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BIK Antibody

Novus Biologicals, part of Bio-Techne | Catalog # NBP2-87074

Novus Biologicals, part of Bio-Techne
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NBP2-87074

Key Product Details

Species Reactivity

Human

Applications

Western Blot

Label

Unconjugated

Antibody Source

Polyclonal Rabbit

Concentration

0.5 mg/ml

Product Specifications

Immunogen

The immunogen is a synthetic peptide directed towards the N-terminal region of Human BIK. Peptide sequence: SEVRPLSRDILMETLLYEQLLEPPTMEVLGMTDSEEDLDPMEDFDSLECM The peptide sequence for this immunogen was taken from within the described region.

Clonality

Polyclonal

Host

Rabbit

Scientific Data Images for BIK Antibody

Western Blot: BIK Antibody [NBP2-87074]

Western Blot: BIK Antibody [NBP2-87074]

Western Blot: BIK Antibody [NBP2-87074] - Host: Rabbit. Target Name: BIK. Sample Type: Fetal Liver lysates. Antibody Dilution: 1.0ug/ml

Applications for BIK Antibody

Application
Recommended Usage

Western Blot

1.0 ug/ml

Formulation, Preparation, and Storage

Purification

Affinity purified

Formulation

PBS, 2% Sucrose

Preservative

0.09% Sodium Azide

Concentration

0.5 mg/ml

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.

Background: BIK

The Bcl-2 family of apoptosis-related genes plays central roles in regulating apoptotic pathways (reviewed in Thomadaki and Scorilas, 2006). Regulation of cell death through apoptosis is critical for the maintenance of homeostasis, defense against infectious agents, and normal development. Bcl-2 family proteins regulate apoptosis primarily through the regulation of mitochondrial outer membrane permeability. In mammals, the family consists of both prosurvival (antiapoptotic) and proapoptotic (prodeath) members. Cellular homeostasis is thought to be dependent on a balance between the actions of prosurvival and proapoptotic proteins. Bcl-2 family proteins can be divided into 3 main subfamilies on the basis of their function and the content of their Bcl-2 homology (BH) domains, for example: 1) Prosurvival: Bcl-2, Bcl-XL, Bcl-W, A1, and Mcl-1 2) Proapoptotic (multidomain): Bax, Bak, and Bok. 3) BH3-only (proapoptotic): Bad, Bcl-XS, Bid, Bik, Bim, Blk, Bmf, Bnip, Noxa, and Puma. Prosurvival members inhibit cells from undergoing apoptosis, whereas proapoptotic and BH3-only subfamily members promote apoptosis. There are 4 BH domains (1-4) conserved among Bcl-2 family proteins. The BH domains are important for function as well as for heterodimerization between family members. Typical prosurvival family members have all four BH domains (1-4), whereas proapoptotic (multidomain) members have BH1, 2 and 3 domains and BH3-only members have only the BH3 domain. Overall, the relative ratio of prosurvival and proapoptotic proteins determines the suseptibility of a cell to various apoptotic stimuli. Many Bcl-2 family proteins are differentially expressed in various malignancies and some are useful prognostic biomarkers. Prosurvival proteins are often elevated in diverse cancers and have the potential to confer resistance to both endogenous cell death stimuli and cancer treatments. Alterations in the ratio or levels of Bcl-2 family proteins have been also associated with nonmalignant diseases including neurodegenerative diseases, autoimmune diseases, AIDs, Down's syndrome, cardiovascular diseases, diabetes, glomerulonephritis, and muscular dystrophy. IMG-5696 recognizes Bik. Human Bik is a 160 amino acid protein, GenBank no. NP_001188.1.

Long Name

Bcl-2 Interacting Killer

Alternate Names

BIP1, BP4, NBK

Gene Symbol

BIK

Additional BIK Products

Product Documents for BIK Antibody

Certificate of Analysis

To download a Certificate of Analysis, please enter a lot number in the search box below.

Product Specific Notices for BIK Antibody

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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