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Characterized cDNA clones of sequences GDH1 and GDH2 (show GLUD2 ELISA Kits) 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.
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 (show GRIN2A ELISA Kits) 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 (show CD59 ELISA Kits).
the existence of two partially unfolded states of GDH at moderate acidic pHs (show PCBD1 ELISA Kits) which may be considered as molten and pre-molten globule-like states.
Data indicate the tetramer as the most active form of glucose-6-phosphate dehydrogenase (G6PDH (show G6PD ELISA Kits)).
mRNA and protein levels of GluD1 were increased in iPSC-derived neurons (show FOXG1 ELISA Kits) from FOXG1(+/-) patients.
Hypoxia-induced expression of GDH relies on the up-regulation of HIF1alpha (show HIF1A ELISA Kits) but not HIF2alpha (show EPAS1 ELISA Kits). HIF1alpha (show HIF1A ELISA Kits) 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 (show GRIN1 ELISA Kits) dehydrogenase (GDH) that might be useful as pharmaceutical agents.
cortisol reduces glucose-6-phosphate (G6P) flux through H6PDH by increasing luminal NADPH (show NQO1 ELISA Kits), thereby allowing more G6P for hydrolysis via G6Pase (show G6PC ELISA Kits)
Missense mutation of GLUD1 is associated with Hyperinsulinism-hyperammonemia syndrome.
GLUD1 is differentially expressed in the cellular and subcellular compartments of numerous tissues.
GLUD1 mutation is associated with congenital hyperinsulinism-hyperammonemia.
Inhibition of glucose-6-phosphate dehydrogenase (show G6PD ELISA Kits) sensitizes cisplatin-resistant cells to death.
Study of the expression of the GDH1/2 in human steroidogenic organs revealed that, while GDH2 (show GLUD2 ELISA Kits) was expressed specifically in steroid-synthesizing cells, GDH1 was expressed both in the cells that produce steroids and in those that lack endocrine function.
mRNA and protein levels of GluD1 were increased in fetal brain of foxg1 (show FOXG1 ELISA Kits)(+/-) mice. mRNA and protein levels of GluD1 were decreased in adult brain of foxg1 (show FOXG1 ELISA Kits)(+/-) mice.
lack of glutamate (show GRIN1 ELISA Kits) oxidation in brain-specific (show CALY ELISA Kits) GDH (show UGDH ELISA Kits) null CnsGlud1-/- mice resulted in a central energy-deprivation state with increased ADP/ATP ratios and phospho-AMPK (show PRKAA1 ELISA Kits) in the hypothalamus.
This study demonstrated a critical requirement for GluD1 in normal spine development in the cortex and hippocampus.
The GDH (show UGDH ELISA Kits) activity in mice is highest in the liver with NAD(+) as a coenzyme and highest GDH (show UGDH ELISA Kits) activity was determined at a glutamate (show GRIN1 ELISA Kits) concentration of 10 mM.
Age-related increases of glutamate (show GRIN1 ELISA Kits) were observed only in the striatum of the glutamate dehydrogenase 1 mice
Glutamate (show GRIN1 ELISA Kits) 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 (show INS ELISA Kits) regulation. MitoNEET (show CISD1 ELISA Kits) 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 (show GRIN1 ELISA Kits) are required for the full development of glucose-stimulated insulin (show INS ELISA Kits) secretion and glutamate (show GRIN1 ELISA Kits) dehydrogenase plays an indispensable role in this process.
these data illustrate the essential role of EIN3-regulated GDH (show UGDH ELISA Kits) activity in metabolic adjustment during anoxia-reoxygenation.
the carboxyl terminus of the GDH (show UGDH ELISA Kits) 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 (show GRIN2A ELISA Kits) dehydrogenase are targeted to the mitochondria of the companion cells.
There are 2 forms of glucose-6-phosphate dehydrogenase. G form is X-linked and H form, encoded by this gene, is autosomally linked. This H form shows activity with other hexose-6-phosphates, especially galactose-6-phosphate, whereas the G form is specific for glucose-6-phosphate. Both forms are present in most tissues, but H form is not found in red cells.
mitochondrial glutamate dehydrogenase 1
, glutamate dehydrogenase 1
, glutamate dehydrogenase 1, mitochondrial-like
, GDH 1
, glutamate dehydrogenase 1, mitochondrial
, glutamate dehydrogenase (NAD(P)+)
, memory-related gene 2 protein
, G6PD, H form
, GDH/6PGL endoplasmic bifunctional protein
, glucose 1- dehydrogenase
, glucose dehydrogenase
, glucose dehyrogenase
, glucose-6-phosphate dehydrogenase, salivary