Literature summary for 6.3.1.2 extracted from

Sohn, B.H.; Park, I.Y.; Shin, J.H.; Yim, S.Y.; Lee, J.S.
Glutamine synthetase mediates sorafenib sensitivity in beta-catenin-active hepatocellular carcinoma cells (2018), Exp. Mol. Med., 50, e421 .

Search for more literature for 6.3.1.2

Protein Variants

Protein Variants	Comment	Organism
additional information	generation of glutamine synthetase-silenced Hep-3B cells by transduction with two independent shRNAs, and glutamine synthetase-overexpressing SK-Hep-1 cells	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P15104	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
HEP-3B cell	-	Homo sapiens	-
Hep-G2 cell	-	Homo sapiens	-
hepatocellular carcinoma cell	-	Homo sapiens	-

Expression

Organism	Comment	Expression
Homo sapiens	beta-catenin regulates the expression of glutamine synthetase	additional information

General Information

General Information	Comment	Organism
malfunction	depletion of the enzyme in Hep-3B cells by transduction with two independent shRNAs reduces LC3-II formation. Conversely, exogenous enzyme overexpression increases autophagic activity in SK-Hep1 cells. Glutamine synthetase (GS) overexpression significantly increases sorafenib sensitivity in hepatocellular carcinoma cells	Homo sapiens
physiological function	glutamine synthetase-mediated autophagy explains the high sensitivity of beta-catenin-active hepatocellular carcinoma cells to sorafenib. beta-Catenin regulates the expression of glutamine synthetase and triggers a series of metabolic changes leading to induction of autophagy in hepatocellular carcinoma cells. Autophagy in beta-catenin-active Hep-3B and Hep-G2 cells is mediated by glutamine synthetase, as silencing of glutamine synthetase significantly reduced autophagic activity	Homo sapiens

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)