Cell Signaling Technology

Product Pathways - Neuroscience

Glutamate Dehydrogenase 1/2 Antibody #9828

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Endogenous 52 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Glutamate Dehydrogenase 1/2 Antibody recognizes endogenous levels of total glutamate dehydrogenase 1 and 2 proteins.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn339 of human glutamate dehydrogenase 1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse brain, rat brain, and Hep G2 cells using Glutamate Dehydrogenase 1/2 Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, either mock transfected (-) or transfected with a construct expressing Myc/DDK-tagged full-length human glutamate dehydrogenase 1 (hGluD1; +) or glutamate dehydrogenase 2 (hGluD2; +), using Glutamate Dehydrogenase 1/2 Antibody.

Background

Glutamate dehydrogenase is a mitochondrial enzyme that catalyzes the oxidative deamination of glutamate to α-ketoglutarate through association with the cofactor nicotinamide adenine dinucleotide phosphate (1). Glutamate dehydrogenase is highly expressed in various tissues such as the liver, brain, kidney, heart, pancreas, ovaries, and testis. Two isoforms produced by two distinct genes are found in mammalian tissues. The GLUD1 gene is ubiquitously expressed (2), while the GLUD2 gene is specifically expressed in neural and testicular tissues (3). Glutamate dehydrogenase links glutamate to the Krebs cycle, thereby playing a critical role in the regulation of energy homeostasis. Research studies have shown that changes in glutamate dehydrogenase activity in pancreatic β-cells can cause a hyperinsulinism syndrome (4).

  1. Blumenthal, K.M. et al. (1975) J Biol Chem 250, 3644-54.
  2. Michaelidis, T.M. et al. (1993) Genomics 16, 150-60.
  3. Shashidharan, P. et al. (1997) J Neurochem 68, 1804-11.
  4. Karaca, M. et al. (2011) Neurochem Int 59, 510-7.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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