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Literature summary for 2.4.1.102 extracted from

  • Mardahl, M.; Schroeter, M.F.; Engelbert, D.; Pink, M.; Sperandio, M.; Hamann, A.; Syrbe, U.
    Core 2 beta1,6-N-acetylglucosaminyltransferase-I, crucial for P-selectin ligand expression is controlled by a distal enhancer regulated by STAT4 and T-bet in CD4+ T helper cells 1 (2016), Mol. Immunol., 77, 132-140 .
    View publication on PubMed
Search for more literature for 2.4.1.102

Cloned(Commentary)

Cloned (Comment) Organism
gene Gcnt1, identification of the Gcnt1 promoter, identification of a putative distal regulatory element of the Gcnt1 gene by mapping H3K4me2 and H3K27me3 across the Gcnt1 locus, sequence comparisons, phylogenetic analysis of promoters, overview. The distal regulatory region is an enhancer forGcnt1 for which STAT4 is functionally important. Prolonged T-bet binding to the Gcnt1 enhancer Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q02742
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Source Tissue

Source Tissue Comment Organism Textmining
helper T-lymphocyte
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 Homo sapiens
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additional information STAT4 controls Gcnt1 expression in Th1 cells, several several conserved and non-conserved predicted STAT4 binding sites are determined. Functional importance of STAT4 for P-lig induction and specifically on the enhancer as a transactivating factor. Prolonged T-bet binding to the Gcnt1 enhancer Homo sapiens
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skin
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 Homo sapiens
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T-lymphocyte
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 Homo sapiens
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Th1 cell
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
C2GlcNAcT-I
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 Homo sapiens
core 2 beta1,6-N-acetylglucosaminyltransferase-I
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 Homo sapiens
GCNT1
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 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens STAT4 controls Gcnt1 expression in Th1 cells, several conserved and non-conserved predicted STAT4 binding sites are determined additional information

General Information

General Information Comment Organism
malfunction Gcnt1-/-Th1 cells lacking C2-GlcNAcT-I expression show impaired P-lig expression similar to Fut4+7-/-Th1 cells. In contrast to impaired P-lig expression,Gcnt1-/-and Fut4 +7-/- maintain their inflammatory competence as assessed by IFNgamma expression. Functional relevance of Gcnt1 deficiency in CD4+T cells in vivo. In line with a lack of Gcnt1 transcription, naive T cells exhibit a closed histone configuration with lowH3K4me2 and prominent H3K27me3 marks. The active H3K4me2 mark in this region increases in a time-dependent manner during Th1 differentiation Homo sapiens
physiological function core 2 beta1,6-N-acetylglucosaminyltransferase-I (C2GlcNAcT-I) is crucial for inflammatory homing of Th1 cells to the skin in vivo, analysis of molecular regulation of the enzyme encoded by gene Gcnt1 in CD4+T helper cells, overview. C2-GlcNAcT-I, encoded by Gcnt1, is essential for generation of P-lig and recruitment of Th1 cells into a skin-DTH reaction. Gcnt1 transcription and subsequent P-lig induction in Th1 cells is governed by binding of STAT4 and T-bet to a distal enhancer and further regulated by epigenetic marks such as H3K27me3. T-cells cultured in vitro under Th1 conditions, i.e. supplemented with IL-12, IFN gamma, and anti-IL-4, but not under Th2 (IL-4, anti-IL-12, anti-IFN gamma) or Th0 (anti-12, anti-IFNgamma and anti-IL-4) conditions, express P-lig, which corresponds to differential Gcnt1 but not Fut7 mRNA expression. STAT4 controls Gcnt1 expression in Th1 cells, several several conserved and non-conserved predicted STAT4 binding sites are determined. Functional importance of STAT4 for P-lig induction and specifically on the enhancer as a transactivating factor. Prolonged T-bet binding to the Gcnt1 enhancer Homo sapiens