Literature summary for 2.4.1.144 extracted from

Gu, J.; Taniguchi, N.
Potential of N-glycan in cell adhesion and migration as either a positive or negative regulator (2008), Cell Adh. Migr., 2, 243-245.

Search for more literature for 2.4.1.144

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
UDP-D-glucose + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R	-	Homo sapiens	UDP + N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,3-(N-acetyl-beta-D-glucosaminyl-1,2-alpha-D-mannosyl-1,6)-(beta-D-glucosyl-1,4)-beta-D-mannosyl-1,4-N-acetyl-beta-D-glucosaminyl-R	-	?

Synonyms

Synonyms	Comment	Organism
GnT-III	-	Homo sapiens
N-acetylglucosaminyltransferase III	-	Homo sapiens

Expression

Organism	Comment	Expression
Homo sapiens	E-cadherin-mediated cell-cell interaction upregulates GnT-III expression, suggesting that regulation of GnT-III and E-cadherin expression may exist as a positive feedback loop	up

General Information

General Information	Comment	Organism
physiological function	integrins are modified by GnT-III, which inhibits cell migration and cancer metastasis. Overexpression of GnT-III results in an inhibition of alpha5beta1 integrin-mediated cell spreading and migration, and the phosphorylation of the focal adhesion kinase. Overexpression of GnT-III in highly metastatic melanoma cells reduces beta1, six branching in cell-surface N-glycans and increases bisected N-glycans. GnT-III is an antagonistic of GnT-V, contributing to the suppression of cancer metastasis, overexpression of GnT-III inhibits GnT-V-induced cell migration. Overexpression of GnT-III slows E-cadherin turnover, resulting in increased E-cadherin expression on the surface of B16 melanoma cells	Homo sapiens

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Release 2023.1 (January 2023)