Bcl-XL Positive Control peptide (STJ505387)

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STJ505387-5

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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.
Gene Symbol: BCL2L1
Gene ID: 598
Uniprot ID: B2CL1_HUMAN
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 1
Bcl2-L-1
Apoptosis Regulator Bcl-X
Database Links Reactome: R-HSA-111453
Reactome: R-HSA-6785807
Reactome: R-HSA-844455
Reactome: R-HSA-9648002
Reactome: R-HSA-9692913
Reactome: R-HSA-9702518
Cellular Localisation Isoform Bcl-X(L): Mitochondrion Inner Membrane
Mitochondrion Outer Membrane
Mitochondrion Matrix
Cytoplasmic Vesicle
Secretory Vesicle
Synaptic Vesicle Membrane
Cytoplasm
Cytosol
Cytoskeleton
Microtubule Organizing Center
Centrosome
Nucleus Membrane
Single-Pass Membrane Protein
Cytoplasmic Side
After Neuronal Stimulation
Translocates From Cytosol To Synaptic Vesicle And Mitochondrion Membrane In A Calmodulin-Dependent Manner
Localizes To The Centrosome When Phosphorylated At Ser-49
Alternative Peptide Names Bcl-2-Like Protein 1 protein
Bcl2-L-1 protein
Apoptosis Regulator Bcl-X protein
BCL2L1 protein
BCL2L protein
BCLX protein

Information sourced from Uniprot.org

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