro and in vivo. The enzyme represses suppressor of cytokine signalling 2 expression in hepatocellular carcinoma through an N6-methyladenosine-reader protein YTHDF2-dependent mechanism
physiological function
the enzyme (METTL3) contributes to transforming growth factor-beta-induced epithelial-mesenchymal transition of lung cancer cells through the regulation of JUNB
physiological function
the enzyme (METTL3) cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-kappaB signaling. METTL3 positively regulates expression of MYD88, a critical upstream regulator of NF-kappaB signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-kappaB, a repressor of osteogenesis, and therefore suppressing osteogenic progression. The METTL3-mediated m6A methylation is dynamically reversed by the demethylase ALKBH5
physiological function
the enzyme (METTL3) inhibits hepatic insulin sensitivity via N6-methyladenosine modification of Fasn mRNA and promoting fatty acid metabolism
physiological function
-
the enzyme (METTL3) interacts with viral RNA-dependent RNA polymerase 3D and induces enhanced sumoylation and ubiquitination of the 3D polymerase that boosts viral replication. The host m6A modification complex interacts with viral proteins to modulate enterovirus 71 (EV71) replication
physiological function
the enzyme (METTL3) is involved in RNA metabolism through N6-methyladenosine modification. The oncoprotein HBXIP up-regulates METTL3 by inhibiting the expression of tumor suppressor let-7g in breast cancer. METTL3 increases the expression of HBXIP, forming a positive feedback loop of HBXIP/let-7g/METTL3/HBXIP in breast cancer cells
physiological function
the enzyme (METTL3) promotes osteosarcoma progression by regulating the m6A level of lymphoid enhancer binding factor 1 (LEF1) and activating Wnt/beta-catenin signaling pathway
physiological function
the enzyme (METTL3) promotes pancreatic cancer cell proliferation and invasion. High METTL3 expression is associated with high pathological stage. Survival is better in patients with low METTL3 expression compared with those with high MTTL3 expression
physiological function
-
the enzyme interacts with viral RNA-dependent RNA polymerase 3D and induces enhanced sumoylation and ubiquitination of the 3D polymerase that boosts viral replication
physiological function
-
the enzyme is essential for rice male gametogenesis
physiological function
the enzyme METTL3 controls cardiac homeostasis, function, stress responses and hypertrophy
physiological function
the enzyme plays a key role of m6A in governing haematopoietic stem cell differentiation
physiological function
the enzyme promotes translation of certain mRNAs including epidermal growth factor receptor and the Hippo pathway effector TAZ in human cancer cells. The enzyme enhances translation of target mRNAs by recruiting eIF3 to the translation initiation complex. The enzyme promotes growth, survival, and invasion of human lung cancer cells
physiological function
the RNA methyltransferase complex of WTAP, METTL3, and METTL14 regulates mitotic clonal expansion in adipogenesis
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RNA N6-methyladenosine methylation in post-transcriptional gene expression regulation
Genes Dev.
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1343-1355
2015
Arabidopsis thaliana, Danio rerio, Saccharomyces cerevisiae, Drosophila melanogaster, Mus musculus
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Homo sapiens
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Homo sapiens (Q86U44 and Q9HCE5)
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Mammalian WTAP is a regulatory subunit of the RNA N6-methyladenosine methyltransferase
Cell Res.
24
177-189
2014
Danio rerio (F1R777), Danio rerio, Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
brenda
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21
290-297
2016
Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
brenda
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NSUN2-mediated m5C methylation and METTL3/METTL14-mediated m6A methylation cooperatively enhance p21 translation
J. Cell. Biochem.
118
2587-2598
2017
Homo sapiens (Q86U44 and Q9HCE5)
brenda
Feng, Z.; Li, Q.; Meng, R.; Yi, B.; Xu, Q.
METTL3 regulates alternative splicing of MyD88 upon the lipopolysaccharide-induced inflammatory response in human dental pulp cells
J. Cell. Mol. Med.
22
2558-2568
2018
Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
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The m(6)A methyltransferase METTL3 promotes translation in human cancer cells
Mol. Cell
62
335-345
2016
Homo sapiens (Q86U44), Homo sapiens
brenda
Wang, P.; Doxtader, K.A.; Nam, Y.
Structural basis for cooperative function of Mettl3 and Mettl14 methyltransferases
Mol. Cell
63
306-317
2016
Homo sapiens (Q86U44 and Q9HCE5)
brenda
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A METTL3-METTL14 complex mediates mammalian nuclear RNA N6-adenosine methylation
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10
93-95
2014
Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
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Structural basis of N(6)-adenosine methylation by the METTL3-METTL14 complex
Nature
534
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2016
Homo sapiens (Q86U44 and Q9HCE5)
brenda
Patil, D.P.; Chen, C.K.; Pickering, B.F.; Chow, A.; Jackson, C.; Guttman, M.; Jaffrey, S.R.
m(6)A RNA methylation promotes XIST-mediated transcriptional repression
Nature
537
369-373
2016
Homo sapiens (Q86U44), Homo sapiens
brenda
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SUMOylation of the m6A-RNA methyltransferase METTL3 modulates its function
Nucleic Acids Res.
46
5195-5208
2018
Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
brenda
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Solution structure of the RNA recognition domain of METTL3-METTL14 N6-methyladenosine methyltransferase
Protein Cell
10
272-284
2018
Homo sapiens (Q86U44 and Q9HCE5)
brenda
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m6A mRNA methylation facilitates resolution of naive pluripotency toward differentiation
Science
347
1002-1006
2015
Mus musculus (Q8C3P7), Mus musculus
brenda
Miao, W.; Chen, J.; Jia, L.; Ma, J.; Song, D.
