产品: BCL-XL 抗体
货号: DF6015
描述: Rabbit polyclonal antibody to BCL-XL
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog
分子量: 26kDa; 26kD(Calculated).
蛋白号: Q07817
RRID: AB_2837990

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat
预测:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%)
克隆:
Polyclonal
特异性:
BCL-XL Antibody detects endogenous levels of total BCL-XL.
RRID:
AB_2837990
引用格式: Affinity Biosciences Cat# DF6015, RRID:AB_2837990.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Apoptosis regulator Bcl X; Apoptosis regulator Bcl-X; Apoptosis regulator BclX; B cell lymphoma 2 like; B2CL1_HUMAN; Bcl 2 like 1 protein; Bcl X; Bcl xL; BCL XL/S; Bcl xS; Bcl-2-like protein 1; Bcl2 Like 1; Bcl2 related gene; Bcl2-L-1; BCL2L; Bcl2l1; BCLX; BclXL; BclXs; DKFZp781P2092; PPP1R52; Protein phosphatase 1 regulatory subunit 52;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
表达:
Q07817 B2CL1_HUMAN:

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.

描述:
The protein encoded by this gene belongs to the BCL-2 protein family. BCL-2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. The proteins encoded by this gene are located at the outer mitochondrial membrane, and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane potential, and thus controls the production of reactive oxygen species and release of cytochrome C by mitochondria, both of which are the potent inducers of cell apoptosis. Two alternatively spliced transcript variants, which encode distinct isoforms, have been reported. The longer isoform acts as an apoptotic inhibitor and the shorter form acts as an apoptotic activator. [provided by RefSeq]
序列:
MSQSNRELVVDFLSYKLSQKGYSWSQFSDVEENRTEAPEGTESEMETPSAINGNPSWHLADSPAVNGATGHSSSLDAREVIPMAAVKQALREAGDEFELRYRRAFSDLTSQLHITPGTAYQSFEQVVNELFRDGVNWGRIVAFFSFGGALCVESVDKEMQVLVSRIAAWMATYLNDHLEPWIQENGGWDTFVELYGNNAAAESRKGQERFNRWFLTGMTVAGVVLLGSLFSRK

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - Q07817 作为底物

Site PTM Type Enzyme
S14 Phosphorylation
K16 Ubiquitination
S28 Phosphorylation
T47 Phosphorylation P45983 (MAPK8) , P45984 (MAPK9)
S49 Phosphorylation Q9H4B4 (PLK3)
S62 Phosphorylation Q16539 (MAPK14) , P49137 (MAPKAPK2) , P49840 (GSK3A) , P53350 (PLK1) , P45984 (MAPK9) , P49841 (GSK3B) , P45983 (MAPK8)
S72 Phosphorylation
S73 Phosphorylation
S74 Phosphorylation
K87 Ubiquitination
T115 Phosphorylation P45983 (MAPK8) , P45984 (MAPK9)

研究背景

功能:

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.

翻译修饰:

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.

细胞定位:

Mitochondrion inner membrane. Mitochondrion outer membrane. Mitochondrion matrix. Cytoplasmic vesicle>Secretory vesicle>Synaptic vesicle membrane. Cytoplasm>Cytosol. Cytoplasm>Cytoskeleton>Microtubule organizing center>Centrosome. Nucleus membrane>Single-pass membrane protein>Cytoplasmic side.
Note: After neuronal stimulation, translocates from cytosol to synaptic vesicle and mitochondrion membrane in a calmodulin-dependent manner (By similarity). Localizes to the centrosome when phosphorylated at Ser-49.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
组织特异性:

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.

亚基结构:

Homodimer. Isoform Bcl-X(L) forms heterodimers with BAX, BAK or BCL2. Heterodimerization with BAX does not seem to be required for anti-apoptotic activity. Interacts with BCL2L11. Interacts with BAD. Interacts (isoform Bcl-X(L)) with SIVA1 (isoform 1); the interaction inhibits the anti-apoptotic activity. Interacts with BECN1 and PGAM5. Isoform Bcl-X(L) interacts with IKZF3. Interacts with HEBP2. Isoform Bcl-X(L) interacts with RTL10/BOP. Interacts with p53/TP53 and BBC3; interaction with BBC3 disrupts the interaction with p53/TP53. Isoform Bcl-X(L) interacts with DNM1L and CLTA; DNM1L and BCL2L1 isoform BCL-X(L) may form a complex in synaptic vesicles that also contains clathrin and MFF. Interacts with ATP5F1A and ATP5F1B; the interactions mediate the association of isoform Bcl-X(L) with the mitochondrial membrane ATP synthase F(1)F(0) ATP synthase. Interacts with VDAC1. Isoform Bcl-X(L) interacts (via the loop between motifs BH4 and BH3) with NLRP1 (via LRR repeats), but not with NLRP2, NLRP3, NLRP4, PYCARD, nor MEFV. Interacts with BCL2L11 (via BH3). Interacts with RNF183. Interacts with GIMAP3/IAN4 and GIMAP5/IAN5. Interacts with GIMAP5 and HSPA8/HSC70; the interaction between HSPA8 and BCL2L1 is impaired in the absence of GIMAP5 (By similarity). Interacts with CLU (isoform 4); this interaction releases and activates BAX and promotes cell death.

蛋白家族:

The BH4 motif is required for anti-apoptotic activity. The BH1 and BH2 motifs are required for both heterodimerization with other Bcl-2 family members and for repression of cell death.

The loop between motifs BH4 and BH3 is required for the interaction with NLRP1.

Belongs to the Bcl-2 family.

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

文献引用

1). Change in Oxidative Stress and Mitochondrial Dynamics in Response to Elevated Cold-Inducible RNA-Binding Protein in Cardiac Surgery-Associated Acute Kidney Injury. Oxidative Medicine and Cellular Longevity, 2022 (PubMed: 35855864)

Application: WB    Species: Human    Sample: HK-2 Cells

Figure 3 CPB induced mitochondrial dynamics disorder and increased inflammatory factor secretion. (a–f) Expression of IL-6, IL-1β, and TNF-α in the serum at 0 and 4 hours after CPB. Compared to the CPB group, C23 administration decreased the expression of IL-6, IL-1β, and TNF-α by 54.0%, 67.5%, and 45.2% at 4 hours, respectively. (g) Western blot analysis of renal Bax, Bcl-2, and cleaved-caspase-3 expression. (h) CPB upregulated the NADPH oxidase via the TLR-4/MyD88 pathway, which promoted the expressions of mitochondrial fission-related proteins Fis1 and Drp1 and reduced the expression of fusion-related protein Mfn2. ∗P < 0.05 vs. sham;

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