Bcl-2-Interacting Killer (BIK) Antibody

Este producto es parte de BIK - BCL2 Interacting Killer
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221€ (50 µg)

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935106861
info@markelab.com
name
Bcl-2-Interacting Killer (BIK) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx324775
tested applications
ELISA, WB, IHC, IF/ICC

Description

BIK Antibody is a Rabbit Polyclonal against BIK.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Bcl-2-Interacting Killer (BIK)
Host
Rabbit
Reactivity
Human
Recommended Dilution
ELISA: 1/10000, WB: 1/500 - 1/2000, IHC: 1/100 - 1/300, IF/ICC: 1/200 - 1/1000. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Purification
Purified by affinity chromatography.
Size 1
50 µg
Size 2
100 µg
Form
Liquid
Tested Applications
ELISA, WB, IHC, IF/ICC
Buffer
PBS containing 50% glycerol, 0.5% BSA and 0.02% 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
Gene ID
638
OMIM
603392
Alias
BIP1,BP4,NBK,Apoptosis inducer NBK
Background
Antibody anti-BIK
Status
RUO
Note
Concentration: 1 mg/ml -

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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