AFfirm™ Bcl-2 Antibody - #BF9103

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Product: Bcl-2 Antibody
Catalog: BF9103
Description: Mouse monoclonal antibody to Bcl-2
Application: WB IHC IF/ICC ELISA
Reactivity: Human, Mouse, Rat
Mol.Wt.: 26 kd; 26kD(Calculated).
Uniprot: P10415
RRID: AB_2837570

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 100ul $280 In stock
 200ul $350 In stock

Lead Time: Same day delivery

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Mouse
Application:
WB 1:1000, 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
Clonality:
Monoclonal [AFfirm063]
Specificity:
The Bcl-2 mouse monoclonal antibody can detect endogenous Bcl-2 proteins.
RRID:
AB_2837570
Cite Format: Affinity Biosciences Cat# BF9103, RRID:AB_2837570.
Conjugate:
Unconjugated.
Purification:
affinity purification.
Storage:
Store at -20°C. Stable for one year from the date of shipment.1mg/ml in PBS, pH 7.4, containing 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 2; Apoptosis regulator Bcl-2; Apoptosis regulator Bcl2; AW986256; B cell CLL/lymphoma 2; B cell leukemia/lymphoma 2; Bcl-2; Bcl2; BCL2_HUMAN; C430015F12Rik; D630044D05Rik; D830018M01Rik; Leukemia/lymphoma, B-cell, 2; Oncogene B-cell leukemia 2; PPP1R50; Protein phosphatase 1, regulatory subunit 50;

Immunogens

Immunogen:

Mouse monoclonal antibody is prepared by immunizing synthetic peptide coupled to KLH.

Uniprot:

P10415(BCL2_HUMAN) >>Visit HPA database.

Gene(ID):
BCL2(596)
Expression:
P10415 BCL2_HUMAN:

Expressed in a variety of tissues.

Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability.
Sequence:
MAHAGRTGYDNREIVMKYIHYKLSQRGYEWDAGDVGAAPPGAAPAPGIFSSQPGHTPHPAASRDPVARTSPLQTPAAPGAAAGPALSPVPPVVHLTLRQAGDDFSRRYRRDFAEMSSQLHLTPFTARGRFATVVEELFRDGVNWGRIVAFFEFGGVMCVESVNREMSPLVDNIALWMTEYLNRHLHTWIQDNGGWDAFVELYGPSMRPLFDFSWLSLKTLLSLALVGACITLGAYLGHK

PTMs - P10415 As Substrate

Site PTM Type Enzyme
Y9 Phosphorylation
K22 Ubiquitination
S24 Phosphorylation
T56 Phosphorylation Q16539 (MAPK14) , P06493 (CDK1) , P53779 (MAPK10) , P28482 (MAPK1) , P27361 (MAPK3)
T69 Phosphorylation P45983 (MAPK8)
S70 Phosphorylation P27361 (MAPK3) , P06493 (CDK1) , P53779 (MAPK10) , P17252 (PRKCA) , Q00534 (CDK6) , P28482 (MAPK1) , P45983 (MAPK8)
T74 Phosphorylation P28482 (MAPK1) , P53779 (MAPK10) , P27361 (MAPK3)
S87 Phosphorylation Q16539 (MAPK14) , P45983 (MAPK8) , Q00534 (CDK6) , P27361 (MAPK3) , P28482 (MAPK1) , P53779 (MAPK10)
C158 S-Nitrosylation
C229 S-Nitrosylation
Y235 Phosphorylation

Research Backgrounds

Function:

Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release.

PTMs:

Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity. Growth factor-stimulated phosphorylation on Ser-70 by PKC is required for the anti-apoptosis activity and occurs during the G2/M phase of the cell cycle. In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases. Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-87, wich stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A) (By similarity).

Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity, causes the release of cytochrome c into the cytosol promoting further caspase activity.

Monoubiquitinated by PRKN, leading to increase its stability. Ubiquitinated by SCF(FBXO10), leading to its degradation by the proteasome.

Subcellular Location:

Mitochondrion outer membrane>Single-pass membrane protein. Nucleus membrane>Single-pass membrane protein. Endoplasmic reticulum membrane>Single-pass membrane protein.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in a variety of tissues.

