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BCL2L11 Recombinant Monoclonal Antibody

Datasheet
Code CSB-RA147388A0HU
Size US$210
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Image
  • Western Blot
    Positive WB detected in: HepG2 whole cell lysate(30µg), U937 whole cell lysate(30µg), HEK293 whole cell lysate(30µg), HeLa whole cell lysate(30µg), COLO205 whole cell lysate(30µg)
    All lanes: BCL2L11 antibody at 1:1000
    Secondary
    Goat polyclonal to rabbit IgG at 1/50000 dilution
    Predicted band size: 22 kDa
    Observed band size: 22 kDa
    Exposure time: 3min
  • IHC image of CSB-RA147388A0HU diluted at 1:100 and staining in paraffin-embedded human colorectal cancer performed on a Leica BondTM system. After dewaxing and hydration, antigen retrieval was mediated by high pressure in a citrate buffer (pH 6.0). Section was blocked with 10% normal goat serum 30min at RT. Then primary antibody (1% BSA) was incubated at 4°C overnight. The primary is detected by a Goat anti-rabbit polymer IgG labeled by HRP and visualized using 0.05% DAB.
  • IHC image of CSB-RA147388A0HU diluted at 1:100 and staining in paraffin-embedded human kidney tissue performed on a Leica BondTM system. After dewaxing and hydration, antigen retrieval was mediated by high pressure in a citrate buffer (pH 6.0). Section was blocked with 10% normal goat serum 30min at RT. Then primary antibody (1% BSA) was incubated at 4°C overnight. The primary is detected by a Goat anti-rabbit polymer IgG labeled by HRP and visualized using 0.05% DAB.
  • Overlay Peak curve showing jurkat cells stained with CSB-RA147388A0HU (red line) at 1:100. The cells were fixed in 4% formaldehyde and permeated by 0.2% TritonX-100 for 10min. Then 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (1ug/1*106cells) for 45min at 4℃. The secondary antibody used was FITC-conjugated goat anti-rabbit IgG (H+L) at 1/200 dilution for 35min at 4℃.Control antibody (green line) was Rabbit IgG (1ug/1*106cells) used under the same conditions. Acquisition of >10,000 events was performed.
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Product Details

Uniprot No.
O43521
Target Names
BCL2L11
Alternative Names
BCL2 like 11 antibody; B2L11_HUMAN antibody; BAM antibody; Bcl 2 interacting protein Bim antibody; Bcl 2 related ovarian death agonist antibody; Bcl-2-like protein 11 antibody; BCL2 interacting mediator of cell death antibody; BCL2 like 11 (apoptosis facilitator) antibody; BCL2 like protein 11 antibody; Bcl2-interacting mediator of cell death antibody; Bcl2-L-11 antibody; Bcl2l11 antibody; BIM alpha6 antibody; BIM antibody; BIM beta6 antibody; BIM beta7 antibody; BimEL antibody; BimL antibody; BOD antibody
Species Reactivity
Human
Immunogen
A synthesized peptide derived from human BCL2L11
Immunogen Species
Homo sapiens (Human)
Conjugate
Non-conjugated
Clonality
Monoclonal
Isotype
Rabbit IgG
Clone No.
13F3
Purification Method
Affinity-chromatography
Concentration
It differs from different batches. Please contact us to confirm it.
Buffer
Rabbit IgG in 10mM phosphate buffered saline , pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.
Form
Liquid
Tested Applications
ELISA, WB, IHC, FC
Recommended Dilution
Application Recommended Dilution
WB 1:500-1:2000
IHC 1:50-1:200
FC 1:50-1:200
Protocols
ELISA Protocol
Western Blotting(WB) Protocol
Immunohistochemistry (IHC) Protocol
Flow Cytometry (FC) Protocol
Troubleshooting and FAQs
Antibody FAQs
Storage
Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time
Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Description

BCL2L11, commonly known as BIM, is a critical pro-apoptotic member of the BCL-2 protein family that plays a central role in initiating the intrinsic apoptosis pathway. As a BH3-only protein, BIM acts as a key sensor of cellular stress and directly activates BAX and BAK to trigger mitochondrial outer membrane permeabilization, making it essential for understanding programmed cell death in both normal physiology and disease contexts. Dysregulation of BIM has been implicated in cancer development, immune cell homeostasis, and responses to chemotherapeutic agents, positioning it as a significant target for oncology and immunology research.

