Application | Comment | Organism |
---|---|---|
medicine | gene ChGn-2 may serve as a plausible target to treat atherosclerotic-related diseases in humans | Homo sapiens |
Protein Variants | Comment | Organism |
---|---|---|
additional information | deletion of the ChGn-2 gene significantly reduces LDL retention in the DIT mouse model. Chondroitin sulfate N-acetylgalactosaminyltransferase-2 deletion alleviates lipoprotein retention in early atherosclerosis and attenuates aortic smooth muscle cell migration. A functional assay of ASMCs prepared from ChGn-2-/- mice displays abrogation of platelet-derived growth factor (PDGF)-mediated migration via reduced PDGF receptor phosphorylation. Evaluation of LDL retention in a diffuse intimal thickening (DIT) model using partial carotid ligation on ChGn-2/LDL receptor double knockout (ChGn-2-/-/LDLr-/-) mice | Mus musculus |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
Golgi apparatus | - |
Homo sapiens | 5794 | - |
Golgi apparatus | - |
Mus musculus | 5794 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | Q8IZ52 | - |
- |
Mus musculus | Q6IQX7 | - |
- |
Mus musculus C57BL/6J | Q6IQX7 | - |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
aortic smooth muscle cell | ASMC | Homo sapiens | - |
aortic smooth muscle cell | ASMC | Mus musculus | - |
coronary artery | - |
Homo sapiens | - |
additional information | ChGn-2 expression on early and advanced atherosclerotic lesions, overview | Homo sapiens | - |
vascular system | vascular wall | Homo sapiens | - |
vascular system | vascular wall | Mus musculus | - |
Synonyms | Comment | Organism |
---|---|---|
ChGn-2 | - |
Homo sapiens |
ChGn-2 | - |
Mus musculus |
chondroitin sulfate N-acetylgalactosaminyltransferase-2 | - |
Homo sapiens |
chondroitin sulfate N-acetylgalactosaminyltransferase-2 | - |
Mus musculus |
CHPF | - |
Homo sapiens |
More | see also EC 2.4.1.175 | Homo sapiens |
More | see also EC 2.4.1.175 | Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | chondroitin sulfate N-acetylgalactosaminyltransferase-2 deletion alleviates lipoprotein retention in early atherosclerosis and attenuates aortic smooth muscle cell (ASMC) migration through attenuating PDGFR phosphorylation. Effects of CHPF gene deletion on the development of atherosclerosis, overview | Homo sapiens |
malfunction | chondroitin sulfate N-acetylgalactosaminyltransferase-2 deletion alleviates lipoprotein retention in early atherosclerosis and attenuates aortic smooth muscle cell migration. Effects of ChGn-2 gene deletion on the development of atherosclerosis, overview | Mus musculus |
physiological function | chondroitin sulfate N-acetylgalactosaminyltransferase-2 (ChGn-2) is a vital Golgi transferase that participates in enzymatic elongation of GAGs. ChGn-2 is functionally involved in the progression of atherosclerosis both in its early and advanced stages. Crucial contributions of ChGn-2 for LDL retention in the intima. Platelet-derived growth factor (PDGF) signaling is heavily involved in the development of plaques and directly regulates SMCs via platelet-derived growth factor receptor, PDGFR-beta, phosphorylation to promote phenotypic changes including smooth muscle cell migration, enzyme chondroitin sulfate N-acetylgalactosaminyltransferase-2 has a regulatory function | Homo sapiens |
physiological function | chondroitin sulfate N-acetylgalactosaminyltransferase-2 (ChGn-2) is a vital Golgi transferase that participates in enzymatic elongation of GAGs. ChGn-2 is functionally involved in the progression of atherosclerosis both in its early and advanced stages. Crucial contributions of ChGn-2 for LDL retention in the intima. Platelet-derived growth factor (PDGF) signaling is heavily involved in the development of plaques and directly regulates SMCs via platelet-derived growth factor receptor, PDGFR-beta, phosphorylation to promote phenotypic changes including smooth muscle cell migration, enzyme chondroitin sulfate N-acetylgalactosaminyltransferase-2 has a regulatory function | Mus musculus |