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Cow (Bovine) Polyclonal GLUD1 Primary Antibody for ELISA, WB - ABIN99811
Anthonio, Brees, Baumgart-Vogt, Hongu, Huybrechts, Van Dijck, Mannaerts, Kanaho, Van Veldhoven, Fransen: Small G proteins in peroxisome biogenesis: the potential involvement of ADP-ribosylation factor 6. in BMC cell biology 2009
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Cow (Bovine) Polyclonal GLUD1 Primary Antibody for IP, ELISA - ABIN269875
Bao, Pal, Hascup, Wang, Wang, Xu, Hui, Agbas, Wang, Michaelis, Choi, Belousov, Gerhardt, Michaelis: Transgenic expression of Glud1 (glutamate dehydrogenase 1) in neurons: in vivo model of enhanced glutamate release, altered synaptic plasticity, and selective neuronal vulnerability. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2009
Show all 3 Pubmed References
Human Polyclonal GLUD1 Primary Antibody for ELISA, ICC - ABIN4314676
Rueda, Johnson, Giddabasappa, Swaroop, Brooks, Sigel, Chaney, Fox: The cellular and compartmental profile of mouse retinal glycolysis, tricarboxylic acid cycle, oxidative phosphorylation, and ~P transferring kinases. in Molecular vision 2016
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Cow (Bovine) Polyclonal GLUD1 Primary Antibody for IHC, WB - ABIN2782330
Kawajiri, Okano, Kuno, Tokuhara, Hase, Inada, Tashiro, Miyazaki, Yamano: Unregulated insulin secretion by pancreatic beta cells in hyperinsulinism/hyperammonemia syndrome: role of glutamate dehydrogenase, ATP-sensitive potassium channel, and nonselective cation channel. in Pediatric research 2006
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Cow (Bovine) Polyclonal GLUD1 Primary Antibody for ELISA, WB - ABIN2473841
Wu, Wen, Chen, Chang, Cherng, Wong: The effect of dexamethasone on spinal glutamine synthetase and glutamate dehydrogenase expression in morphine-tolerant rats. in Anesthesia and analgesia 2007
Human Polyclonal GLUD1 Primary Antibody for IHC, IHC (p) - ABIN4890436
Li, Li, Li, Zhong, Ji, Yu, Zhang, Wen, Zhang, Goscinski, Nesland, Suo: PDHA1 gene knockout in prostate cancer cells results in metabolic reprogramming towards greater glutamine dependence. in Oncotarget 2016
Human Polyclonal GLUD1 Primary Antibody for ELISA, ICC - ABIN4314675
Jozwik, Pietrzycki, Jozwik, Anthony: Expression of enzymes regulating placental ammonia homeostasis in human fetal growth restricted pregnancies. in Placenta 2009
near-atomic resolution cryoelectron microscopy structures, at resolutions ranging from 3.2 A to 3.6 A for GDH complexes, is reported.
Data show that glutamate dehydrogenase activity in an enzymatic catalyzed reaction by tracing the increasing of oxidation current of NADH.
Data show that heat inactivation of the native GDH enzyme occurred with a rate constant of inactivation of 0.252 min-1.
the existence of two partially unfolded states of GDH at moderate acidic pHs which may be considered as molten and pre-molten globule-like states.
Results showt superactivation is caused by cleavage at the N terminus of the protein and not the C-terminal allosteric site, as has previously been suggested.
Characterized cDNA clones of sequences GDH1 and GDH2 that code for putative alpha- and beta-subunits of the NADH dependent enzyme. Although the gene transcripts are co-localized in roots of etiolated seedlings, the ratio of the two subunits varies among tissues.
This study provides insight into the molecular mechanism by which GDH1-mediated metabolic reprogramming of glutaminolysis mediates lung cancer metastasis and offers a therapeutic strategy for patients with LKB1-deficient lung cancer.
Phenotypic heterogeneity of GDH-hyperinsulinemia patients was observed within the Chinese cohort in the present study. The fact that most patients had a GLUD1 p. S445L mutation implies that this site could be a hotspot in Chinese patients.
structural model of a complex of human Sirt4 and GDH in order to elucidate the molecular mechanism underlying the ADP-ribosylation of GDH by Sirt4
Upregulation of GLUD1 and SLC25A13 was associated with tumor aggressiveness and poorer prognosis in colorectal cancer patients.
This study showed that SIRT5 supports the anaplerotic entry of glutamine into the TCA cycle in malignant phenotypes of CRC via activating GLUD1.
the present study shows that the GDHS445L enzyme is highly sensitive to the allosteric activator ADP, explaining the hyperactivity of this mutant. INS-1E beta-cells expressing GDHS445L responded to glutamine stimulation by increasing the mitochondrial respiration and ATP production, as well as by a rise in cytosolic calcium.
We have shown that alpha-ketoglutarate substrate inhibition kinetics of GDH, which include both random and obligatory ordered association/dissociation reactions, robustly control the ratio between glutamate and ammonium under a wide range of intracellular substrate variation. Dysregulation of this activity under pericentral nitrogen insufficiency contributes to the breaking down of ammonia homeostasis and thereby can s...
mRNA and protein levels of GluD1 were increased in iPSC-derived neurons from FOXG1(+/-) patients.
Hypoxia-induced expression of GDH relies on the up-regulation of HIF1alpha but not HIF2alpha. HIF1alpha binds the promoter of GDH and promotes the transcription of GDH gene in lung cancer cells.
Results indicate that it is possible to use high-throughput screening methods to find activators for glutamate dehydrogenase (GDH) that might be useful as pharmaceutical agents.
