FunctionPotent inhibitor of cell death. Inhibits activation of caspases (By similarity). Appears to regulate cell death by blocking the voltage-dependent anion channnel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Isoform Bcl-X(S) promotes apoptosis.
Tissue specificityBcl-X(S) is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes. In contrast, Bcl-X(L) is found in tissues containing long-lived postmitotic cells, such as adult brain.
Sequence similaritiesBelongs to the Bcl-2 family.
DomainThe BH4 motif is required for anti-apoptotic activity. The BH1 and BH2 motifs are required for both heterodimerization with other Bcl-2 family members and for repression of cell death.
Post-translational modificationsProteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity.
Cellular localizationMitochondrion membrane. Nucleus membrane. Mitochondrial membranes and perinuclear envelope.
Formalin fixed paraffin embedded section of dog ischemic brain cortex stained for Bcl-XL expression using ab47123 at 1/2000. At 2 hr post ischemia, Bcl-XL staining was seen in the dying neurons that had morphological features of apoptosis (arrows). In contrast, mophologically normal appearing neurons lacked Bcl-X staining (arrowheads). Hematoxylin-eosin counterstain.
Formalin fixed paraffin embedded human tissue sections stained for Bcl-XL expression using ab47123 at 1/2000. A. Cortex from the brain of an Alzheimer's disease patient. The degenerating neurons are positive for Bcl-XL expression, the intact neurons are not. B. Normal bone marrow. The cells positive for Bcl-XLexpression appear to be of erythropoetic lineage. Hematoxylin-eosin counterstain.
References for Anti-Bcl-XL antibody (ab47123)
This product has been referenced in:
Loughran ST et al. Bfl-1 is a crucial pro-survival nuclear factor-?B target gene in Hodgkin/Reed-Sternberg cells. Int J Cancer129:2787-96 (2011).
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