Recombinant Mouse Apoptosis regulator Bcl-2(Bcl2),partial

In Stock
Code CSB-EP002611MO
Size US$2466
  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.

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Product Details


In the production of recombinant Mouse Bcl2 protein, the gene for Bcl2 (E.coli) was cloned into a vector and expressed as Bcl2 protein in E.coli. The plasmids with the copy of Bcl2, or the expression vector, were often used to enhance gene expression. Every step of production was undergone with a strict QC system. N-terminal 6xHis tag was used in the process. The purity is 90% determined by SDS-PAGE.

Bcl-2 was the first identified cellular protein that functions as an oncogene by blocking apoptotic cell death. Bcl-2 was initially cloned from the breakpoint of the t(14:18) chromosomal translocation found in the majority of patients with follicular lymphoma. Its oncogenic activity was established when transgenic mice bearing a BCL-2 immunoglobulin minigene fusion that recapitulates the t(14:18) translocation were found to develop follicular hyperplasia and lymphoma.For almost two decades, Bcl-2 has been thought to act by inhibiting one specific form of programmed cell death, apoptosis. Nearly all of the effects of Bcl-2 in cancer have been attributed to its effects on the apoptotic pathway, although it is known that Bcl-2 family members are multifunctional proteins that can influence other cellular processes, including cell cycle progression, calcineurin signaling, glucose homeostasis, and transcriptional repression by p53.

Purity Greater than 90% as determined by SDS-PAGE.
Target Names Bcl2
Uniprot No. P10417
Research Area Others
Alternative Names
Bcl2; Bcl-2; Apoptosis regulator Bcl-2
Species Mus musculus (Mouse)
Source E.coli
Expression Region 5-205aa
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 26.7kDa
Protein Length Partial
Tag Info N-terminal 6xHis-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time 3-7 business days
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

