BCL2 Like 1 (BCL2L1) Antibody
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Description
BCL2L1 Antibody is a Rabbit Polyclonal against BCL2L1.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | BCL2 Like 1 (BCL2L1) |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | ELISA: 1/5000, WB: 1/500 - 1/2000, IHC: 1/100 - 1/300, IF/ICC: 1/200 - 1/1000. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Purified by affinity chromatography. |
| Size 1 | 50 µg |
| Size 2 | 100 µg |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC, IF/ICC |
| Buffer | PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q07817 |
| Gene ID | 598 |
| Alias | BCLX,BCL2L,Bcl-X,PPP1R52; BCL-XL/S,Apoptosis regulator Bcl-X |
| Background | Antibody anti-BCL2L1 |
| Status | RUO |
Descripción
BCL2 like 1 (BCL2L1), also known as BCL-XL, is a well-known anti-apoptotic protein that regulates cell survival by preventing mitochondrial apoptosis BCL2L1 is part of the Bcl-2 family of proteins, which includes both pro- and anti-apoptotic members, and it plays a crucial role in inhibiting the release of cytochrome c from mitochondria, thus blocking caspase activation and preventing apoptosis BCL2L1 is highly expressed in various cell types, including immune cells, neurons, and cancer cells, where it supports cell survival and promotes tissue homeostasis Dysregulation of BCL2L1 has been associated with cancer, where its overexpression protects tumor cells from chemotherapy-induced apoptosis and promotes tumor progression In addition to its role in cancer, BCL2L1 is involved in regulating immune responses and neuronal function, particularly in protecting against neurodegenerative diseases like Alzheimer’s and Parkinson’s Recent studies also highlight its importance in cell metabolism, autophagy, and inflammation, further emphasizing its role as a critical regulator of cellular fate and survival
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anti- BCL2L1 antibody
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.
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anti- BCL2L1 antibody
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.
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