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Key Documents

SAB1403849

Sigma-Aldrich

Monoclonal Anti-GAD1 antibody produced in mouse

clone 1D12, ascites fluid

Synonyme(s) :

FLJ45882, GAD, SCP

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

ascites fluid

Type de produit anticorps

primary antibodies

Clone

1D12, monoclonal

Poids mol.

antigen ~91.45 kDa

Espèces réactives

human

Technique(s)

indirect ELISA: suitable
western blot: 1:500-1:1000

Isotype

IgMκ

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... GAD1(2571)

Description générale

This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes. The enzyme encoded is responsible for catalyzing the production of gamma-aminobutyric acid from L-glutamic acid. A pathogenic role for this enzyme has been identified in the human pancreas since it has been identified as an autoantigen and an autoreactive T cell target in insulin-dependent diabetes. This gene may also play a role in the stiff man syndrome. Deficiency in this enzyme has been shown to lead to pyridoxine dependency with seizures. Alternative splicing of this gene results in two products, the predominant 67-kD form and a less-frequent 25-kD form. (provided by RefSeq)

Immunogène

GAD1 (AAH26349, 1 a.a. ~ 594 a.a) full-length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
MASSTPSSSATSSNAGADPNTTNLRPTTYDTWCGVAHGCTRKLGLKICGFLQRTNSLEEKSRLVSAFKERQSSKNLLSCENSDRDARFRRTETDFSNLFARDLLPAKNGEEQTVQFLLEVVDILLNYVRKTFDRSTKVLDFHHPHQLLEGMEGFNLELSDHPESLEQILVDCRDTLKYGVRTGHPRFFNQLSTGLDIIGLAGEWLTSTANTNMFTYEIAPVFVLMEQITLKKMREIVGWSSKDGDGIFSPGGAISNMYSIMAARYKYFPEVKTKGMAAVPKLVLFTSEQSHYSIKKAGAALGFGTDNVILIKCNERGKIIPADFEAKILEAKQKGYVPFYVNATAGTTVYGAFDPIQEIADICEKYNLWLHVDAAWGGGLLMSRKHRHKLNGIERANSVTWNPHKMMGVLLQCSAILVKEKGILQGCNQMCAGYLFQPDKQYDVSYDTGDKAIQCGRHVDIFKFWLMWKAKGTVGFENQINKCLELAEYLYAKIKNREEFEMVFNGEPEHTNVCFWYIPQSLRGVPDSPQRREKLHKVAPKIKALMMESGTTMVGYQPQGDKANFFRMVISNPAATQSDIDFLIEEIERLGQDL

Forme physique

Clear solution

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Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Shuzhuo Zhang et al.
Pain, 155(8), 1504-1515 (2014-05-06)
Anxiety disorder is a comorbid condition of chronic pain. Analgesics and anxiolytics, subject to addiction and abuse, are currently used to manage pain and anxiety symptoms. However, the cellular mechanism underlying chronic pain and anxiety interaction remains to be elucidated.
YeeWen Candace Wu et al.
Psychoneuroendocrinology, 45, 167-178 (2014-05-23)
Gender differences in the neurodevelopmental disorder, schizophrenia, have been described for nearly all features of the illness. Reduced hippocampal expression of the GABAergic interneuron marker, parvalbumin (PV), and GABA synthesizing enzyme, GAD67, are consistently reported in schizophrenia. However, little is
Chuan-Ching Lai et al.
Neurochemical research, 39(11), 2180-2188 (2014-08-20)
The combined abuse of recreational drugs such as ketamine (Ket) and amphetamine (Amph) should be seriously considered important social and health issues. Numerous studies have documented the behavioral and neurochemical changes associated with polydrug administration; however, most studies have only
Laetitia Buret et al.
The international journal of neuropsychopharmacology, 17(8), 1221-1232 (2014-02-22)
Stress exposure during adolescence/early adulthood has been shown to increase the risk for psychiatric disorders such as schizophrenia. Reelin plays an essential role in brain development and its levels are decreased in schizophrenia. However, the relationship between stress exposure and
Bo Han et al.
Anesthesiology, 121(5), 999-1009 (2014-07-25)
Numerous studies demonstrate that anesthetic-induced unconsciousness is accompanied by activation of hypothalamic sleep-promoting neurons, which occurs through both pre- and postsynaptic mechanisms. However, the correlation between drug exposure, neuronal activation, and onset of hypnosis remains incompletely understood. Moreover, the degree

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