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Key Documents

B5897

Sigma-Aldrich

Anti-Bak antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Synonym(s):

Anti-Bcl-2 Homologous Antagonist/Killer

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.46

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 28 kDa

species reactivity

human

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:100 using sections of human colon carcinoma
microarray: suitable
western blot: 1:2,000 using human epidermal carcinoma A431 whole cell extract

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... BAK1(578)

General description

Bak (Bcl-2 homologous antagonist/killer, Bak1) belongs to the B-cell lymphoma 2 (Bcl-2) family of proteins. The bak gene is mapped to chromosome 6 and encodes a 233 amino acid protein with a predicted MW of 23.4 kDa. Bak shares homology with Bcl-2 in the Bcl‐2 homology (BH) domains (BH1 and BH2). Bak is expressed in a wide variety of cell types and tissues, with the highest levels observed in heart and skeletal muscle.

Immunogen

synthetic peptide corresponding to the N-terminus of human Bak amino acids 23-38 with C-terminally added lysine, conjugated to KLH.

Application

Anti-Bak antibody produced in rabbit has been used in immunoblotting and immunohistochemistry.

Biochem/physiol Actions

Bak (Bcl-2 homologous antagonist/killer, Bak1) is involved in regulating apoptosis. Bak can accelerate the rate of apoptosis when overexpressed in some cell lines. Increased Bak expression in normal and neoplastic intestinal epithelial cells results in apoptosis. However, expression of Bak in a human lymphoblastoid cell line, provided protection from apoptosis induced by serum deprivation and the oxidant menadione, suggesting that the function of Bak may be context dependent.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, 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 Code

10 - Combustible liquids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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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Association of Bax and Bak Homo-oligomers in Mitochondria Bax REQUIREMENT FOR Bak REORGANIZATION AND CYTOCHROMEc RELEASE
Mikhailov V, et al.
Test, 278, 5367-5376 (2003)
Up regulation of Bax and down regulation of Bcl2 during 3-NC mediated apoptosis in human cancer cells
Naseri MH, et al.
Cancer Cell International, 15(1), 55-55 (2015)
Stephen Ma et al.
The Journal of biological chemistry, 288(36), 26027-26038 (2013-07-31)
Bak and Bax are the essential effectors of the intrinsic pathway of apoptosis. Following an apoptotic stimulus, both undergo significant changes in conformation that facilitates their self-association to form pores in the mitochondrial outer membrane. However, the molecular structures of
Rachel T Uren et al.
eLife, 6 (2017-02-10)
During apoptosis, Bak and Bax undergo major conformational change and form symmetric dimers that coalesce to perforate the mitochondrial outer membrane via an unknown mechanism. We have employed cysteine labelling and linkage analysis to the full length of Bak in
DNA damage-related gene expression as biomarkers to assess cellular response after gamma irradiation of a human lymphoblastoid cell line
Bishay K, et al.
Oncogene, 19(7), 916-916 (2000)

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