Bik BH3 Domain Antibody

Este producto es parte de BIK - BCL2 Interacting Killer
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292.5€ (80 µl)

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935106861
info@markelab.com
name
Bik BH3 Domain Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx027273
tested applications
ELISA, WB, IHC

Description

The Bik protein is known to interact with cellular and viral survival-promoting proteins, such as BCL2 and the Epstein-Barr virus in order to enhance programmed cell death. Because its activity is suppressed in the presence of survival-promoting proteins, this protein is suggested as a likely target for antiapoptotic proteins. This protein shares a critical BH3 domain with other death-promoting proteins, BAX and BAK.

Documents del producto

Instrucciones
Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
Bik BH3 Domain
Host
Rabbit
Reactivity
Human
Recommended Dilution
WB: 1/2000, IHC-P: 1/50 - 1/100. Not tested in IHC-F. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Purification
Purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS.
Size 1
80 µl
Size 2
400 µl
Form
Liquid
Tested Applications
ELISA, WB, IHC
Buffer
PBS containing 0.09% sodium azide.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q13323
NCBI Accession
NP_001188.1
Alias
BIP1,BP4,NBK,Apoptosis inducer NBK
Background
Antibody anti-BIK
Status
RUO

Descripción

BIK is a pro-apoptotic member of the BCL-2 family that promotes programmed cell death by interacting with anti-apoptotic proteins, such as BCL-2 and BCL-XL, and neutralizing their function. BIK functions in the intrinsic apoptotic pathway, where it localizes to the mitochondria and induces mitochondrial outer membrane permeabilization (MOMP), leading to cytochrome c release and caspase activation. It acts as a BH3-only protein, a subclass of BCL-2 family proteins that serve as stress sensors for cellular damage, DNA replication errors, and oncogenic signaling. BIK is transcriptionally regulated by p53 and is involved in eliminating damaged or transformed cells, thus functioning as a tumor suppressor. BIK is often downregulated or silenced in cancers, where its loss contributes to apoptosis resistance, cell survival, and tumor progression. Overexpression studies show enhanced cell death, whereas knockdown studies reveal reduced apoptosis and increased tumor cell survival, highlighting BIK’s essential role in apoptosis induction, tumor suppression, and cellular stress responses.

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