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Key Documents

PLA0302

Sigma-Aldrich

Goat anti-GAPDH Antibody, Affinity Purified

Powered by Bethyl Laboratories, Inc.

Synonim(y):

G3PD, GAPD, GAPDH, HEL-S-162eP, aging-associated gene 9 protein, epididymis secretory sperm binding protein Li 162eP, peptidyl-cysteine S-nitrosylase GAPDH

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About This Item

Kod UNSPSC:
12352203
NACRES:
NA.41

pochodzenie biologiczne

goat

Poziom jakości

100

forma przeciwciała

affinity purified immunoglobulin

rodzaj przeciwciała

primary antibodies

klasa czystości

Powered by Bethyl Laboratories, Inc.

reaktywność gatunkowa

human, mouse

stężenie

1 mg/mL

metody

immunohistochemistry: 1:500-1:2,000
western blot: 1:500- 1:2,500

nr dostępu

NP_002037.2

numer dostępu UniProt

P04406

Warunki transportu

wet ice

temp. przechowywania

2-8°C

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

goat ... GAPDH(2597)

Immunogen

The epitope recognized by PLA0302 maps to a region between residue 175 and 225 of human Glyceraldehyde-3-Phosphate Dehydrogenase using the numbering given in entry NP_002037.2 (GeneID 2597).

Postać fizyczna

Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide

Inne uwagi

In the process of carbohydrate metabolism, GAPDH (glyceraldehydes-3-phosphate dehydrogenase) catalyzes the oxidative phosphorylation of glyceraldehydes-3-phosphate to 1,3-diphosphoglycerate in the presence of nicotinamide adenine dinucleotide (NAD) and inorganic phosphate. In addition to its role in the oxidation of glucose, GAPDH has been shown to be involved in other cellular processes such as vesicle transport, DNA repair, DNA replication, cytoskeletal modulation, and tRNA export.

Oświadczenie o zrzeczeniu się odpowiedzialności

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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Kod klasy składowania

12 - Non Combustible Liquids

Klasa zagrożenia wodnego (WGK)

nwg

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable

Certyfikaty analizy (CoA)

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

Xiaolei Lian et al.
Acta neuropathologica communications, 9(1), 88-88 (2021-05-19)
Diffuse intrinsic pontine glioma (DIPG), a rare pediatric brain tumor, afflicts approximately 350 new patients each year in the United States. DIPG is noted for its lethality, as fewer than 1% of patients survive to five years. Multiple clinical trials
Lesya V Zelenchuk et al.
PloS one, 9(5), e97326-e97326 (2014-05-21)
PHEX or DMP1 mutations cause hypophosphatemic-rickets and altered energy metabolism. PHEX binds to DMP1-ASARM-motif to form a complex with α5β3 integrin that suppresses FGF23 expression. ASARM-peptides increase FGF23 by disrupting the PHEX-DMP1-Integrin complex. We used a 4.2 kDa peptide (SPR4)
Amane Araki et al.
Neurology, 82(20), 1813-1821 (2014-04-25)
The aim of this study was to clarify myocardial involvement and its clinical implications in subjects with spinal and bulbar muscular atrophy (SBMA), a neuromuscular disease affecting both neuronal and nonneuronal tissues. Two independent cardiologists evaluated ECGs from a total
Bo Cao et al.
Oncotarget, 5(6), 1646-1656 (2014-04-12)
Upregulation of constitutively-active androgen receptor splice variants (AR-Vs) has been implicated in AR-driven tumor progression in castration-resistant prostate cancer. To date, functional studies of AR-Vs have been focused mainly on their ability to regulate gene expression independent of the full-length
Paul Cottu et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 20(16), 4314-4325 (2014-06-21)
Patients with luminal breast cancer (LBC) often become endocrine resistant over time. We investigated the molecular changes associated with acquired hormonoresistances in patient-derived xenografts of LBC. Two LBC xenografts (HBCx22 and HBCx34) were treated with different endocrine treatments (ET) to
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