This recombinant rabbit monoclonal antibody (clone 13F3) offers the reproducibility and consistency that demanding experimental workflows require. Generated against a synthetic peptide derived from human BCL2L11 and produced through recombinant technology, this antibody provides sequence-defined specificity with minimal lot-to-lot variation, ensuring reliable results across extended studies.

Validation testing demonstrates robust performance across multiple applications. Western blot analysis confirms detection of the expected 22 kDa band across diverse human cell lines including HepG2, U937, HEK293, HeLa, and COLO205, with optimal results at 1:500–1:2000 dilution. Immunohistochemistry studies show clear staining in paraffin-embedded human colorectal cancer and kidney tissue sections at 1:100 dilution using citrate buffer antigen retrieval. Flow cytometry validation in Jurkat cells demonstrates effective intracellular detection of BIM following fixation and permeabilization.

This antibody serves researchers investigating apoptotic signaling, cancer biology, drug resistance mechanisms, and immune cell development where precise detection of BIM expression is essential for advancing their work.

Usage
For Research Use Only. Not for use in diagnostic or therapeutic procedures.

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Target Background

Function
Induces apoptosis and anoikis. Isoform BimL is more potent than isoform BimEL. Isoform Bim-alpha1, isoform Bim-alpha2 and isoform Bim-alpha3 induce apoptosis, although less potent than isoform BimEL, isoform BimL and isoform BimS. Isoform Bim-gamma induces apoptosis. Isoform Bim-alpha3 induces apoptosis possibly through a caspase-mediated pathway. Isoform BimAC and isoform BimABC lack the ability to induce apoptosis.
Gene References into Functions
  1. POH1 knockdown induced cell apoptosis through increased expression of p53 and Bim. PMID: 29573636
  2. BIM deletion polymorphism was associated with significantly shorter progression-free survival (PFS) and slightly shorter overall survival (OS), compared to the WT group. Moreover, patients with BIM deletion polymorphism showed significantly inferior response to EGFR TKIs. In conclusion, our analysis confirmed that lung cancer patients harboring the BIM deletion have inferior survival and TKI responses. PMID: 30213299
  3. Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11 PMID: 30249504
  4. FoxO3a overexpression increased the transcription and protein expression of Bcl2like protein 11 and cyclindependent kinase inhibitor 1B, and inhibited cyclin D1 transcription and expression. PMID: 29257235
  5. Data indicate that miR-34a enhanced the sensitivity to cisplatin by upregulation of c-Myc and Bim pathway. PMID: 29060932
  6. Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant non-small cell lung cancer (NSCLC)cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291 PMID: 28765329
  7. TMEM16A expression was found to correlate with greater tumor size, less Bim expression, and less apoptotic activity overall in head and neck squamous cell carcinomas (HNSCCs). PMID: 28899969
  8. Hypermethylation of the proapoptotic genes BCL2 L11 and TNFRSF25 is observed in pleomorphic adenoma of the salivary glands. However, this phenomenon did not impact mRNA transcription. PMID: 28941993
  9. Data suggest that regulation of pancreatic beta-cell function and survival/apoptosis involves alternative splicing modulated by key splicing regulator SRP55; SRP55-regulated alternative splicing includes modulation of function of pro-apoptotic proteins (BIM, BAX), JNK signaling, and endoplasmic reticulum stress. (SRP55 = pre-mRNA-splicing factor SRP55; BAX = apoptosis regulator BAX) PMID: 29246973
  10. Bim expression was significantly different in the four molecular subtypes of breast cancer. PMID: 28582840
  11. BIM deletion is a significant predictor of shorter PFS and OS on EGFR-TKIs. Further studies to determine its effect on response to other BIM-dependent therapeutic agents are needed, so that alternative treatment strategies may be devised. PMID: 28467813