Subunit Structure:

Forms homodimers, and heterodimers with BAX, BAD, BAK and Bcl-X(L). Heterodimerization with BAX requires intact BH1 and BH2 motifs, and is necessary for anti-apoptotic activity. Interacts with EI24 (By similarity). Also interacts with APAF1, BBC3, BCL2L1, BNIPL, MRPL41 and TP53BP2. Binding to FKBP8 seems to target BCL2 to the mitochondria and probably interferes with the binding of BCL2 to its targets. Interacts with BAG1 in an ATP-dependent manner. Interacts with RAF1 (the 'Ser-338' and 'Ser-339' phosphorylated form). Interacts (via the BH4 domain) with EGLN3; the interaction prevents the formation of the BAX-BCL2 complex and inhibits the anti-apoptotic activity of BCL2. Interacts with G0S2; this interaction also prevents the formation of the anti-apoptotic BAX-BCL2 complex. Interacts with RTL10/BOP. Interacts with the SCF(FBXO10) complex. 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 GIMAP3/IAN4, GIMAP4/IAN1 and GIMAP5/IAN5 (By similarity).

Family&Domains:

BH1 and BH2 domains are required for the interaction with BAX and for anti-apoptotic activity.

The BH4 motif is required for anti-apoptotic activity and for interaction with RAF1 and EGLN3.

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)

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

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

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

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

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

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

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

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

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum.   (View pathway)

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

· Human Diseases > Drug resistance: Antineoplastic > Endocrine 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: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

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

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

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

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

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

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

· Organismal Systems > Circulatory system > Adrenergic signaling in cardiomyocytes.   (View pathway)

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

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Cholinergic synapse.

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

References

1). Celastrol upregulated ATG7 triggers autophagy via targeting Nur77 in colorectal cancer. Phytomedicine (PubMed: 35752079) [IF=7.9]
2). Protective mechanisms of 10-gingerol against myocardial ischemia may involve activation of JAK2/STAT3 pathway and regulation of Ca2+ homeostasis. BIOMEDICINE & PHARMACOTHERAPY (PubMed: 35569350) [IF=7.5]

Application: WB    Species: Rat    Sample: myocardial tissues

Fig. 6. Effects of 10-Gin on the Bax, Bcl-2, Caspase-3 protein expressions in myocardial tissues (A). The band gray values of Bcl-2 (B), Bax (C), and Caspase-3 (D) were analyzed by normalization to β-actin. Data are represented as mean ± SEM. * P < 0.05, ** P < 0.01 vs. CONT; # P < 0.05, ## P < 0.01 vs. ISO group, n = 5.
3). Ginkgolide A targets forkhead box O1 to protect against lipopolysaccharide‐induced septic cardiomyopathy. Phytotherapy Research (PubMed: 36932920) [IF=7.2]
4). Chang qing formula ameliorates colitis-associated colorectal cancer via suppressing IL-17/NF-κB/STAT3 pathway in mice as revealed by network pharmacology study. Frontiers in Pharmacology (PubMed: 35991881) [IF=5.6]

Application: WB    Species: Mice    Sample: colon tissue

FIGURE 7 CQF suppressed the phosphorylation of STAT3 and altered the expression of its downstream proteins. (A,B) Expression of MMP9, p-STAT3, STAT3, Bcl-2, and Bax proteins in colon tissue (n = 4 per group). (C) Immunofluorescence staining of colon tissue, green: p-STAT3, red: MMP9, blue: DAPI. Values are expressed as mean ± SEM. # p < 0.05, ## p < 0.01, compared with normal mice; * p < 0.05, ** p < 0.01, compared with AOM/DSS-treated mice.
5). Activation of STING Pathway Contributed to Cisplatin-Induced Cardiac Dysfunction via Promoting the Activation of TNF-α-AP-1 Signal Pathway. Frontiers in Pharmacology (PubMed: 34483919) [IF=5.6]

Application: WB    Species: Mice    Sample: HL-1 cells

FIGURE 1 Activation of the cGAS-STING pathway was detected in cisplatin-induced HL-1 cells (A) HL-1 cells were incubated with CDDP (10, 20, 30, 40 μM) for 24 h and then the cell viability of HL-1 cells was examined by CCK8 analysis (n = 5 independent experiments; ### p < 0.001, vs. the 0 group). (B) HL-1 cells were incubated with CDDP (10, 20, 30, 40 μM) for 24 h, and then total protein was collected. The protein level of BAX and BCL2 in HL-1 cells was detected by Western blot. (C–D) HL-1 cells were incubated with CDDP (10, 20, 30, 40 μM) for 24 h, and then cell apoptosis induced by CDDP was detected by TUNEL staining. (C) Representative images of TUNEL staining in HL-1 cells (Green: TUNEL positive cell, DAPI: nucleus; Scale Bar: 25 μm, ×400 magnification). (D) Quantification of TUNEL-positive cells (E) HL-1 cells were incubated with CDDP (10, 20, 30, 40 μM) for 1 h, and total protein was collected. The protein level of p-STING, STING, p-TBK1, TBK1 in HL-1 cells was detected by Western blot (n = 3 independent experiments; # p < 0.05, ## p < 0.01, ### p < 0.001, vs. Vehicle group).
6). CTRP1 attenuates cerebral ischemia/reperfusion injury via the PERK signaling pathway. Frontiers in Cell and Developmental Biology (PubMed: 34422821) [IF=5.5]

