BCL2L1 Antikörper (AA 3-14)
Kurzübersicht für BCL2L1 Antikörper (AA 3-14) (ABIN135025)
Target
Alle BCL2L1 Antikörper anzeigenReaktivität
Wirt
Klonalität
Konjugat
Applikation
Klon
-
-
Bindungsspezifität
- AA 3-14
-
Spezifität
- Mouse/Rat/Human Bcl-xL
-
Produktmerkmale
- Mouse Anti-Bcl-xL-UNLB
-
Aufreinigung
- Purified
-
Immunogen
- Bcl-xL peptide (a.a. 3-14) common to mouse and human
-
Isotyp
- IgG2a
-
-
-
-
Applikationshinweise
-
- 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
-
Probenmenge
- 1 mL
-
Beschränkungen
- Nur für Forschungszwecke einsetzbar
-
-
-
Konzentration
- 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
-
Konservierungsmittel
- Without preservative
-
Handhabung
- Each reagent is stable for the period shown on the bottle label if stored as directed.
-
Lagerung
- 4 °C
-
Informationen zur Lagerung
- Store at 2-8°C
-
-
- BCL2L1 (BCL2-Like 1 (BCL2L1))
-
Andere Bezeichnung
- Bcl-xL
-
Hintergrund
- 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
- Apoptose, Negative Regulation of intrinsic apoptotic Signaling
Target
-