BCL2L1 antibody (AA 3-14)

Catalog No. ABIN135025

This Mouse Monoclonal antibody specifically detects BCL2L1 in WB. It exhibits reactivity toward Human and Mouse.

Quick Overview for BCL2L1 antibody (AA 3-14) (ABIN135025)

Target: BCL2L1 (BCL2-Like 1 (BCL2L1))

Reactivity: Human, Mouse

Host: Mouse

Clonality: Monoclonal

Conjugate: This BCL2L1 antibody is un-conjugated

Application: Western Blotting (WB)

Clone: 2H12

Product Details anti-BCL2L1 Antibody

Binding Specificity: AA 3-14

Specificity: Mouse/Rat/Human Bcl-xL

Characteristics: Mouse Anti-Bcl-xL-UNLB

Purification: Purified

Immunogen: Bcl-xL peptide (a.a. 3-14) common to mouse and human

Isotype: IgG2a

Application Details

Application Notes:

• Applications: WB - Quality tested , IP - Reported in literature , FC - Reported in literature , IHC-PS - Reported in literature , ELISA - Reported in literature
• Working Dilutions: Immunoblotting Purified (UNLB) antibody ≤ 2 g/mL

Sample Volume: 1 mL

Restrictions: For Research Use only

Handling

Concentration: 0.1 mg/mL

Buffer: 0.1 mg of purified immunoglobulin in 1.0 mL of borate buffered saline,  pH 8.2. No preservatives or amine-containing buffer salts added

Preservative: Without preservative

Handling Advice: Each reagent is stable for the period shown on the bottle label if stored as directed.

Storage: 4 °C

Storage Comment: Store at 2-8°C

Target Details for BCL2L1

Target: BCL2L1 (BCL2-Like 1 (BCL2L1))

Alternative Name: Bcl-xL

Background: Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems. It plays a key role in tissue and organ development as well as in adult tissues during cell turnover. Apoptosis can be induced by a variety of internal and external stimuli including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation and glucocorticoid treatment. Bcl-2 and one of its homologues, Bcl-xL, protect cells from apoptosis, while other homologues of Bcl-2 such as Bax, Bad and Bak have been shown to enhance apoptosis. Bcl-xL has been shown to block apoptosis which is induced by a variety of stimuli and, under certain conditions, offers greater protection against apoptosis than Bcl-2. In contrast, Bad and Bax inhibit the protective functions of Bcl-xL and Bcl-2, respectively. Although heterodimerization between Bcl-xL/Bad and Bcl-2/Bax was originally thought to be essential for the differential anti-apoptotic activity of Bcl-xL and Bcl-2, other results suggest that the formation of heterodimers may not be necessary for this death-repressing activity.

Pathways: Apoptosis, Negative Regulation of intrinsic apoptotic Signaling