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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.


Glutaminase, LGA
catalyzes the conversion of L-glutamine and H2O to L-glutamate and NH3 in glutamine catabolism [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, CAN, HAD, V1a, AGE
Papers on Glutaminase
Analysis of specific proteolytic digestion of the peptidoglutaminase-asparaginase of koji molds.
Koyama et al., Noda, Japan. In J Biosci Bioeng, 30 Sep 2014
AsGahB, a peptidoglutaminase-asparaginase acting as the main glutaminase in Aspergillus sojae, was previously purified from the cytoplasm of overexpressing strains.
The glutaminase activity of L-asparaginase is not required for anticancer activity against ASNS-negative cells.
Weinstein et al., Houston, United States. In Blood, Jul 2014
Its mechanism of action, however, is still poorly understood, in part because of its dual asparaginase and glutaminase activities.
Celiac disease or non-celiac gluten sensitivity? An approach to clinical differential diagnosis.
Kelly et al., Boston, United States. In Am J Gastroenterol, May 2014
The positive likelihood ratio for diagnosis of CD of a >2× upper limit of normal IgA trans-glutaminase antibody (tTG) or IgA/IgG deaminated gliadan peptide antibody (DGP) with clinical response to GFD was 130 (confidence interval (CI): 18.5-918.3).
Effects of acute versus repeated cocaine exposure on the expression of endocannabinoid signaling-related proteins in the mouse cerebellum.
Suárez et al., Málaga, Spain. In Front Integr Neurosci, Dec 2013
In addition, we analyzed the gene expression of relevant components of the glutamate signaling system [glutamate synthesizing enzymes liver-type glutaminase isoform (LGA) and kidney-type glutaminase isoform (KGA), metabotropic glutamatergic receptor (mGluR3/5), NMDA-ionotropic glutamatergic receptor (NR1/2A/2B/2C) and AMPA-ionotropic receptor subunits (GluR1/2/3/4)] and the gene expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, because noradrenergic terminals innervate the cerebellar cortex.
Fetal growth in relation to maternal and fetal IGF-axes: a systematic review and meta-analysis.
Lashen et al., Libya. In Acta Obstet Gynecol Scand, Sep 2013
Cord IGF-I (p < 0.0001) and IGFBP-3 (p = 0.003) were significantly higher in large-for-gestational age (LGA) than appropriate-for-gestational age (AGA) babies.
Actinobacteriological research in India.
Kamat et al., Taleigao, India. In Indian J Exp Biol, Aug 2013
Research on enzymes mostly covered lipases, amylases, proteases, endoglucanases, a-galactosidases, pectin lyases, xylanases, L-asparaginases, L-glutaminase and cellulases.
Targeting the glutamatergic system for the treatment of HIV-associated neurocognitive disorders.
Slusher et al., Baltimore, United States. In J Neuroimmune Pharmacol, Jun 2013
One alternative to direct receptor blockade has been the inhibition of enzymes responsible for the production of glutamate such as glutaminase and glutamate carboxypeptidase II.
Effect of different maternal metabolic characteristics on fetal growth in women with gestational diabetes mellitus.
Jamal et al., Tehrān, Iran. In Iran J Reprod Med, Apr 2013
After adjustment for confounding variables, maternal hypertriglyceridemia remained as a significant risk factor for delivering large for gestational age (LGA) newborns (p=0.04); and according to spearman test the increase of TG level was correlated with increase of insulin resistance and HOMA-IR (p<0.001,
In vivo HIF-mediated reductive carboxylation is regulated by citrate levels and sensitizes VHL-deficient cells to glutamine deprivation.
Iliopoulos et al., United States. In Cell Metab, Apr 2013
Lastly, HIF rendered VHL-deficient cells sensitive to glutamine deprivation in vitro, and systemic administration of glutaminase inhibitors suppressed the growth of RCC cells as mice xenografts.
Cancer cell metabolism: implications for therapeutic targets.
Lee et al., Seoul, South Korea. In Exp Mol Med, 2012
In this review, we will discuss dysregulated and reprogrammed cancer metabolism followed by clinical relevance of the metabolic enzymes, such as hexokinase, phosphofructokinase, pyruvate kinase M2, lactate dehydrogenase, pyruvate dehydrogenase kinase and glutaminase.
Targeting cellular metabolism to improve cancer therapeutics.
Tan et al., Chengdu, China. In Cell Death Dis, 2012
From this unique angle, this review article will discuss the relationship between dysregulated cellular metabolism and cancer drug resistance and how targeting of metabolic enzymes, such as glucose transporters, hexokinase, pyruvate kinase M2, lactate dehydrogenase A, pyruvate dehydrogenase kinase, fatty acid synthase and glutaminase can enhance the efficacy of common therapeutic agents or overcome resistance to chemotherapy or radiotherapy.
Structural basis for the allosteric inhibitory mechanism of human kidney-type glutaminase (KGA) and its regulation by Raf-Mek-Erk signaling in cancer cell metabolism.
Sivaraman et al., Singapore, Singapore. In Proc Natl Acad Sci U S A, 2012
KGA activity in cells is stimulated by EGF, and KGA associates with all three kinase components of the Raf-1/Mek2/Erk signaling module.
Synaptic underpinnings of altered hippocampal function in glutaminase-deficient mice during maturation.
Rayport et al., New York City, United States. In Hippocampus, 2012
In wild-type (WT) mice, GLS1 gene expression was highest in the hippocampus and cortex, where it was reduced by about 50% in Glutaminase-deficient mice.
Proteomic analysis identifies dysfunction in cellular transport, energy, and protein metabolism in different brain regions of atypical frontotemporal lobar degeneration.
Bahn et al., Cambridge, United Kingdom. In J Proteome Res, 2012
A protein encoded by this locus was found to be differentially expressed in postmortem brains from patients with atypical frontotemporal lobar degeneration.
The metabolic profile of tumors depends on both the responsible genetic lesion and tissue type.
Bishop et al., San Francisco, United States. In Cell Metab, 2012
Inhibition of Gls1 kills lung cancer cells that overexpress MYC and catabolize glutamine.
Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells.
Dang et al., Baltimore, United States. In Cell Metab, 2012
The essential role of glutamine metabolism in cell survival and proliferation under hypoxia and glucose deficiency makes them susceptible to the glutaminase inhibitor BPTES and hence could be targeted for cancer therapy.
Interferon-α regulates glutaminase 1 promoter through STAT1 phosphorylation: relevance to HIV-1 associated neurocognitive disorders.
Zheng et al., Omaha, United States. In Plos One, 2011
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.
Mammalian glutaminase Gls2 gene encodes two functional alternative transcripts by a surrogate promoter usage mechanism.
Márquez et al., Málaga, Spain. In Plos One, 2011
Study demonstrated expression of alternative transcripts of the mammalian Gls2 gene. Transcriptional mechanisms giving rise to GLS2 variants and isolation of novel GLS2 transcripts in human, rat and mouse are presented.
Targeting mitochondrial glutaminase activity inhibits oncogenic transformation.
Cerione et al., Ithaca, United States. In Cancer Cell, 2010
We identify the target of this inhibitor to be the metabolic enzyme glutaminase, which catalyzes the hydrolysis of glutamine to glutamate.
c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.
Dang et al., Baltimore, United States. In Nature, 2009
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
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