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Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Additionally we are shipping BCL2 Kits (24) and BCL2 Proteins (11) and many more products for this protein.
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These results suggest a role for mitochondrial p53 (show TP53 Antibodies) activity in promoting hair cell death due to aminoglycosides, likely upstream of Bax (show BAX Antibodies) and Bcl2.
Zebrafish gene expressions of P53 (show TP53 Antibodies), Bcl-2, Bax (show BAX Antibodies) and caspase-3 (show CASP3 Antibodies) were elevated after exposure with microcystin-LR under different ambient temperatures.
Analysis using clinical biopsy specimens revealed autophagy and increased levels of BCL2, S1P1 (show S1PR1 Antibodies), and ICAM1 (show ICAM1 Antibodies) in human T-lymphoblastic lymphoma compared with T-lymphoblastic leukemia.
Real-time RT-PCR revealed acetaminophen treatment of zebrafish embryos decreased the expression of cox2 (show COX2 Antibodies) and bcl2, but increased p53 (show TP53 Antibodies) expression.
Leukemia onset was dramatically accelerated in transgenic fish overexpressing human Notch1 (show NOTCH1 Antibodies) and fish bcl-2, indicating synergy between the Notch (show NOTCH1 Antibodies) pathway and the bcl2-mediated antiapoptotic pathway.
Bcl-2 is an essential regulator in the survival of doublecortin (show DCX Antibodies)-expressing immature neurons.
Results show that the deletion of BCL-2, on its own or in concert with MCL-1 (show MCL1 Antibodies), does not affect platelet production or platelet lifespan.
the expression changes observed within the BCL2 family did not depend on STAT3 (show STAT3 Antibodies) signalling, in line with its initiating role early in the process, but rather appear to result from relief of repression by STAT5 (show STAT5A Antibodies).
Bcl-2-caspase-9 (show CASP9 Antibodies) apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related proteins.
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
Studied the protein expression of BCL2, FGF-R1, and HSP70 (show HSP70 Antibodies) after short-time magnetic thermoablative tumor treatment using immunohistochemistry in a human BT474 breast cancer mouse xenograft model.
The increased level of Bcl-2 caused by the decrease in miR (show MLXIP Antibodies)-181c protected mitochondrial morphology from the tumour necrosis factor alpha (show TNF Antibodies)-induced apoptosis.
The expression of GRP78 (show HSPA5 Antibodies) and Bcl-2 was significantly higher in astrocytes pretreated with recombinant Shh (show SHH Antibodies). These findings suggest that the expression of Shh (show SHH Antibodies) may inhibit cell death by activating Bcl-2 through a GRP78 (show HSPA5 Antibodies)-dependent pathway.
Knockdown of NF-kappaB (show NFKB1 Antibodies) p65 (show NFkBP65 Antibodies) 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.
Studies suggest targeting the BCL-2 family for treating diseases with dysregulated apoptosis.
bcl-2 and bax (show BAX Antibodies) were expressed strongly in denervated guinea-pig facial muscle. [bcl-2; bax (show BAX Antibodies)]
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).
, B-cell leukemia/lymphoma 2
, apoptosis regulator Bcl-2
, B-cell CLL/lymphoma 2
, B cell lymphoma 2 associated oncogene
, Bcl2-like protein