Application: WB    Species: Rat    Sample: cortex

FIGURE 4 CTRP1 protected against cerebral ischemia reperfusion injury via alleviating neuron injury and apoptosis. (A) Neuron injury was analyzed by double labeling immunofluorescence staining. n = 3 per group. The representative images were acquired under × 400 magnification, scale bars = 50 μm. (B) Apoptosis in the cortex was analyzed by TUNEL, n = 3 per group. The representative images were acquired under × 200 magnification, scale bars = 100 μm. (C) Western blot analyzed the expression of CTRP1, BAX, Bcl-2, and CHOP in cortex. n = 4 per group. ****p < 0.0001, ***p < 0.01, **p < 0.01, *p < 0.05 vs. sham group; ####p < 0.0001, ##p < 0.01, #p < 0.05 vs. MCAO/R + LV-NC group.
7). Peptidase Inhibitor 16 Attenuates Left Ventricular Injury and Remodeling After Myocardial Infarction by Inhibiting the HDAC1‐Wnt3a‐β‐Catenin Signaling Axis. Journal of the American Heart Association (PubMed: 37158154) [IF=5.4]

Application: WB    Species: Mouse    Sample: heart tissue

Figure 3. PI16 inhibited the loss of cardiomyocytes and LV dysfunction at 24 hours after MI. A and E, Representative M‐mode images and echocardiographic data, including ejection fraction and fraction shortening from PI16‐Tg and WT mice subjected to MI or sham surgery after 24 hours (n=6). B, Representative images and quantification of heart sections with Evans blue (blue) and TTC staining (red) in WT and PI16‐Tg mice 24 hours after being subjected to MI (n=5). Scale bar, 5 mm. C, Representative Western blotting and quantitative analysis of PI16, Bax, Bcl‐2, Bax/Bcl2, and cleaved caspase 3 in heart tissue from PI16‐Tg and WT mice 24 hours after being subjected to MI or sham surgery (n=6). D, Representative images of TUNEL staining and quantitative data in the infarcted zone from WT and PI16‐Tg mice 24 hours after MI (n=5). Scale bar, 50 μm. E, Representative M‐mode images and echocardiographic data from PI16+/− and PI16−/− mice 24 hours after being subjected to MI or sham surgery (n=6). F, Representative heart images and quantitation of Evans blue and TTC staining from PI16+/− and PI16−/− mice 24 hours after being subjected to MI (n=5). Scale bar, 5 mm. G, Representative Western blotting and quantitation of apoptosis‐associated proteins in the hearts from PI16+/− and PI16−/− mice (n=6). H, Representative images of TUNEL staining and quantitative data from infarcted PI16+/− and PI16−/− hearts (n=4–5). Scale bar, 50 μm. Data are presented as the mean±SEM and are representative of 3 independent experiments. B, D, F, and H, A Student t test was used to assess the difference. A, C, E, and G, One‐way ANOVA was used to assess the difference. *P
8). Hepatocyte nuclear factor 4 gamma (HNF4G) is correlated with poor prognosis and promotes tumor cell growth by inhibiting caspase-dependent intrinsic apoptosis in colorectal cancer. European Journal of Pharmacology (PubMed: 34965388) [IF=5.0]
9). The miR-345-3p/PPP2CA signaling axis promotes proliferation and invasion of breast cancer cells Get access Arrow. CARCINOGENESIS (PubMed: 34922339) [IF=4.7]
10). LncRNA PVT1 promotes the malignant progression of acute myeloid leukaemia via sponging miR-29 family to increase WAVE1 expression. PATHOLOGY (PubMed: 33558065) [IF=4.5]

Application: WB    Species: Human    Sample: tumour tissues

Fig. 6 PVT1/WAVE1 axis regulates xenograft growth in vivo. (A) Photograph of the xenograft tumours from different groups. (B) Tumour volumes at the indicated time points and (C) tumour weight are presented. (D) Apoptosis in tumour tissues was evaluated by TUNEL assay. (E) Expression of Ki-67 in tumour tissues was determined by immunohistochemical staining. (F) The protein levels of Bax, Bcl-2, cleaved Caspase 3, p21, and cyclin D1 in tumour tissues was assessed by western blotting. All data are expressed as mean ± standard deviation. *p<0.05, **p<0.01, ***p<0.001 versus the indicated group.
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