Recombinant Human Glutaminase kidney isoform, mitochondrial (GLS), partial

1. Overexpressing glutaminase abolished the inhibitory effects of miR-1-3p on bladder cancer cell proliferation, migration, and invasion and glutaminase depletion resulted in the prolonged expression of gammaH2AX, an established biomarker for DNA damage. PMID: 30458442
2. These results reveal that GAC is post-translationally regulated by phosphorylation, which affects cellular glutamine metabolism and glutaminase-related cell phenotype. PMID: 30092248
3. In silico analysis potentially links GLS SNPs with Alzheimer disease and type 2 diabetes. PMID: 29441491
4. Del11q-positive CLL lymphocytes exhibit altered glutamine metabolism and differential response to GLS1 and glucose metabolism inhibition. PMID: 29367649
5. Overexpression of miR-513c suppresses neuroblastoma cells' migration, invasion, and proliferation. We demonstrate the glutaminase (GLS) is a direct target of miR-513c in human neuroblastoma cells. PMID: 28800318
6. the present findings enriched our knowledge by demonstrating a significant association of PKM2 and GLS1 with oxaliplatin-resistance in CRC. PMID: 28498807
7. miR-137 was decreased in melanoma tissue, and the low miR-137 levels and high glutaminase expression are independent risk factors in melanoma. miR-137 suppressed the proliferation and glutamine catabolism of melanoma cells. PMID: 29097210
8. ZIC5 positively regulated the proliferation, migration (Fig. 2), and survival (Fig. 5) of PCa and CRC cells PMID: 29032577
9. the crystal structure of full-length KGA and present a small-angle X-ray scattering model for full-length GLS2. These structures explain these proteins' compromised ability to assemble into catalytically active supra-tetrameric filaments, as previously shown for GAC. PMID: 28526749
10. GLS1 inhibition using BPTES reduced metabolic intermediates including thymidine and carbamoyl phosphate. Reduction of thymidine and carbamoyl-phosphate synthesis by BPTES treatment exacerbated pyrimidine supply by combination with 5-FU, which induced cell death synergistically in NSCLC PMID: 27338638
11. studies show that the formation of large GAC oligomers is not a pre-requisite for full enzymatic activity. They also offer a mechanism by which the binding of activators like inorganic phosphate enables the activation loop to communicate with the active site to ensure maximal rates of catalysis, and promotes the opening of the lid to achieve optimal product release. PMID: 27542409
12. Glutaminase expression in tumor cells was significantly associated with a low level of tumor-infiltrating lymphocytesand poor disease-free survival in triple-negative breast cancers presenting with lymph node metastasis and high levels of tumor-infiltrating lymphocytes. PMID: 28185053
13. Study reports that GLS1 is a direct target of miR-23a in retinal pigment epithelium cells (RPE) providing evidence for a role in maintaining RPE cell function. PMID: 27411920
14. The relative expression of microRNA-153 and glutaminase in glioblastoma versus matched non-tumor tissues showed a reverse correlation, further indicating that microRNA-153 may negatively regulate glutaminase in vivo. PMID: 28218035
15. High GLS1 expression is associated with epithelial-mesenchymal transition in cancer. PMID: 26771232
16. Data suggest that glutaminase C (GAC) inhibition maybe a potential treatment strategy for acquired erlotinib-resistant non-small cell lung cancer (NSCLC). PMID: 26575584
17. Findings indicate a role for transcription factor c-Jun as a driver of cancer cell metabolic reprogramming, and suggest that cancers overexpressing JUN may be especially sensitive to glutaminase (GLS)-targeted therapies. PMID: 27089238
18. GLS1 was identified as a potential downstream target of the miR-192/-204-HOTTIP axis in hepatocellular carcinoma. PMID: 26710269
19. Our findings support the role of the GLS long microsatellite in the development of HE; this could be important for identifying susceptible patients and for the prevention of this condition. PMID: 25880019
20. GABAergic neurons and astrocytes express Gls and Gls2 isoenzymes in nucleus and mitochondria, in addition to glutamatergic neurons PMID: 25297978
21. studies demonstrate that GLS is required for tumorigenesis and support small molecule and genetic inhibition of GLS as potential approaches for targeting the tumor cell-autonomous dependence on GLS for cancer therapy. PMID: 25915584
22. GLS1 has a key role in coupling glutaminolysis of the TCA cycle with elevated glucose uptake and consequently the growth of prostate cancer cells PMID: 25482439
23. These results suggest that the expression of GLS1 is upregulated and correlates with clinicopathological factors in colorectal cancer. PMID: 24696726
