BCL-XL Antibody - #AF6414

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Product: BCL-XL Antibody
Catalog: AF6414
Description: Rabbit polyclonal antibody to BCL-XL
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 30kDa; 26kD(Calculated).
Uniprot: Q07817
RRID: AB_2835244

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 100ul $280 In stock
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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
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: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(89%), Bovine(89%), Horse(100%), Sheep(89%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
BCL-XL Antibody detects endogenous levels of total BCL-XL.
RRID:
AB_2835244
Cite Format: Affinity Biosciences Cat# AF6414, RRID:AB_2835244.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:
Uniprot:

Q07817(B2CL1_HUMAN) >>Visit HPA database.

Gene(ID):
BCL2L1(598)
Expression:
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.

Description:
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.
Sequence:
MSQSNRELVVDFLSYKLSQKGYSWSQFSDVEENRTEAPEGTESEMETPSAINGNPSWHLADSPAVNGATGHSSSLDAREVIPMAAVKQALREAGDEFELRYRRAFSDLTSQLHITPGTAYQSFEQVVNELFRDGVNWGRIVAFFSFGGALCVESVDKEMQVLVSRIAAWMATYLNDHLEPWIQENGGWDTFVELYGNNAAAESRKGQERFNRWFLTGMTVAGVVLLGSLFSRK

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Horse
100
Dog
100
Rabbit
100
Pig
89
Bovine
89
Sheep
89
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q07817 As Substrate

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)

Research Backgrounds

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.

PTMs:

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.

Subcellular Location:

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
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.

Subunit Structure:

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.

Family&Domains:

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.

Research Fields

· 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)

References

1). Astragaloside IV attenuates myocardial dysfunction in diabetic cardiomyopathy rats through downregulation of CD36-mediated ferroptosis. Phytotherapy Research, 2023 (PubMed: 36882189) [IF=7.2]
2). Poly(ADP-ribose) polymerase family member 14 promotes functional recovery after spinal cord injury through regulating microglia M1/M2 polarization via STAT1/6 pathway. Neural Regeneration Research, 2023 (PubMed: 36751810) [IF=6.1]

Application: WB    Species: Mouse    Sample:

Figure 3 PARP14 deficiency exacerbates SCI-induced neuronal apoptosis at 7 days post-SCI. (A) Representative images and quantitative analysis of Nissl staining in each group. Lv-shPARP14 injection increased SCI-induced neuronal loss. (B, C) Representative images and quantitative analysis showing TUNEL+/NeuN+ immunofluorescence staining. Lv-shPARP14 injection increased SCI-induced neuronal apoptosis. White arrows indicate TUNEL+ (green, apoptosis cells)/NeuN+ (red, Cy3-labeled, neuronal marker) cells. Scale bars: 50 µm in A and B. (D) Western blot analysis of cleaved caspase 3, bax, Bcl-2, and Bcl-xl in each group. Lv-shPARP14 injection enhanced the SCI-induced increase in cleaved caspase 3 and bax (pro-apoptotic factors) expression and decrease in Bcl-2 and Bcl-xl (anti-apoptotic factors) expression. Values are shown as mean ± SD (n = 6). *P < 0.05, **P < 0.01 (one-way analysis of variance followed by Tukey’s post hoc test). Images were taken from the gray matter ventral horn at the injury site. Spinal cord tissues from the injury site were used for western blot detection. DAPI: 4′,6-Diamidino-2-phenylindole; PARP14: poly(ADP-ribose)polymerase, member 14; SCI: spinal cord injury; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling.
3). Irisin Enhances Doxorubicin-Induced Cell Apoptosis in Pancreatic Cancer by Inhibiting the PI3K/AKT/NF-κB Pathway. MEDICAL SCIENCE MONITOR, 2019 (PubMed: 31412018) [IF=3.1]

Application: WB    Species: human    Sample: MIA PaCa-2 and BxPC-3 cells

Figure 3.| Irisin enhances DOX-induced apoptosis in PC cells. MIA PaCa-2 cells were exposed to 100 nM irisin alone, 0.75 μg/mL DOX alone, or DOX combined with irisin for 24 h. BxPC-3 cells were exposed to 100 nM irisin alone, 1.5 μg/mL DOX alone, or DOX combined with irisin for 24 h. (C) Western blot analysis of the levels of cleaved PARP, cleaved caspase-3, BCL-2, and BCL-xL protein in MIA PaCa-2 (a) and BxPC-3 (b) cells. b-actin served as the loading control.
4). miR-374 improves cerebral ischemia reperfusion injury by targeting Wnt5a. EXPERIMENTAL ANIMALS, 2021 (PubMed: 33116025) [IF=2.4]

Application: WB    Species: rat    Sample: brain

Fig. 3. |Overexpression of miR-374 attenuated cerebral IR-induced apoptosis. (B) Western blot showing expression of apoptosis-related proteins (BCL-XL, BCL-2, and BAX) in brain tissues. Data are presented as the mean ± SD, and they were analyzed by unpaired t-test. Comparison of the sham group with the IR group and the IR + NC agomir group with the IR + miR-374 agomir group: *P<0.05; ***P<0.001; ****P<0.0001.

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