The m6A methyltransferase METTL3 promotes osteosarcoma progression by regulating the m6A level of LEF1
Biochem. Biophys. Res. Commun.
516
719-725
2019
Homo sapiens (Q86U44), Homo sapiens
brenda
Xie, W.; Ma, L.; Xu, Y.; Wang, B.; Li, S.
METTL3 inhibits hepatic insulin sensitivity via N6-methyladenosine modification of Fasn mRNA and promoting fatty acid metabolism
Biochem. Biophys. Res. Commun.
518
120-126
2019
Mus musculus (Q8C3P7), Mus musculus
brenda
Wanna-Udom, S.; Terashima, M.; Lyu, H.; Ishimura, A.; Takino, T.; Sakari, M.; Tsukahara, T.; Suzuki, T.
The m6A methyltransferase METTL3 contributes to transforming growth factor-beta-induced epithelial-mesenchymal transition of lung cancer cells through the regulation of JUNB
Biochem. Biophys. Res. Commun.
524
150-155
2020
Homo sapiens (Q86U44)
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Nakano, M.; Ondo, K.; Takemoto, S.; Fukami, T.; Nakajima, M.
Methylation of adenosine at the N6 position post-transcriptionally regulates hepatic P450s expression
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171
113697
2020
Homo sapiens (Q86U44 and Q9HCE5), Homo sapiens
brenda
Cai, X.; Wang, X.; Cao, C.; Gao, Y.; Zhang, S.; Yang, Z.; Liu, Y.; Zhang, X.; Zhang, W.; Ye, L.
HBXIP-elevated methyltransferase METTL3 promotes the progression of breast cancer via inhibiting tumor suppressor et-7g
Cancer Lett.
415
11-19
2018
Homo sapiens (Q86U44)
brenda
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Human MettL3-MettL14 complex is a sequence-specific DNA adenine methyltransferase active on single-strand and unpaired DNA in vitro
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63
2019
Homo sapiens (Q86U44 and Q9HCE5)
brenda
Selberg, S.; Blokhina, D.; Aatonen, M.; Koivisto, P.; Siltanen, A.; Mervaala, E.; Kankuri, E.; Karelson, M.
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3762-3771
2019
Homo sapiens (Q86U44)
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Zhang, Z.; Wang, M.; Xie, D.; Huang, Z.; Zhang, L.; Yang, Y.; Ma, D.; Li, W.; Zhou, Q.; Yang, Y.G.; Wang, X.J.
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1050-1061
2018
Mus musculus (Q8C3P7), Mus musculus
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952-954
2018
Mus musculus (Q8C3P7 and Q3UIK4)
brenda
Dorn, L.E.; Lasman, L.; Chen, J.; Xu, X.; Hund, T.J.; Medvedovic, M.; Hanna, J.H.; van Berlo, J.H.; Accornero, F.
The N6-methyladenosine mRNA methylase METTL3 controls cardiac homeostasis and hypertrophy
Circulation
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2019
Mus musculus (Q8C3P7), Mus musculus
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RNA N6-methyladenosine methyltransferase-like 3 promotes liver cancer progression through YTHDF2-dependent posttranscriptional silencing of SOCS2
Hepatology
67
2254-2270
2018
Homo sapiens
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Homo sapiens (Q86U44), Homo sapiens (Q9HCE5)
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2020
Homo sapiens (Q86U44)
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Mus musculus (Q8C3P7 and Q3UIK4)
brenda
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21
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2019
Mus musculus (Q8C3P7)
brenda
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Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation
Nat. Commun.
10
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2019
Mus musculus (Q8C3P7)
brenda
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Nat. Commun.
9
4772
2018
Mus musculus (Q8C3P7)
brenda
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N6-methyladenosine marks primary microRNAs for processing.
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2015
Homo sapiens (Q86U44)
brenda
Wang, X.; Feng, J.; Xue, Y.; Guan, Z.; Zhang, D.; Liu, Z.; Gong, Z.; Wang, Q.; Huang, J.; Tang, C.; Zou, T.; Yin, P.
Corrigendum Structural basis of N6-adenosine methylation by the METTL3-METTL14 complex
Nature
542
260
2017
Homo sapiens
brenda
Hao, H.; Hao, S.; Chen, H.; Chen, Z.; Zhang, Y.; Wang, J.; Wang, H.; Zhang, B.; Qiu, J.; Deng, F.; Guan, W.
N6-methyladenosine modification and METTL3 modulate enterovirus 71 replication
Nucleic Acids Res.
47
362-374
2019
Chlorocebus aethiops, Chlorocebus sabaeus
brenda
Xia, T.; Wu, X.; Cao, M.; Zhang, P.; Shi, G.; Zhang, J.; Lu, Z.; Wu, P.; Cai, B.; Miao, Y.; Jiang, K.
The RNA m6A methyltransferase METTL3 promotes pancreatic cancer cell proliferation and invasion
Pathol. Res. Pract.
215
152666
2019
Homo sapiens (Q86U44), Homo sapiens
brenda
Zhang, F.; Zhang, Y.C.; Liao, J.Y.; Yu, Y.; Zhou, Y.F.; Feng, Y.Z.; Yang, Y.W.; Lei, M.Q.; Bai, M.; Wu, H.; Chen, Y.Q.
The subunit of RNA N6-methyladenosine methyltransferase OsFIP regulates early degeneration of microspores in rice.
PLoS Genet.
15
e1008120
2019
Oryza sativa
brenda
Yu, J.; Li, Y.; Wang, T.; Zhong, X.
Modification of N6-methyladenosine RNA methylation on heat shock protein expression
PLoS ONE
13
e0198604
2018
Homo sapiens (Q86U44 and Q9HCE5)
brenda