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Bcl-2 antibody (AA 49-76)

This anti-Bcl-2 antibody is a Rabbit Polyclonal antibody detecting Bcl-2 in WB. Suitable for Human.
Catalog No. ABIN1881105

Quick Overview for Bcl-2 antibody (AA 49-76) (ABIN1881105)

Target

See all Bcl-2 (BCL2) Antibodies
Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))

Reactivity

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Human

Host

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Rabbit

Clonality

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Polyclonal

Conjugate

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This Bcl-2 antibody is un-conjugated

Application

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Western Blotting (WB)

Clone

RB42026
  • Binding Specificity

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    AA 49-76

    Purification

    This antibody is purified through a protein A column, followed by peptide affinity purification.

    Immunogen

    This Bcl-2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 49-76 amino acids from the Central region of human Bcl-2.

    Isotype

    Ig Fraction
  • Application Notes

    WB: 1:1000

    Restrictions

    For Research Use only
  • Format

    Liquid

    Buffer

    Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

    Preservative

    Sodium azide

    Precaution of Use

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

    Storage

    4 °C,-20 °C

    Expiry Date

    6 months
  • Target

    Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))

    Alternative Name

    Bcl-2

    Background

    Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1).

    Molecular Weight

    26266

    NCBI Accession

    NP_000624

    UniProt

    P10415

    Pathways

    MAPK Signaling, PI3K-Akt Signaling, Apoptosis, Caspase Cascade in Apoptosis, Regulation of Muscle Cell Differentiation, Cell-Cell Junction Organization, Skeletal Muscle Fiber Development, Autophagy, Smooth Muscle Cell Migration, Negative Regulation of intrinsic apoptotic Signaling
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