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Merck
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Documenti fondamentali

ABN443

Sigma-Aldrich

Anti-Glud1 Antibody

from rabbit, purified by affinity chromatography

Sinonimo/i:

Glutamate dehydrogenase 1, mitochondrial, GDH 1

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About This Item

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

Origine biologica

rabbit

Livello qualitativo

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Purificato mediante

affinity chromatography

Reattività contro le specie

human, mouse

Reattività contro le specie (prevista in base all’omologia)

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

tecniche

immunohistochemistry: suitable
western blot: suitable

N° accesso NCBI

N° accesso UniProt

Condizioni di spedizione

wet ice

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... GLUD1(2746)

Descrizione generale

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.

Immunogeno

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

Applicazioni

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.

Qualità

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.

Descrizione del bersaglio

~58 kDa observed

Stato fisico

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

Stoccaggio e stabilità

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

Altre note

Concentration: Please refer to lot specific datasheet.

Esclusione di responsabilità

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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Codice della classe di stoccaggio

12 - Non Combustible Liquids

Classe di pericolosità dell'acqua (WGK)

WGK 1

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘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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