BAD antibody (AA 90-118)

Catalog No. ABIN6243058

This anti-BAD antibody is a Rabbit Polyclonal antibody detecting BAD in WB. Suitable for Mouse.

Quick Overview for BAD antibody (AA 90-118) (ABIN6243058)

Target: BAD (BCL2-Associated Agonist of Cell Death (BAD))

Reactivity: Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This BAD antibody is un-conjugated

Application: Western Blotting (WB)

Clone: RB39400

Product Details anti-BAD Antibody

Binding Specificity: AA 90-118

Predicted Reactivity: Rat

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

Immunogen: This mouse BAD antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 90-118 amino acids from the Central region of mouse BAD.

Isotype: Ig Fraction

Application Details

Application Notes: WB: 1:1000. WB: 1:1000

Restrictions: For Research Use only

Handling

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 Details for BAD

Target: BAD (BCL2-Associated Agonist of Cell Death (BAD))

Alternative Name: BAD

Background: BAD promotes cell death. It successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.

Molecular Weight: 22080

NCBI Accession: NP_031548

UniProt: Q61337

Pathways: MAPK Signaling, PI3K-Akt Signaling, RTK Signaling, Apoptosis, Fc-epsilon Receptor Signaling Pathway, Positive Regulation of Peptide Hormone Secretion, Carbohydrate Homeostasis, Positive Regulation of Endopeptidase Activity, Regulation of Carbohydrate Metabolic Process, Hepatitis C, CXCR4-mediated Signaling Events