Missense mutation of GLUD1 is associated with Hyperinsulinism-hyperammonemia syndrome.
Analysis of Serbian patients with Hyperinsulinism/hyperammonemia syndrome confirms the association of p.S445L and p.R221C mutations with hypoglycaemic seizures noted within the first three months of life and with subsequent risk for cognitive impairment and/or epilepsy.
GLUD1 is differentially expressed in the cellular and subcellular compartments of numerous tissues.
GLUD1 mutation is associated with congenital hyperinsulinism-hyperammonemia.
Study of the expression of the GDH1/2 in human steroidogenic organs revealed that, while GDH2 was expressed specifically in steroid-synthesizing cells, GDH1 was expressed both in the cells that produce steroids and in those that lack endocrine function.
GDH plays a critical role in colorectal cancer progression
Mutation in the GLUD1 gene is associated with hyperinsulinism/hyperammonemia.
side-chain interactions between 409 and 443 positions in the 'antenna' region of GDH are crucial for basal catalytic activity, allosteric regulation, and relative resistance to thermal inactivation
argeting GDH1 by shRNA or a small molecule inhibitor R162 resulted in imbalanced redox homeostasis, leading to attenuated cancer cell proliferation and tumor growth.
SIRT3 and glutamate dehydrogenase are altered in follicular cells of women with reduced ovarian reserve or advanced maternal age
Findings demonstrate that hippocampal synapse assembly and maintenance require a tripartite molecular complex in which the ligand Cbln2 binds with presynaptic neurexin 1beta (+S4) and postsynaptic GluD1.
Data suggest that metabolism of glutamine and related analogs by Gdh in intestinal L-cells explains why Glp1 secretion, but not that of insulin by pancreatic beta-cells, is activated by these secretagogues. (Gdh = glutamate dehydrogenase; Glp1 = glucagon-like peptide 1)
mRNA and protein levels of GluD1 were increased in fetal brain of foxg1(+/-) mice. mRNA and protein levels of GluD1 were decreased in adult brain of foxg1(+/-) mice.
lack of glutamate oxidation in brain-specific GDH null CnsGlud1-/- mice resulted in a central energy-deprivation state with increased ADP/ATP ratios and phospho-AMPK in the hypothalamus.
This study demonstrated a critical requirement for GluD1 in normal spine development in the cortex and hippocampus.
The GDH activity in mice is highest in the liver with NAD(+) as a coenzyme and highest GDH activity was determined at a glutamate concentration of 10 mM.
Age-related increases of glutamate were observed only in the striatum of the glutamate dehydrogenase 1 mice
Glutamate hyperactivity caused gene expression changes in the hippocampus at all ages
GluD1 regulates the connectivity of parallel fiber-interneuron synapses and promotes differentiation of interneurons.
The GDH1 is a key metabolic enzyme with emerging roles in insulin regulation. MitoNEET forms a covalent complex with GDH1 through disulfide bond formation and acts as an activator.
GluD1 is crucial for normal functioning of synapses and absence of GluD1 leads to specific abnormalities in learning and memory.
Permissive levels of glutamate are required for the full development of glucose-stimulated insulin secretion and glutamate dehydrogenase plays an indispensable role in this process.
Mice deficient in Glud1 exhibit deficient oxidative catabolism of glutamate in astrocytes, showing that GDH is required for Krebs cycle pathway; however, lack of GDH modifies metabolic handling of glutamate without altering synaptic transmission.
These results suggest that GluD1 might contribute to the formation of specific synapses in the hippocampus such as those formed by the projecting neurons of the entorhinal cortex.
Data show that Balb/c Glud1 transgenic mice had significantly increased depolarization-induced glutamate release compared with wild type littermates.
In betaGlud1(-/-) mice, the reduced secretory capacity resulted in lower plasma insulin levels in response to both feeding and glucose load, while body weight gain was preserved
these data illustrate the essential role of EIN3-regulated GDH activity in metabolic adjustment during anoxia-reoxygenation.
the carboxyl terminus of the GDH subunit is involved in the stabilization of the oligomeric structure of the enzyme.
In leaves and stems of arabidopsis and tobacco, both the alpha- and beta-subunits of Glutamate dehydrogenase are targeted to the mitochondria of the companion cells.
role in amino acid breakdown under C-deficient conditions
GDH has a major effect on the control of metabolic composition during tomato fruit ripening, but not at other stages of development.
These results indicate that GDH beta-subunit could modulate the heteromeric isoforms of GDH in response to the environment and physiology of the tomato fruit.
This gene encodes glutamate dehydrogenase protein\; a mitochondrial matrix enzyme that catalyzes the oxidative deamination of glutamate to alpha-ketoglutarate and ammonia. This enzyme has an important role in regulating amino acid induced insulin secretion and activating mutations in this gene are a common cause of congenital hyperinsulinism. This enzyme is allosterically activated by ADP and inhibited by GTP and ATP. The related glutamate dehydrogenase 2 gene on the human X-chromosome originated from this gene via retrotransposition and encodes a soluble form of glutamate dehydrogenase. Multiple pseudogenes of this gene are present in humans.
, glutamate dehydrogenase 1, mitochondrial
, glutamate dehydrogenase 1
, mitochondrial glutamate dehydrogenase 1
, glutamate dehydrogenase (NAD(P)+)
, memory-related gene 2 protein
, glutamate dehydrogenase 1, mitochondrial-like
, NADH-glutamate dehydrogenase
, glutamate dehydrogenase