Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 2.4.1.175 extracted from

  • Adhikara, I.M.; Yagi, K.; Mayasari, D.S.; Ikeda, K.; Kitagawa, H.; Miyata, O.; Igarashi, M.; Hatakeyama, K.; Asada, Y.; Hirata, K.I.; Emoto, N.
    Chondroitin sulfate N-acetylgalactosaminyltransferase-2 deletion alleviates lipoprotein retention in early atherosclerosis and attenuates aortic smooth muscle cell migration (2019), Biochem. Biophys. Res. Commun., 509, 89-95 .
    View publication on PubMed

Application

Application Comment Organism
medicine gene ChGn-2 may serve as a plausible target to treat atherosclerotic-related diseases in humans Homo sapiens

Protein Variants

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

Localization Comment Organism GeneOntology No. Textmining
Golgi apparatus
-
Homo sapiens 5794
-
Golgi apparatus
-
Mus musculus 5794
-

Organism

Organism UniProt Comment Textmining
Homo sapiens Q8IZ52
-
-
Mus musculus Q6IQX7
-
-
Mus musculus C57BL/6J Q6IQX7
-
-

Source Tissue

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

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 2.4.1.226 Homo sapiens
More see also EC 2.4.1.226 Mus musculus

General Information

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