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Literature summary for 2.3.1.48 extracted from

  • Wang, Y.; Yun, C.; Gao, B.; Xu, Y.; Zhang, Y.; Wang, Y.; Kong, Q.; Zhao, F.; Wang, C.R.; Dent, S.Y.R.; Wang, J.; Xu, X.; Li, H.B.; Fang, D.
    The lysine acetyltransferase GCN5 is required for iNKT cell development through EGR2 acetylation (2017), Cell Rep., 20, 600-612 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.3.1.48

Cloned(Commentary)

Cloned (Comment) Organism
gene Kat2a, recombinant expression of FLAG-tagged enzyme in DN32.D3 cells, interaction of FLAG-tagged GCN5 with HA-tagged EGR2 in transiently transfected DN32.D3 cells by coimmunoprecipitation and immunoblotting Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of a strain of T cell-specific Gcn5 knockout (GCN5 KO) mice by breeding Lck-Cre transgenic mice with Gcn5 floxed mice. In these mice, Cre recombinase expression driven by the Lck promoter mediates Gcn5 deletion from the CD4/CD8 double-negative stage. Immunoblot analysis demonstrates that GCN5 is efficiently deleted from thymic T cells. The percentages of cells at CD4/CD8 double-positive and single-positive stages are not altered in the thymus of GCN5 KO mice. But GCN5 gene deletion results in an about 20% reduction in the total thymocyte numbers in mice. As a consequence, a similar level reduction in the absolute numbers of CD4/CD8 double-positive and single-positive cells. While a slight but statistically significant increase in the percentage of double-negative cells is observed upon Gcn5 gene deletion, their absolute number is not altered due to the reduction in total thymocytes in GCN5 KO mice. Ectopic GCN5 expression significantly enhances EGR2 acetylation without affecting total protein expression levels. Gene expression profiles in the GCN5 knockdown DN32, overview Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
acetyl-CoA + [EGR2]-L-lysine Mus musculus
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 CoA + [EGR2]-N6-acetyl-L-lysine
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 ?
acetyl-CoA + [EGR2]-L-lysine Mus musculus C57BL/6
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 CoA + [EGR2]-N6-acetyl-L-lysine
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 ?
acetyl-CoA + [protein]-L-lysine Mus musculus endogenous GCN5 and EGR2 in iNKT cells CoA + [protein]-N6-acetyl-L-lysine
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 ?
acetyl-CoA + [protein]-L-lysine Mus musculus C57BL/6 endogenous GCN5 and EGR2 in iNKT cells CoA + [protein]-N6-acetyl-L-lysine
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 ?

Organism

Organism UniProt Comment Textmining
Mus musculus Q9JHD2
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Mus musculus C57BL/6 Q9JHD2
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-

Source Tissue

Source Tissue Comment Organism Textmining
natural killer cell invariant natural killer T (iNKT) cells. Enzyme GCN5 promotes iNKT development during the maturation stage. iNKT cells undergo several well-defined developmental stages in the thymus. Dramatic accumulation of iNKT cells at the stage 0 in thymus of Gcn5 knockout mice Mus musculus
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T-lymphocyte
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 Mus musculus
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thymocyte
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 Mus musculus
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thymus
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 Mus musculus
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Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
acetyl-CoA + [EGR2]-L-lysine
-
 Mus musculus CoA + [EGR2]-N6-acetyl-L-lysine
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 ?
acetyl-CoA + [EGR2]-L-lysine
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 Mus musculus C57BL/6 CoA + [EGR2]-N6-acetyl-L-lysine
-
 ?
acetyl-CoA + [protein]-L-lysine
-
 Mus musculus CoA + [protein]-N6-acetyl-L-lysine
-
 ?
acetyl-CoA + [protein]-L-lysine endogenous GCN5 and EGR2 in iNKT cells Mus musculus CoA + [protein]-N6-acetyl-L-lysine
-
 ?
acetyl-CoA + [protein]-L-lysine
-
 Mus musculus C57BL/6 CoA + [protein]-N6-acetyl-L-lysine
-
 ?
acetyl-CoA + [protein]-L-lysine endogenous GCN5 and EGR2 in iNKT cells Mus musculus C57BL/6 CoA + [protein]-N6-acetyl-L-lysine
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 ?

Synonyms

Synonyms Comment Organism
Gcn5
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 Mus musculus
histone acetyltransferase
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 Mus musculus
Kat2A
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 Mus musculus
lysine acetyltransferase
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 Mus musculus

Cofactor

Cofactor Comment Organism Structure
acetyl-CoA
-
 Mus musculus

General Information

General Information Comment Organism
malfunction GCN5 loss leads to a modest impairment in T cell development. The generation of iNKT cells, identified by TCRbeta antibody and NK1.1 or CD1d-alphaGalCer tetramer, is largely diminished in the thymus of GCN5 KO mice. This block cannot be compensated in the periphery, as indicated by a profound decrease in iNKT cell frequencies and numbers in the spleen and liver of GCN5 KO mice. Impaired iNKT cell development is unlikely due to elevated cell death, as annexin V-positive populations of iNKT cells in the thymus, spleen, and liver are indistinguishable between wild-type and GCN5 KO mice. Dramatic accumulation of iNKT cells at the stage 0 in thymus of Gcn5 knockout mice. Phenotype, overview. GCN5 knockdown inhibits EGR2 acetylation Mus musculus
physiological function lysine acetyltransferases GCN5 is a transcription-related histone acetyltransferase. GCN5 is a specific lysine acetyltransferase of EGR2, a transcription factor required for CD1d-restricted invariant natural killer T (iNKT) cell development. The histone acetyltransferase GCN5 is essential for iNKT cell development during the maturation stage. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibits the transcription of EGR2 target genes in iNKT cells, including Runx1, PLZF, IL-2Rb, and T-bet. Therefore, GCN5-mediated EGR2 acetylation is a molecular mechanism that regulates iNKT development. GCN5 has been shown to play critical roles in a variety of important biological functions including metabolic regulation, cell growth and survival, DNA damage repair, and embryonic development. Role of GCN5 in T cell immunity, overview. GCN5 is required for the development of iNKT cells in mice. GCN5 regulates the expression of genes driving iNKT development through EGR2 Mus musculus