| Applications: |
WB |
| Note: |
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS. |
| Short Description: |
Bcl-XL Positive Control is synthetically produced from the sequence and is suitable for use in western blot applications. |
| Formulation: |
Provided as 100 uL ready-to-use, in SDS-PAGE sample buffer (Laemelli's buffer) containing Tris, pH 6.8, 1 % SDS, Glycerol and Bromophenolblue blue as tracking dye. The sample is reduced by adding 2% beta mercaptoethanol. The protein concentration is |
| Dilution Range: |
WB: 1:500 |
| Storage Instruction: |
Store at-20°C for long term storage. Avoid freeze-thaw cycles. |
| Tissue Specificity | Bcl-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. |
| 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. |
| 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. Isoform Bcl-X(S) promotes apoptosis. |
| Peptide Name | Bcl-2-Like Protein 1Bcl2-L-1Apoptosis Regulator Bcl-X |
| Database Links | Reactome: R-HSA-111453Reactome: R-HSA-6785807Reactome: R-HSA-844455Reactome: R-HSA-9648002Reactome: R-HSA-9692913Reactome: R-HSA-9702518 |
| Cellular Localisation | Isoform Bcl-X(L): Mitochondrion Inner MembraneMitochondrion Outer MembraneMitochondrion MatrixCytoplasmic VesicleSecretory VesicleSynaptic Vesicle MembraneCytoplasmCytosolCytoskeletonMicrotubule Organizing CenterCentrosomeNucleus MembraneSingle-Pass Membrane ProteinCytoplasmic SideAfter Neuronal StimulationTranslocates From Cytosol To Synaptic Vesicle And Mitochondrion Membrane In A Calmodulin-Dependent MannerLocalizes To The Centrosome When Phosphorylated At Ser-49 |
| Alternative Peptide Names | Bcl-2-Like Protein 1 proteinBcl2-L-1 proteinApoptosis Regulator Bcl-X proteinBCL2L1 proteinBCL2L proteinBCLX protein |
Information sourced from Uniprot.org
12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance
