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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


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
Dlx-2 and glutaminase upregulate epithelial-mesenchymal transition and glycolytic switch.
Kang et al., Pusan, South Korea. In Oncotarget, Feb 2016
Here we show that Dlx-2 also induces the expression of the crucial Gln metabolism enzyme glutaminase (GLS1), which converts Gln to glutamate.
Mitochondrial thiol modification by a targeted electrophile inhibits metabolism in breast adenocarcinoma cells by inhibiting enzyme activity and protein levels.
Landar et al., Birmingham, United States. In Redox Biol, Feb 2016
Additionally, the inhibition of glutaminolysis corresponded to decreased glutaminase C (GAC) protein levels, although other protein levels were unaffected.
ω-Amidase: an underappreciated, but important enzyme in L-glutamine and L-asparagine metabolism; relevance to sulfur and nitrogen metabolism, tumor biology and hyperammonemic diseases.
Krasnikov et al., Valhalla, United States. In Amino Acids, Jan 2016
However, another major pathway exists in mammals for the conversion of L-glutamine to α-ketoglutarate (the glutaminase II pathway) in which L-glutamine is first transaminated to α-ketoglutaramate (KGM) followed by hydrolysis of KGM to α-ketoglutarate and ammonia catalyzed by an amidase known as ω-amidase.
First trimester pregnancy-associated plasma protein-A and birth weight.
Jelliffe-Pawlowski et al., Richmond, United States. In Eur J Obstet Gynecol Reprod Biol, Jan 2016
The frequency of small or large for gestational age (SGA, ≤10%; LGA, ≥90%) versus appropriately grown for gestational age birth was examined by PAPP-A percentile.
L-asparaginase as a critical component to combat Acute Lymphoblastic Leukaemia (ALL): A novel approach to target ALL.
Mumtaz et al., Wuhan, China. In Eur J Pharmacol, Jan 2016
Moreover, an overview has also been provided in the current review regarding the contradiction among various researchers regarding the significance of the enzyme's glutaminase activity.
How microglia kill neurons.
Vilalta et al., Cambridge, United Kingdom. In Brain Res, Jan 2016
A number of mechanisms by which activated microglia kill neurons have been identified, including: (i) stimulation of the phagocyte NADPH oxidase (PHOX) to produce superoxide and derivative oxidants, (ii) expression of inducible nitric oxide synthase (iNOS) producing NO and derivative oxidants, (iii) release of glutamate and glutaminase, (iv) release of TNFα, (v) release of cathepsin B, (vi) phagocytosis of stressed neurons, and (vii) decreased release of nutritive BDNF and IGF-1.
Oncogenic Myc Induces Expression of Glutamine Synthetase through Promoter Demethylation.
Zong et al., Stony Brook, United States. In Cell Metab, Jan 2016
c-Myc is known to promote glutamine usage by upregulating glutaminase (GLS), which converts glutamine to glutamate that is catabolized in the TCA cycle.
Biochemical, Epigenetic, and Metabolic Approaches to Target IDH Mutations in Acute Myeloid Leukemia.
Emadi et al., Baltimore, United States. In Semin Hematol, Jul 2015
Other therapeutic approaches under preclinical and clinical investigation in this population include DNA methyltransferase inhibitors and agents that target glutamine metabolism through inhibition of glutaminase or depletion of serum glutamine by asparaginase products.
Clinical analysis on anti-N-methyl-D-aspartate receptor encephalitis cases: Chinese experience.
Jia et al., Beijing, China. In Int J Clin Exp Med, 2014
With diverse clinical manifestations, most patients displayed positively by NMDAR antibody test and 63.6% of them were associated with elevated CSF-lgA.
Targeting Glutamine Induces Apoptosis: A Cancer Therapy Approach.
Cui et al., China. In Int J Mol Sci, 2014
In order to be well used by cells, glutamine must be transported to cells by specific transporters and converted to glutamate by glutaminase.
Genetic Pharmacotherapy as an Early CNS Drug Development Strategy: Testing Glutaminase Inhibition for Schizophrenia Treatment in Adult Mice.
Rayport et al., New York City, United States. In Front Syst Neurosci, 2014
Here for the first time, we have implemented this strategy to address the potential therapeutic value of a glutamate-based pharmacotherapy for schizophrenia involving inhibition of the glutamate recycling enzyme phosphate-activated glutaminase.
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, 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.
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.
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