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Literature summary for 2.4.1.102 extracted from
- Small-molecule inhibition of GCNT3 disrupts mucin biosynthesis and malignant cellular behaviors in pancreatic cancer (2016), Cancer Res., 76, 1965-1974.
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| gene GCNT3 expression analysis in pancreatic cancer and in healthy pancreatic tissue, gene expression profiling and transcriptome analysis | Homo sapiens |
| gene GCNT3 expression analysis in pancreatic cancer and in healthy pancreatic tissue, gene expression profiling and transcriptome analysis | Mus musculus |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | p48Cre/+-LSL-KrasG12D+þ GEM with Kras mutations display significant dysregulation of EGF receptor and upregulation of mucin biosynthesis in PanIN lesions and pancreatic ductal adenocarcinoma, genotyping | Mus musculus |
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| talniflumate | selectively binds to enzyme GCNT3 via three notable hydrogen bonds between talniflumate and GCNT3. Synthesis and in silico small molecular docking simulation, overview | Homo sapiens |  |
| talniflumate | selectively binds to enzyme GCNT3 via three notable hydrogen bonds between talniflumate and GCNT3. Synthesis and in silico small molecular docking simulation, overview | Mus musculus | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | O95395 | - |
- |
| Mus musculus | Q5JCT0 | LSL-KrasG12D/+ and p48Cre/+ mice | - |
| Mus musculus C57BL/6 | Q5JCT0 | LSL-KrasG12D/+ and p48Cre/+ mice | - |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| BxPC-3 cell | - |
Homo sapiens | - |
| MiaPaCa cell | - |
Homo sapiens | - |
| additional information | human pancreatic cancer tissue array consisting of 90 cases of tumor and matched normal adjacent tissue with survival data, overview | Homo sapiens | - |
| additional information | transcriptome analysis in pacreatic carcinomas and healthy tissues | Mus musculus | - |
| PANC-1 cell | - |
Homo sapiens | - |
| pancreas | - |
Homo sapiens | - |
| pancreas | - |
Mus musculus | - |
| pancreatic cancer cell | - |
Homo sapiens | - |
| pancreatic cancer cell | genetically engineered Kras-driven mouse pancreatic tumors | Mus musculus | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| UDP-N-acetyl-alpha-D-glucosamine + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R | - |
Homo sapiens | UDP + beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl-R | - |
? | |
| UDP-N-acetyl-alpha-D-glucosamine + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R | - |
Mus musculus | UDP + beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl-R | - |
? | |
| UDP-N-acetyl-alpha-D-glucosamine + beta-D-galactosyl-(1->3)-N-acetyl-alpha-D-galactosaminyl-R | - |
Mus musculus C57BL/6 | UDP + beta-D-galactosyl-(1->3)-[N-acetyl-beta-D-glucosaminyl-(1->6)]-N-acetyl-alpha-D-galactosaminyl-R | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| core 2 beta-1,6 N-acetylglucosaminyltransferase | - |
Homo sapiens |
| core 2 beta-1,6 N-acetylglucosaminyltransferase | - |
Mus musculus |
| gcnt3 | - |
Homo sapiens |
| gcnt3 | - |
Mus musculus |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Homo sapiens | inhibitor talniflumate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro | down |
| Mus musculus | inhibitor talniflumate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro | down |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | aberrant GCNT3 expression is associated with increased mucin production, aggressive tumorigenesis, and reduced patient survival, and CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells reduces proliferation and spheroid formation. Inhibitor talniflumate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro | Homo sapiens |
| malfunction | in mouse pancreatic cancer tumors, GCNT3 103fold upregulation is correlated with increased expression of mucins by 5-87fold. Inhibitor talniflumate alone and in combination with low-dose gefitinib reduced GCNT3 expression, leading to the disrupted production of mucins in vivo and in vitro. CRISPR GCNT3-KO leads to reduced cell viability and spheroid formation | Mus musculus |
| physiological function | the mucin-synthesizing core 2 beta-1,6 N-acetylglucosaminyltransferase (GCNT3/C2GNT) plays a significant role in mucin biosynthesis | Mus musculus |
| physiological function | the mucin-synthesizing core 2 beta-1,6 N-acetylglucosaminyltransferase (GCNT3/C2GNT) plays a significant role in mucin biosynthesis. Correlation between GCNT3 expression and patient survival in human pancreatic cancer | Homo sapiens |
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