Recombinant Mouse Bcl-XL protein (His tag)
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Recombinant Mouse Bcl-XL protein (His tag) is a Human Fragment protein, in the 1 to 209 aa range, expressed in Escherichia coli, with >95%, suitable for SDS-PAGE, Mass Spec.
View Alternative Names
BCL2L, BCLX, BCL2L1, Bcl-2-like protein 1, Bcl2-L-1, Apoptosis regulator Bcl-X
- SDS-PAGE
Supplier Data
SDS-PAGE - Recombinant Mouse Bcl-XL protein (His tag) (AB206811)
15% SDS-PAGE analysis of ab206811 (3μg).
Reactivity data
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage duration
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Aliquoting information
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
This protein acts as an anti-apoptotic molecule within the mitochondria and is part of the Bcl-2 family complex. Bcl-XL modulates the balance between pro-apoptotic and anti-apoptotic signals impacting cell fate. By binding and sequestering pro-apoptotic members such as Bax and Bak Bcl-XL prevents mitochondrial outer membrane permeabilization important for avoiding programmed cell death. This function not only supports cellular longevity but also understanding cancer cell survival.
Pathways
The Bcl-XL protein holds a significant position in the apoptotic signaling pathways. It is particularly involved in the intrinsic pathway where its interactions with mitochondrial proteins Bax and Bak determine cell survival or death. It is interconnected with the PI3K/AKT pathway where AKT kinase activity can upregulate Bcl-XL expression demonstrating how survival signals are transmitted. These interactions highlight its pivotal role in balancing life and death at the cellular level.
Specifications
Form
Liquid
Additional notes
ab206811 was purified using conventional chromatography techniques.
General info
Function
Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage-dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis.. Isoform Bcl-X(L) also regulates presynaptic plasticity, including neurotransmitter release and recovery, number of axonal mitochondria as well as size and number of synaptic vesicle clusters. During synaptic stimulation, increases ATP availability from mitochondria through regulation of mitochondrial membrane ATP synthase F(1)F(0) activity and regulates endocytic vesicle retrieval in hippocampal neurons through association with DMN1L and stimulation of its GTPase activity in synaptic vesicles. May attenuate inflammation impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed : 17418785).. Isoform Bcl-X(S) promotes apoptosis.
Sequence similarities
Belongs to the Bcl-2 family.
Post-translational modifications
Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity.. Phosphorylated on Ser-62 by CDK1. This phosphorylation is partial in normal mitotic cells, but complete in G2-arrested cells upon DNA-damage, thus promoting subsequent apoptosis probably by triggering caspases-mediated proteolysis. Phosphorylated by PLK3, leading to regulate the G2 checkpoint and progression to cytokinesis during mitosis. Phosphorylation at Ser-49 appears during the S phase and G2, disappears rapidly in early mitosis during prometaphase, metaphase and early anaphase, and re-appears during telophase and cytokinesis.. Ubiquitinated by RNF183 during prolonged ER stress, leading to degradation by the proteosome.
Subcellular localisation
Mitochondrion inner membrane
Target data
Product promise
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