24. Silencing GLS or overexpressing GLS2 induces growth inhibition in glioma cell lines. PMID: 24276018
25. our data indicate that ErbB2 activation promotes GLS1 expression via a PI3K-Akt-independent NF-kappaB pathway in breast cancer cells, identifying another oncogenic signaling pathway which stimulates GLS1 expression PMID: 24122876
26. The rate of Glu decarboxylation into GABA by Glnase is an order of magnitude lower than that of Glutamate decarboxylase. Potential impact on the mechanistic aspects of Gln-Glu shuttle in neuroscience and glutaminolysis in tumors, is discussed. PMID: 24755074
27. STAT1 regulates human glutaminase 1 promoter activity PMID: 24086752
28. Inhibition of glutaminase selectively suppresses the growth of primary acute myeloid leukemia cells with IDH mutations. PMID: 24333121
29. A glutaminase inhibitor reduced conversion of (13)C-pyruvate to alanine. PMID: 23722553
30. HER2- type breast cancer had the highest expression of stromal GLS1, tumoral GDH, stromal GDH, and tumoral ASCT, while TNBC had the lowest tumoral GDH expression. PMID: 23507704
31. activated glutaminase C (GAC) self-assembles into a helical, fiber-like double-stranded oligomer and propose a molecular model consisting of seven tetramer copies per turn per strand interacting via the N-terminal domains PMID: 23935106
32. stromal expression of the glutamine-metabolism-related proteins GLS1, GDH, ASCT2 increases with worsening histological phyllodes tumor grade. PMID: 23636801
33. neuronal glutaminase is a potential component of neurotoxicity during inflammation and modulation of glutaminase may provide therapeutic avenues for neurodegenerative diseases. PMID: 23578284
34. NSCLC cell lines depend on Gln for glutaminolysis to a varying degree, in which the GLS1 splice variant GAC plays an essential role and is a potential target for cancer metabolism-directed therapy. PMID: 22892846
35. Data indicate that both HIV-1 infection and IFN-alpha treatment increase glutaminase 1 (GLS1) expression through STAT1 phosphorylation and by binding to the GLS1 promoter. PMID: 22479354
36. KGA activity in cells is stimulated by EGF, and KGA associates with all three kinase components of the Raf-1/Mek2/Erk signaling module. PMID: 22538822
37. Inhibition of Gls1 kills lung cancer cells that overexpress MYC and catabolize glutamine. PMID: 22326218
38. GLS1 differs from PFKFB3 in that its recognition by APC/C-Cdh1 during S phase requires the presence of both a Lys-Glu-Asn box (KEN box) and a destruction box (D box) rather than a KEN box alone. PMID: 22106309
39. first report of full-length crystal structure of a splice variant of GLS1 in presence/absence of BPTES, an allosteric inhibitor: 2 BPTES molecules bind at interface of GLS1 tetramer; appear to lock GLS1 tetramer into nonproductive conformation PMID: 22049910
40. Glutamine synthetase is a genetic determinant of cell type-specific glutamine independence in breast epithelia PMID: 21852960
41. This studt demonistrated that the genetic variation in the glutaminase gene GLS1 is related the glutamine/glutamate ratio in brain. PMID: 21457947
42. Glutaminase: a hot spot for regulation of cancer cell metabolism. PMID: 21234284
43. Data show that the ability to selectively slow growth in cells with IDH1 mutations by inhibiting glutaminase suggesting a unique reprogramming of intermediary metabolism and a potential therapeutic strategy. PMID: 21045145
44. This study identifies mutations in the gene sequence for glutaminase that are associated with development of hepatic encephalopathy in patients with cirrhosis PMID: 20820037
45. Data suggest that glutaminase is an important factor in melanoma cell proliferation. PMID: 12579526
46. human neutrophils appeared to utilize glutamine and posess the appropriate glutaminase enzyme for metabolizing glutamine. PMID: 14722097
47. possible role for intestinal glutaminase in the pathogenesis of hepatic encephalopathy PMID: 15246207
48. K glutaminase isoform is up-regulated with increased rates of proliferation in cancer cells, whereas prevalence of the L isoform seems to be related with resting or quiescent cell states PMID: 15496140
49. c-Myc transcriptionally represses miR-23a and miR-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells PMID: 19219026
50. Release of glutaminase from dysfunctional macrophages is a possible mechanism of glutaminase-mediated production of excitotoxic glutamate during the pathogenic process of human immunodeficiency virus (HIV)-1 associated dementia. PMID: 19222703

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HGNC: 4331

OMIM: 138280

KEGG: hsa:2744

STRING: 9606.ENSP00000317379

UniGene: Hs.116448