GLS (Glutaminase)

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URI: http://hdl.handle.net/2042/70527  |   DOI : https://doi.org/10.4267/2042/70527
Title: GLS (Glutaminase)
Author: Campos-Sandoval, José A.; Martin-Rufián, Mercedes; Márquez, Javier
Abstract: After metabolic reprogramming, many cancer cells become glutamine addicted, that is, they depend on a high consumption of this amino acid for their survival and proliferation. Glutaminase catalyzes the stoichiometric conversion of L-glutamine to L-glutamate and ammonium ions, the first step of glutaminolysis. GLS gene encodes two isoforms, known as kidney-type glutaminase (KGA) and glutaminase C (GAC). Upregulation of GLS is a common feature of many tumors and, in recent years, this enzyme and its interacting partners have attracted much attention as potential new targets for cancer therapy. Considerable effort is being devoted towards the development of small-molecule inhibitors of GLS.
Subject: Glutaminase; glutamine addiction; anticancer therapy; BPTES; CB-839; compound 968; breast cancer; colorectal cancer; glioblastoma; hepatocellular carcinoma; leukemia; lung cancer; melanoma; ovarian cancer; prostate cancer; Genes Section; Adult; Aged; Animals; Big Data; CRISPR-Cas Systems; Carcinoma, Hepatocellular/drug therapy/genetics/metabolism/*pathology; Cell Line, Tumor; Female; Gene Expression Regulation, Neoplastic; Gene Knockout Techniques; Glutaminase/antagonists & inhibitors/*genetics/*metabolism; Hep G2 Cells; Humans; Liver Neoplasms/drug therapy/genetics/metabolism/*pathology; Male; Mice; Middle Aged; Neoplasm Transplantation; Neoplastic Stem Cells/drug effects/*metabolism; Prognosis; Reactive Oxygen Species/*metabolism
Publisher: ARMGHM - Atlas Génétique des Cancers
Date: 2019

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