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Key Documents

ABN443

Sigma-Aldrich

Anti-Glud1 Antibody

from rabbit, purified by affinity chromatography

Synonym(s):

Glutamate dehydrogenase 1, mitochondrial, GDH 1

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

human, mouse

species reactivity (predicted by homology)

monkey (based on 100% sequence homology), bat (based on 100% sequence homology), baboon (based on 100% sequence homology), bovine (based on 100% sequence homology)

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... GLUD1(2746)

General description

GLUD1/GDH1 is a mitochondrial glutamate dehydrogenase that converts L-glutamate into alpha keto-glutarate which is an important intermediate in the TCA cycle. GLUD1/GDH1, because it metabolizes glutamate which is also an important neurotransmitter, plays a role in learning and memory reactions mediated by glutamate, as well as certain neurodegenerative disorders associated with altered glutamate metabolism. Mutations in GLUD1/GDH1 are the most common cause of persistent hyperinsulinism hypoglycemia (HHF6). Interestingly GLUD1/GDH1 may also be involved in glutamate toxicity that accompanies aging. It appears that a decline in GLUD1/GDH1 function, even in over expressing mice, leads to buildup of glutamate and subsequent glutamate induced neurotoxicity.

Immunogen

Epitope: Near N-terminal
KLH-conjugated linear peptide corresponding to human Glud1 near the N-terminal.

Application

Immunohistochemistry Analysis: A 1:50-1,000 dilution from a representative lot detected Glud1 in mouse hindbrain, human thalamus, and human cerebral cortex tissue.
Research Category
Neuroscience
Research Sub Category
Developmental Signaling
This Anti-Glud1 Antibody is validated for use in Western Blotting and Immunohistochemistry for the detection of Glud1.

Quality

Evaluated by Western Blotting in human hippocampus tissue lysate.

Western Blotting Analysis: 1.0 µg/mL of this antibody detected Glud1 in 10 µg of human hippocampus tissue lysate.

Target description

~58 kDa observed

Physical form

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Other Notes

Concentration: Please refer to lot specific datasheet.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Metabolism changes during aging in the hippocampus and striatum of glud1 (glutamate dehydrogenase 1) transgenic mice.
Choi, IY; Lee, P; Wang, WT; Hui, D; Wang, X; Brooks, WM; Michaelis, EK
Neurochemical Research null
The human glutamate dehydrogenase gene family: gene organization and structural characterization.
Michaelidis, TM; Tzimagiorgis, G; Moschonas, NK; Papamatheakis, J
Genomics null
Nicholas P Lesner et al.
Metabolic engineering, 60, 157-167 (2020-04-25)
Pathogenic mutations in the mitochondrial genome (mtDNA) impair organellar ATP production, requiring mutant cells to activate metabolic adaptations for survival. Understanding how metabolism adapts to clinically relevant mtDNA mutations may provide insight into cellular strategies for metabolic flexibility. In this

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