Dieser Maus Monoklonal Antikörper detektiert spezifisch BCL2L1 in FACS. Es zeigt Reaktivität gegenüber Proben von Human.Es wurde in 1 Publikation zitiert.
Applications: FC - Quality tested , IHC-PS - Reported in literature , ICC - Reported in literature , WB - Reported in literature , IP - Reported in literature , ELISA - Reported in literature
Working Dilutions: Flow Cytometry FITC and BIOT conjugates 3 g/106 cells PE conjugate 0.3 g/106 cells For flow cytometry, the suggested use of these reagents is in a final volume of 100 L Immunoblotting Purified (UNLB) antibody 1 g/mL
Probenmenge
1 mL
Beschränkungen
Nur für Forschungszwecke einsetzbar
Konzentration
0.1 mg/mL
Buffer
0.1 mg in 1.0 mL PBS/Sodium azide
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handhabung
Protect conjugated products from light. 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
Gottschalk, Boise, Oltvai, Accavitti, Korsmeyer, Quintáns, Thompson: "The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated." in: Cell death and differentiation, Vol. 3, Issue 1, pp. 113-8, (2006) (PubMed).
Target
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.