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Literature summary for 3.6.4.13 extracted from

  • Szappanos, D.; Tschismarov, R.; Perlot, T.; Westermayer, S.; Fischer, K.; Platanitis, E.; Kallinger, F.; Novatchkova, M.; Lassnig, C.; Mueller, M.; Sexl, V.; Bennett, K.L.; Foong-Sobis, M.; Penninger, J.M.; Decker, T.
    The RNA helicase DDX3X is an essential mediator of innate antimicrobial immunity (2018), PLoS Pathog., 14, e1007397 .
    View publication on PubMedView publication on EuropePMC

Cloned(Commentary)

Cloned (Comment) Organism
X-chromosome-encoded RNA helicase DDX3X Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of Ddx3xfl/fl mice, analysis of DDX3X and DDX3Y activity in fibroblasts from gene-targeted mice. Mouse embryonic fibroblasts (MEFs) derived from female Ddx3xfl/fl CreERT2 mice are treated with 4-OHT to delete Ddx3x. Innate immunity of DDX3X-deficient cells and of Ddx3xfl/y Vav-iCre mice is analyzed, overview. Mice lacking DDX3X in hematopoietic cells have reduced numbers of lymphocytes and natural killer cells. Mice lacking DDX3X in the hematopoietic system produce reduced amounts of serum IL-12 and IFNgamma after Listeria monocytogenes infection compromising the immune response of macrophages Mus musculus

Localization

Localization Comment Organism GeneOntology No. Textmining
nucleolus
-
Mus musculus 5730
-

Metals/Ions

Metals/Ions Comment Organism Structure
Mg2+ required Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + H2O Mus musculus
-
ADP + phosphate
-
?

Organism

Organism UniProt Comment Textmining
Mus musculus Q62167
-
-

Source Tissue

Source Tissue Comment Organism Textmining
embryonic fibroblast MEF, from female and male mice Mus musculus
-
hematopoietic cell
-
Mus musculus
-
macrophage
-
Mus musculus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + H2O
-
Mus musculus ADP + phosphate
-
?

Synonyms

Synonyms Comment Organism
ATP-dependent RNA helicase DDX3X UniProt Mus musculus
DDX3
-
Mus musculus
DDX3X
-
Mus musculus
DEAD box RNA helicase
-
Mus musculus
DExD/H box RNA helicase
-
Mus musculus
RNA helicase DDX3X
-
Mus musculus

General Information

General Information Comment Organism
malfunction mice lacking DDX3X during hematopoiesis show an altered leukocyte composition in bone marrow and spleen and a striking inability to combat infection with Listeria monocytogenes. Mice lacking DDX3X in the hematopoietic system show alterations of bone marrow and splenic cell populations. Alterations in innate immune responses result from decreased effector cell availability and function as well as a sex-dependent impairment of cytokine synthesis. Production of important cytokines such as IL12 or IFNgamma is reduced, DDX3X-deficient macrophages show reduced ability to restrict Listeria monocytogenes growth. Owing to partial redundancy with its close Y chromosomal homologue, DDX3Y, the observed effects differ between mouse sexes. DDX3Y, either alone or together with additional Y-chromosomal genes, partially compensates for the loss of the Ddx3x gene, as homozygous female cells and mice show more severe loss-of-function phenotypes Mus musculus
metabolism pivotal and sex-specific role for the heterosomal isoforms of the DEAD box RNA helicase DDX3 in the immune system. Mechanism of DDX3X action, redundancy with DDX3Y, overview Mus musculus
physiological function the RNA helicase DDX3X is an essential mediator of innate antimicrobial immunity, essential contribution of a non-RLR DExD/H RNA helicase to innate immunity. Enzyme DDX3 is an interactor of the S/T kinase TBK1 which regulates the production of type I Interferons (IFN-I), contributions of DDX3X to hematopoiesis. DDX3X is critically involved in enhancing the expression of numerous antimicrobial genes. DDX3X may contribute to sex differences in immunity to pathogens and inflammatory disease. Besides its role in the regulation of the TBK1-IRF3 axis, DDX3X controls the NFkappaB signaling pathway and has a profound impact on inflammatory cytokine production. DDX3Y, either alone or together with additional Y-chromosomal genes, partially compensates for the loss of the Ddx3x gene, as homozygous female cells and mice show more severe loss-of-function phenotypes Mus musculus