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Key Documents

B7931

Sigma-Aldrich

Anti-BNIP3 antibody, Mouse monoclonal

clone ANa40, purified from hybridoma cell culture

Sinónimos:

Monoclonal Anti-BNIP3 antibody produced in mouse

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About This Item

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

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

ANa40, monoclonal

form

buffered aqueous solution

mol wt

antigen 21.5 kDa

species reactivity

human

concentration

~2 mg/mL

technique(s)

immunocytochemistry: suitable
immunoprecipitation (IP): suitable
indirect ELISA: suitable
microarray: suitable
western blot: 2-4 μg/mL using whole extract of transfected 293T (human embryonal kidney) cells expressing human BNIP3.

isotype

IgG2b

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... BNIP3(664)

General description

Monoclonal Anti-BNIP3 (mouse IgG2b isotype) is derived from the ANa40 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mouse immunized with a recombinant human BNIP3. B-cell lymphoma 2 (BCL2) Interacting Protein 3 (BNIP3) is a pro-apoptotic protein localized in mitochondria and belongs to Bcl-2 family. Its Bcl-2 homology 3 (BH3) domain is less conserved in mammalian cells and yeast.

Specificity

Rabbit monoclonal clone ANa40 anti-BNIP3 recognizes human BNIP3. The epitope recognized by the antibody resides within amino acids 112-124 of human BNIP3 molecule.

Immunogen

recombinant human BNIP3 (amino acids 1-163, BNIP3ΔTM2).

Application

Anti-BNIP3 antibody, Mouse monoclonal has been used in
  • western blotting
  • immunoblotting
  • immunocytochemistry
  • immunoprecipitation enzyme linked immunosorbent assay (ELISA)
  • immunofluorescence analysis

Rabbit monoclonal clone ANa40 anti-BNIP3 is used to tag BNIP3 for detection and quantitation by immunocytochemical and immunohistochemical (IHC) techniques such as ELISA, immunoblotting, and immunoprecipitation. It is used as a probe to determine the presence and roles of BNIP3 in the regulation of mitochondrial and non-mitochondrial mediated apoptosis.
The product is useful in ELISA, immunoblotting (21.5 kDa, apparent molecular mass in SDS-PAGE is approximately 30 and 60 kDa, for monomer and dimer, respectively), immunocytochemistry (4% formaldehyde), and immunoprecipitation.

Biochem/physiol Actions

B-cell lymphoma 2 (BCL2) Interacting Protein 3 (BNIP3) functions without a typical Bcl-2 homology 3 (BH3) domain. It interacts withcell death abnormality gene 9 (CED-9). BNIP3 interaction with B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra-large (Bcl-XL) regulates apoptosis in mitochondria l and non-mitochondrial sites. Endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N-terminus in the cytoplasm and the C-terminus in the membrane during induction of cell death. This is accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial permeability transition (PT) pore, proton electrochemical gradient (Dym) suppression, and increased reactive oxygen species production.

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

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Visite la Librería de documentos

Yanxiang Shao et al.
International journal of oncology, 54(1), 348-360 (2018-10-27)
The majority of clear cell renal cell carcinomas (ccRCCs) are caused by an accumulation of hypoxia‑inducible factor (HIF) and the overexpression of downstream genes in response to the von Hippel‑Lindau (VHL) gene becoming inactivated. In the present study, our hypothesis
Bnip3-mediated mitochondrial autophagy is independent of the mitochondrial permeability transition pore
Quinsay MN, et al.
Autophagy, 6(7), 855-862 (2010)
BNIP3 Heterodimerizes with Bcl-2/Bcl-XL and Induces Cell Death Independent of a Bcl-2 Homology 3 (BH3) Domain at Both Mitochondrial and Nonmitochondrial Sites
Ray R, et al.
The Journal of Biological Chemistry, 275(2), 1439-1448 (2000)
Bnip3 as a Dual Regulator of Mitochondrial Turnover and Cell Death in the Myocardium
Gustafsson AA, et al.
Pediatric Cardiology, 32(3), 267-267 (2011)
BNIP3 protects HepG2 cells against etoposide-induced cell death under hypoxia by an autophagy-independent pathway
Cosse JP, et al.
Biochemical Pharmacology, 80(8), 1160-1169 (2010)

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