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04-080

Sigma-Aldrich

Anti-BAF250a/ARID1a Antibody, clone PSG3

clone PSG3, Upstate®, from mouse

Synonyme(s) :

Anti-B120, Anti-BAF250, Anti-BAF250a, Anti-BM029, Anti-C1orf4, Anti-CSS2, Anti-ELD, Anti-MRD14, Anti-OSA1, Anti-P270, Anti-SMARCF1, Anti-hELD, Anti-hOSA1

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About This Item

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

Source biologique

mouse

Niveau de qualité

100

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

PSG3, monoclonal

Espèces réactives

human

Fabricant/nom de marque

Upstate®

Technique(s)

immunofluorescence: suitable
western blot: suitable

Isotype

IgG

Numéro d'accès NCBI

NM_006015.4
NM_139135.2

Numéro d'accès UniProt

O14497

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ARID1A (8289)

Spécificité

BAF250a/ARID1a

Immunogène

GST fusion protein corresponding to 419 residues in the mid-portion of human BAF250a/ARID1a

Application

Anti-BAF250a/ARID1a Antibody, clone PSG3 is an antibody against BAF250a/ARID1a for use in WB, ChIP, IC & IHC.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Chromatin Biology

Transcription Factors

Qualité

Routinely evaluated by immunoblot.

Description de la cible

~270 kDa

Forme physique

100 μg of Protein A purified mouse monoclonal IgG in 100μl of 1X PBS, pH 7.0, 0.1% Azide.
Format: Purified
Protein A purified

Stockage et stabilité

2 years at -20°C from date of shipment

Informations légales

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Clause de non-responsabilité

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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Réf. du produit
Description
Tarif

Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Coexistent ARID1A-PIK3CA mutations promote ovarian clear-cell tumorigenesis through pro-tumorigenic inflammatory cytokine signalling.
Chandler, RL; Damrauer, JS; Raab, JR; Schisler, JC; Wilkerson, MD; Didion, JP; Starmer et al.
Nature Communications null
Radhika Mathur et al.
Nature genetics, 49(2), 296-302 (2016-12-13)
Genes encoding subunits of SWI/SNF (BAF) chromatin-remodeling complexes are collectively mutated in ∼20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here we demonstrate that
Guillermo Pablo Vicent et al.
The Journal of biological chemistry, 285(4), 2622-2631 (2009-11-27)
Steroid hormones induce transcription of their responsive genes by complex mechanisms including synergism between the hormone receptors and other transcription factors. On the mouse mammary tumor virus (MMTV) promoter progesterone induction is mediated by the reciprocal synergism between progesterone receptor
Xiaomei Wang et al.
The Biochemical journal, 383(Pt 2), 319-325 (2004-06-02)
p270 (ARID1A) is a member of the ARID family of DNA-binding proteins and a subunit of human SWI/SNF-related complexes, which use the energy generated by an integral ATPase subunit to remodel chromatin. ARID1B is an independent gene product with an
Hiroko Inoue et al.
The Journal of biological chemistry, 277(44), 41674-41685 (2002-08-30)
The mammalian SWI/SNF-related complexes facilitate gene transcription by remodeling chromatin using the energy of ATP hydrolysis. The recruitment of these complexes to promoters remains poorly understood and may involve histone modifications or direct interactions with site-specific transcription factors or other
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