Bcl-2-Interacting Killer (BIK) Antibody

Este producto es parte de BIK - BCL2 Interacting Killer
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455€ (100 µg)

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935106861
info@markelab.com
name
Bcl-2-Interacting Killer (BIK) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx411860
tested applications
WB, IHC

Description

Bcl-2-Interacting Killer (BIK) Antibody is a Rabbit Polyclonal antibody against Bcl-2-Interacting Killer (BIK).

Documents del producto

Instrucciones
Data sheet
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Product specifications

CategoryPrimary Antibodies
Immunogen TargetBcl-2-Interacting Killer (BIK)
HostRabbit
ReactivityHuman
Recommended DilutionValidated in IHC-F. Optimal dilutions/concentrations should be determined by the end user.
ClonalityPolyclonal
ConjugationUnconjugated
IsotypeIgG
PurificationPurified
Size 1100 µg
FormLiquid
Tested ApplicationsWB, IHC
BufferPBS. Contains sodium azide.
AvailabilityShipped within 3-7 working days.
StorageAliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry IceNo
UniProt IDQ13323
AliasBIP1,BP4,NBK,Apoptosis inducer NBK
BackgroundAntibody anti-BIK
StatusRUO
NoteConcentration: 1.0 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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