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H9912

Sigma-Aldrich

Anti-hSNF5/INI1 antibody produced in rabbit

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 42-45 kDa (doublet)

species reactivity

human

concentration

~1 mg/mL

technique(s)

indirect immunofluorescence: 1-2 μg/mL using paraformaldehyde/Triton fixed hSNF5/INI1-transfected 293T cell line
microarray: suitable
western blot: 0.5-1 μg/mL using HeLa nuclear extracts

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SMARCB1(6598)
mouse ... Smarcb1(20587)

General description

INI1/SNF5, also known as SWItch/sucrose non-fermentable (SWI/SNF) related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1, is encoded by the gene mapped to human chromosome 22q11.2. This gene codes for an essential component of chromatin-remodelling SWI/SNF multiprotein complexes.

Immunogen

synthetic peptide corresponding to amino acids 276-288 of human SNF5. The sequence is conserved in mouse.

Application

Anti-hSNF5/INI1 antibody produced in rabbit has been used in microarray and immunofluorescence.

Biochem/physiol Actions

INI1/sucrose non-fermentable 5 (SNF5) plays a vital role in transcriptional activation of inducible genes through chromatin remodelling. hSNF5/INI1 interacts with the protooncogene c-Myc and the SWI complex is necessary for c-Myc mediated transactivation. hSNF5 displays properties of a tumor-suppressor gene, as sporadic rhabdoid tumors show biallelic loss-of-function mutations and germline mutations confer an autosomal-dominant syndrome that predisposes patients to a variety of rhabdoid cancers. Loss of function mutations of the gene is associated with the pathogenesis of aggressive pediatric cancer and epithelioid schwannoma. SNF5 interacts with E1 protein of human papillomavirus (HPV) and thus, enhances the efficiency of HPV DNA replication.

Physical form

Solution in 0.01 M phosphate buffered saline containing 15 mM sodium azide.

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

10 - Combustible liquids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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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Cytoplasmic Recruitment of INI1 and PML on Incoming HIV Preintegration Complexes: Interference with Early Steps of Viral Replication
Turelli P, et al.
Molecular Cell, 7(6), 1245-1254 (2001)
Human SNF5/INI1, a Component of the Human SWI/SNF Chromatin Remodeling Complex, Promotes Nucleotide Excision Repair by Influencing ATM Recruitment and Downstream H2AX Phosphorylation
Ray A, et al.
Molecular and Cellular Biology, 29(23), 6206-6219 (2009)
Further intracellular proteins and signaling pathways regulated by angiotensin- in human endothelial cells
Meinert C, et al.
Data in Brief, 354-363 (2017)
SMARCB1/INI1 Loss in Epithelioid Schwannoma: A Clinicopathologic and Immunohistochemical Study of 65 Cases
Jo VY, et al.
The American journal of surgical pathology, 41(8), 1013-1022 (2017)
I Versteege et al.
Nature, 394(6689), 203-206 (1998-07-22)
Malignant rhabdoid tumours (MRTs) are extremely aggressive cancers of early childhood. They can occur in various locations, mainly the kidney, brain and soft tissues. Cytogenetic and molecular analyses have shown that the deletion of region 11.2 of the long arm

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