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Literature summary for 2.4.1.122 extracted from

  • Chou, C.H.; Huang, M.J.; Liao, Y.Y.; Chen, C.H.; Huang, M.C.
    C1GALT1 seems to promote in vitro disease progression in ovarian cancer (2017), Int. J. Gynecol. Cancer, 27, 863-871 .
    View publication on PubMed
Search for more literature for 2.4.1.122

Inhibitors

Inhibitors Comment Organism Structure
itraconazole mediates its suppressive effects on malignant phenotypes and EGFR activity by inhibiting C1GALT1 in HNSCC cells. C1GALT1 inhibitor itraconazole can also suppress tumor growth Homo sapiens
additional information homology modeling and docking simulation with potential C1GALT1 inhibitors Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor Homo sapiens
-
 UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
 ?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R Homo sapiens
-
 UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q9NS00
-
-

Posttranslational Modification

Posttranslational Modification Comment Organism
additional information the effect of itraconazole on C1GALT1 protein levels might be through posttranslational modifications, analysis of mechanism by which itraconazole promotes C1GALT1 degradation Homo sapiens

Source Tissue

Source Tissue Comment Organism Textmining
head and neck squamous cell carcinoma cell C1GALT1 expression is upregulated in HNSCC tumors Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
 Homo sapiens UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-epidermal growth factor receptor
-
 ?
UDP-alpha-D-galactose + N-acetyl-alpha-D-galactosaminyl-R
-
 Homo sapiens UDP + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R
-
 ?

Synonyms

Synonyms Comment Organism
C1GALT1
-
 Homo sapiens
core 1 beta1,3-galactosyltransferase
-
 Homo sapiens

Expression

Organism Comment Expression
Homo sapiens real-time RT-PCR analysis shows that C1GALT1 messenger RNA expression is not significantly affected, implying that the effect of itraconazole on C1GALT1 protein levels might be through posttranslational modifications. Itraconazole increases ubiquitinated C1GALT1. C1GALT1 degradation induced by itraconazole is primarily through the proteasomal degradation pathway additional information

General Information

General Information Comment Organism
malfunction C1GALT1 overexpression enhances HNSCC cell viability, migration, and invasion, which can be reversed by erlotinib. Silencing of C1GALT1 suppresses the malignant behavior both in vitro and in vivo. C1GALT1 knockdown decreases the EGFR signaling in SAS, OEC-M1, and FaDu cells. Decreased C1GALT1 causes accumulation of Tn antigens Homo sapiens
physiological function core 1 beta1,3-galactosyltransferase (C1GALT1) controls the crucial step of GalNAc-type O-glycosylation and is overexpressed in various human malignancies with a role in head and neck squamous cell carcinoma (HNSCC). Enzyme C1GALT1 seems to promote in vitro disease progression in ovarian cancer. C1GALT1 modifies O-glycans on epidermal growth factor receptor (EGFR). C1GALT1 regulates phosphorylation, EGF-binding affinity, and O-glycosylation of EGFR to enhance malignant phenotypes in HNSCC cells. C1GALT1 regulates EGF-binding affinity of EGFR in HNSCC cells. C1GALT1 transfers galactose to Tn antigen to form T antigen. C1GALT1 is overexpressed in head and neck squamous cell carcinoma (HNSCC) tumors and high C1GALT1 expression predicts poor prognosis Homo sapiens