  12. These findings indicate the importance of developing HDAC3-selective inhibitors, and their combined use with osimertinib, for treating EGFR-mutated lung cancers carrying the BIM deletion polymorphism PMID: 27986747
  13. Low BIM expression is associated with renal cell carcinoma. PMID: 27582546
  14. The decreased miR-101-3p caused elevated Bim expression by targeting its 3'-untranslated region (3'-UTR). PMID: 28518140
  15. The mitochondrial apoptotic pathway, activated by BH3-only proteins, BIM and PUMA, is essential for endoplasmic reticulum stress-induced cell death; DR5 as well as caspase-8 are not required for this process. PMID: 28409774
  16. sequestration of Bim by Mcl-1 is a mechanism of intrinsic ABT-199 resistance and supports the clinical development of ABT-199 in combination with cytarabine or daunorubicin for the treatment of AML. PMID: 27103402
  17. Knock down of VDR and BIM reduces the enhancement of cell death treated with Cytarabine (AraC) followed by the addition of Doxercalciferol together with Carnosic acid (CA). PMID: 27144333
  18. UMI-77 enhances TRAIL-induced apoptosis by unsequestering Bim and Bak, which provides a novel therapeutic strategy for the treatment of gliomas. PMID: 28337703
  19. Conversion of Bim-BH3 from Activator to Inhibitor of Bak through Structure-Based Design. PMID: 29149594
  20. in FOXO3-death-resistant cells no point mutations in the TP53-DBD were found-in these cells FOXO3-TP53 complexes are formed and FOXO3-binding to the BIM-promoter, but not the induction of the detoxifying protein SESN3, were prevented, which in turn increased chemo-protection in this type of high-stage-derived neuroblastoma cells PMID: 28869600
  21. At BCL2L11, the authors identify a haematopoietic enhancer hub that is inactivated by the Epstein-Barr virus repressors EBNA3A and EBNA3C through recruitment of the H3K27 methyltransferase EZH2. PMID: 27490482
  22. observations suggest that an association of a deletion polymorphism of BIM and the response to induction therapy in B-cell precursor acute lymphoblastic leukemia may be clinically minimal PMID: 28641145
  23. expression of Bim is mediated by FoxO1 and indirectly downregulated by thyroid hormone/thyroid hormone receptor, leading to chemotherapy resistance and doxorubicin-promoted metastasis of hepatoma cells. PMID: 27490929
  24. BIM is associated with favorable prognostic markers for prediction of disease-free survival and overall survival in cervical cancer. PMID: 28870908
  25. this study shows that BIM deletion polymorphisms are associated with a poor clinical response to erlotinib and represents an independent prognostic factor for patients with EGFR positive non-small-cell lung cancer PMID: 27926478
  26. The Bim deletion polymorphism was found to be associated with primary resistance to crizotinib in patients with ALK fusion-positive NSCLC. PMID: 28346673
  27. increased apoptosis resistance was associated with significantly reduced up-regulation of proapoptotic Bim in T cells from patients with primary sclerosing cholangitis. PMID: 27630216
  28. Results suggest that valproic acid (VPA) reduces paraoxonase 2 (PON2) expression in glioblastoma multiforme (GBM) cells, which in turn increases reactive oxygen species (ROS) production and induces Bim protein production that inhibits cancer progression via the PON2-Bim cascade. PMID: 28108734
  29. Little difference in Bim expression among CD20+ cells was seen between tonsil primary follicles, tonsil germinal centers, and lupus nephritis renal tissue. The frequency of Bim-positive cells among CD4+ lymphocytes was significantly lower in lupus nephritis kidneys compared to tonsil controls. PMID: 27159593
  30. Inhibition of mTORC1-mediated 4EBP1 phosphorylation leads to decreased expression of c-MYC and subsequent upregulation of the proapoptotic BCL2 family member PUMA, whereas inhibition of mTORC2 results in nuclear factor-kappaB-mediated expression of the Early Growth Response 1 (EGR1) gene, which encodes a transcription factor that binds and transactivates the proapoptotic BCL2L11 locus encoding BIM. PMID: 26917778
  31. miR-423-3p activates oncogenic and Beclin-1-dependent autophagy and promotes GC progression by reducing the expression of Bim. The newly identified miR-423-3p-Bim axis might be a potential therapeutic target in GC. PMID: 28254439
