Bcl-XL antibody

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935106861
info@markelab.com
name
Bcl-XL antibody
category
Primary Antibodies
provider
FineTest
reference
FNab00842
tested applications
ELISA, IHC, IP, IF, WB

Description

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.

Documents del producto

Instrucciones
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Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
BCL2-like 1 (Bcl-XL)
Host
Rabbit
Reactivity
Human, Mouse, Rat
Recommended Dilution
WB: 1:500-1:2000; IHC: 1:50-1:500; IF: 1:50-1:500
Clonality
polyclonal
Conjugation
Unconjugated
Isotype
IgG
Observed MW
30 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Immunogen affinity purified
Size 1
100µg
Form
liquid
Tested Applications
ELISA, IHC, IP, IF, WB
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
UniProt ID
Q07817
Gene ID
598
Alias
Bcl-2-like protein 1 (Bcl2-L-1),Apoptosis regulator Bcl-X,BCL2L1,BCL2L,BCLX
Background
Antibody anti-Bcl-XL
Status
RUO
Note
Mol. Weight 30 kDa

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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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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