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Target Background

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). Also acts as an inhibitor of autophagy: interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function. May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release.
Gene References into Functions
  1. data demonstrate that disruption of the beclin 1-BCL2 complex is an effective mechanism to increase autophagy, prevent premature ageing, improve healthspan and promote longevity in mammals PMID: 29849149
  2. Results support a link between age-related apoptosis in auditory cortex neurons and miR-34a/Bcl-2 signaling, which may serve as a potential mechanism of the expression of age-related hearing loss in the auditory cortex. PMID: 28817812
  3. MiR-146a inhibits proliferation and induces apoptosis in murine osteoblastic MC3T3-E1 by regulating Bcl2 PMID: 28975995
  4. Ru(II)/diphenylphosphine/pyridine-6-thiolate complexes induce S-180 cell apoptosis through intrinsic mitochondrial pathway involving inhibition of Bcl-2 and p53/Bax activation. PMID: 28795366
  5. The results suggest that SPK2 interacts with Bcl2 via its BH3 domain, thereby dissociating it from Beclin-1 and activating autophagy while protecting neurons against ischemic injury. PMID: 28682313
  6. The findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins, BCL2, Mcl1, and BCL2A1, rather than by a single anti-apoptotic protein. PMID: 28362427
  7. Bcl-2 is strongly expressed in the inner hair cells and spiral ganglion neurons of young mice. In addition, moderate Bcl-2 expression is also detected in the outer hair cells and in the neurons of the auditory cortex. A significant reduction of Bcl-2 expression in the cochlea or auditory cortex is also associated with elevated hearing thresholds and hair cell loss during aging. PMID: 27925611
  8. Bcl2 is the autophagy-related target of miR-449a. PMID: 27351886
  9. anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L. PMID: 27367565
  10. Acute ethanol exposure induced autophagy-mediated heart toxicity and injury mainly through the ROS-JNK-Bcl-2 signaling pathway. PMID: 28369910
  11. Th17 cells are resistant to glucocorticoid-induced apoptosis and cytokine suppression, at least in part due to high levels of BCL-2. These findings support a role of Th17 cells in glucocorticoid-resistant inflammatory conditions such as certain endotypes of asthma. PMID: 26752231
  12. E2 protects skeletal myoblasts against apoptosis induced by H2 O2 modulating p53 and FoxO transcription factors and then their target genes Bcl-2, Bim, Puma, PERP, and MDM2, without affecting Noxa gene. PMID: 27249370
  13. Bcl-2 expression has a significant impact on the mineralogical content of enamel crystals of tooth structure PMID: 28610838
  14. The results suggest that CARP can protect against hypoxia-reperfusion induced cardiomyocyte apoptosis, possibly through increasing anti-apoptosis Bcl2 gene expression. PMID: 27713078
  15. This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 overexpression to promote B-cell lymphoma. PMID: 28288979
  16. an essential role for the binding of BCL2 to BIM in the survival of noncycling NK cells. PMID: 28057804
  17. LIGHT signalling pathway combined with IFN-gamma induces beta cells apoptosis via an NF-kappaB/Bcl2-dependent mitochondrial pathway. PMID: 27241100
  18. Bcl-2 was highly expressed in tubulointerstitial infiltrates in (NZB x NZW)F1 (NZB/NZW) lupus-prone mice. PMID: 27159593
  19. Bcell lymphoma 2, an antiapoptotic gene, was the target of mmumiR96. PMID: 28259902
  20. The abnormal expression of epidermal cytokeratins suggests that Ha-Ras and Bcl-2 suppress the terminal differentiation and sustain the stem cell-like features in epidermal keratinocytes PMID: 27655119
  21. the augmentation of endogenous MTA1 expression during neuronal ischemic injury acts additionally to an endocrinous cascade orchestrating intimate interactions between ERalpha and BCL2 pathways. PMID: 26728277
  22. Interestingly, SKPs showed higher protein levels of Bcl-2, Nrf2, and HO-1 than FBs. SKPs exert a beneficial effect on resisting UVB-induced apoptosis, which may be associated with Bcl-2 and Nrf2 upregulation. PMID: 27635399
  23. Bcl-2 is an essential regulator in the survival of doublecortin-expressing immature neurons. PMID: 26266948
  24. Results show that the deletion of BCL-2, on its own or in concert with MCL-1, does not affect platelet production or platelet lifespan. PMID: 25880088
  25. the expression changes observed within the BCL2 family did not depend on STAT3 signalling, in line with its initiating role early in the process, but rather appear to result from relief of repression by STAT5. PMID: 26045049
  26. Bcl-2-caspase-9 apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related proteins. PMID: 26938720
  27. Bcl-2 expression in the endothelium plays a significant role during postnatal retinal vascularization, and pathological choroidal but not retinal neovascularization, suggesting vascular bed specific Bcl-2 function in the endothelium PMID: 26444547
  28. Studied the protein expression of BCL2, FGF-R1, and HSP70 after short-time magnetic thermoablative tumor treatment using immunohistochemistry in a human BT474 breast cancer mouse xenograft model. PMID: 25792827
  29. The increased level of Bcl-2 caused by the decrease in miR-181c protected mitochondrial morphology from the tumour necrosis factor alpha-induced apoptosis. PMID: 25898913
  30. The expression of GRP78 and Bcl-2 was significantly higher in astrocytes pretreated with recombinant Shh. These findings suggest that the expression of Shh may inhibit cell death by activating Bcl-2 through a GRP78-dependent pathway. PMID: 25961032
  31. Knockdown of NF-kappaB p65 subunit expression can significantly inhibit the growth of nude mouse Lewis tumour cell xenografts by inducing tumour cell apoptosis and downregulating pro-apoptotic protein Bcl-2 expression. PMID: 26178579
  32. Studies suggest targeting the BCL-2 family for treating diseases with dysregulated apoptosis. PMID: 26344567
  33. Deletion of AU-rich elements within the Bcl2 3'UTR reduces protein expression and B cell survival PMID: 25680182
  34. The nuclear-penetrating anti-dsDNA autoantibodies could possibly function as a pathogenic factor for lupus nephritis by up-regulating ERK activation and Bcl-2 production in mesangial cells. PMID: 26189065
  35. Enhanced splicing of XBP-1 was observed in BCL-2 overexpressing cells implicating BCL-2 in the complex regulation of IRE1alpha activity. PMID: 26319553
  36. Bcl-2 counteracts palmitate-induced beta-cell death by maintaining mitochondrial membrane integrity and augmenting NF-kappaB activity, but not by affecting ROS production and ER stress PMID: 25266628
  37. BCL2-overexpressing B cells required multiple GC transits before acquiring FL-associated developmental arrest and presenting as GC B cells with constitutive activation-induced cytidine deaminase (AID) mutator activity. PMID: 25384217
  38. ZFP36L1 interacts with and mediates degradation of anti-apoptotic BCL2 mRNA as its important target in malignant B-cells. PMID: 25014217
  39. MPT64 could inhibit the apoptosis of RAW264.7 macrophages through the NF-kappaB-miRNA21-Bcl-2 pathway PMID: 25000291
  40. Suggest that when encountering harmful stress (hypoxia), melanoma cells overexpress Bcl-2 and turn to senescence, a permanent cell-cycle arrest, for prolonged survival. PMID: 24966955
  41. Bcl2 deficiency activates FoxO1 and FoxO3a through Akt inactivation and causes an increase in bone mass and osteoblast apoptosis. PMID: 24466179
  42. we demonstrate that inhibition of Bcl-2 increasingly stimulates NSCs proliferation, so that, it suggests that Bcl-2 controls NSCs differentiation to neurons. PMID: 25470948
  43. sigmaR1 regulates endoplasmic reticulum stress in retinal Muller cells and that the role of sigmaR1 in retinal neuroprotection probably involves BCL2. PMID: 24469320
  44. But not the IL-15 effect on Bcl-2 proteins. PMID: 24825007
  45. Data indicate that triggering receptor expressed on myeloid cells 1 (TREM-1) induces anti-apoptotic protein Bcl-2 and prolongs macrophage survival. PMID: 24711453
  46. Data suggest, in pancreatic beta-cells exposed to nonesterified fatty acid/palmitate, microRNA 34a expression is upregulated, apoptosis is promoted, and expression of Bcl2 is downregulated; silencing of Bcl2 gene expression promotes apoptosis. PMID: 24829923
  47. Differences in cell-death susceptibility between the undifferentiated and differentiated states showed that the mitochondria-localised anti-apoptotic protein Bcl-2 was highly expressed in undifferentiated Embryonic stem cells PMID: 24293136
  48. Bcl-2 levels are upregulated following traumatic brain injury, contributing to neuronal cell death. PMID: 25057207
  49. Myotubes of differentiated C2C12 cells with low levels of Bcl-2 expression are particularly vulnerable to apoptosis. PMID: 24129924
  50. In resistant Bcl2-expressing mouse lymphoma cells, 2 missense mutations within the Bcl2 BH3 domain were identified. Both F101C and F101L mutations impeded ABT-199 binding to the BH3 domain, therefore suppressing mitochondrial apoptosis PMID: 24786774

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Subcellular Location Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein.
Protein Families Bcl-2 family
Tissue Specificity Expressed in a variety of tissues.
Database Links

KEGG: mmu:12043

STRING: 10090.ENSMUSP00000108371

UniGene: Mm.257460

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