  32. activation of the PI3K pathway does not suppress activation of the ARF or BIM gene by over-expressed E2F1 PMID: 27888102
  33. have shown that Bim protein expression in CM is an independent predictor for advanced disease confirming that this pro-apoptotic BH3-only protein might be a potent biomarker and promising therapeutic target PMID: 27356803
  34. BIM deletion polymorphism does not account for intrinsic resistance to EGFR-TKI in Patients With Lung Adenocarcinoma PMID: 27077907
  35. Mechanistically, G-Rg1 promoted the phosphorylation of Akt and FoxO3a and led to the cytoplasmic translocation of FoxO3a, which in turn suppressed FoxO3a-modulated expression of proapoptotic Bim and elevated the ratio of Bcl-2 to Bax. PMID: 27522666
  36. Dnd1 facilitates apoptosis by increasing the expression of Bim via its competitive combining with miR-221 in Bim-3'UTR. PMID: 28191469
  37. patients with BIM-g had significantly shorter progression-free survival than those without BIM-gamma (median: 304 vs. 732 days; p=0.023). CONCLUSION: Expression of BIM-gamma mRNA and BIM deletion polymorphism were strongly associated. BIM-gamma overexpression may have a role in apoptosis related to EGFR-tyrosine kinase inhibitor PMID: 27807070
  38. MicroRNA-301b directly targets the expression of Bim, a well-known pro-apoptotic protein. PMID: 27352910
  39. FOXO4 has an inhibitory effect in clearcell renal carcinoma cells, at least in part through inducing apoptosis via upregulation of Bim in the mitochondria-dependent pathway. PMID: 26780985
  40. Results indicate that upregulation of miR-124 could regulate apoptosis and impaired autophagy process in the MPTP model of Parkinson's disease, thus reducing the loss of dopaminergic neurons PMID: 25976060
  41. the Bim activated by doxorubicin-induced DNA damage might directly interrupt the interaction of Bcl-xl with pro-apoptotic proteins, Bak/Bax, to activate mitochondriadriven apoptosis. PMID: 26694174
  42. the BIM deletion polymorphism enhanced the emergence of populations with complete imatinib resistance, mimicking the situation in patients. PMID: 26517680
  43. BimEL-Bax pro-apoptotic cascade is activated by cAMP signalling of Bordetella adenylate cyclase toxin through SHP-1 phosphatase in phagocytes. PMID: 26334669
  44. miR-24 was found to be up-regulated while the expression of BCL2L11 was inhibited in tumor tissues of gastric cancer PMID: 26758252
  45. The potent antitumor activity of RHL may be mediated through downregulation of Bcl-2 and cyclin D expression and upregulation of BAX and Bim expression. PMID: 26707131
  46. mRNA expression of BIM and MTOR in 57 patients with EGFR-mutant non-small-cell lung cancer. PMID: 26639561
  47. miR-24 promotes tumor growth and angiogenesis by suppressing Bim expression in a model of pancreatic carcinoma PMID: 26517093
  48. miR-181b/Bim pathway may be a novel target used to overcome the chemoresistance in breast cancer PMID: 26572075
  49. Bcl-2 dependent NB cell lines are exquisitely sensitive to ABT-199 . Treatment with ABT-199 displaces Bim from Bcl-2 in NB to activate caspase 3, confirming the restoration of mitochondrial apoptosis PMID: 26874859
  50. Fluorizoline bind to prohibitin, inducing mitochondrial apoptotic pathway through NOXA and BIM upregulation. PMID: 26497683

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Subcellular Location
Endomembrane system; Peripheral membrane protein.; [Isoform BimEL]: Mitochondrion. Note=Translocates from microtubules to mitochondria on loss of cell adherence.; [Isoform BimL]: Mitochondrion.; [Isoform BimS]: Mitochondrion.; [Isoform Bim-alpha1]: Mitochondrion.
Protein Families
Bcl-2 family
Tissue Specificity
Isoform BimEL, isoform BimL and isoform BimS are the predominant isoforms and are widely expressed with tissue-specific variation. Isoform Bim-gamma is most abundantly expressed in small intestine and colon, and in lower levels in spleen, prostate, testis
Database Links

HGNC: 994

OMIM: 603827

KEGG: hsa:10018

STRING: 9606.ENSP00000376943

UniGene: Hs.469658

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