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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 Antibodies (11) and many more products for this protein.
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These results suggest a role for mitochondrial p53 (show TP53 Proteins) activity in promoting hair cell death due to aminoglycosides, likely upstream of Bax (show BAX Proteins) and Bcl2.
Zebrafish gene expressions of P53 (show TP53 Proteins), Bcl-2, Bax (show BAX Proteins) and caspase-3 (show CASP3 Proteins) 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 Proteins), and ICAM1 (show ICAM1 Proteins) 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 and bcl2, but increased p53 (show TP53 Proteins) expression.
Leukemia onset was dramatically accelerated in transgenic fish overexpressing human Notch1 (show NOTCH1 Proteins) and fish bcl-2, indicating synergy between the Notch (show NOTCH1 Proteins) pathway and the bcl2-mediated antiapoptotic pathway.
Bcl-2 is an essential regulator in the survival of doublecortin (show DCX Proteins)-expressing immature neurons.
Results show that the deletion of BCL-2, on its own or in concert with MCL-1 (show MCL1 Proteins), does not affect platelet production or platelet lifespan.
the expression changes observed within the BCL2 family did not depend on STAT3 (show STAT3 Proteins) signalling, in line with its initiating role early in the process, but rather appear to result from relief of repression by STAT5 (show STAT5A Proteins).
Bcl-2-caspase-9 (show CASP9 Proteins) 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 Proteins) 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 Proteins)-181c protected mitochondrial morphology from the tumour necrosis factor alpha (show TNF Proteins)-induced apoptosis.
The expression of GRP78 (show HSPA5 Proteins) and Bcl-2 was significantly higher in astrocytes pretreated with recombinant Shh (show SHH Proteins). These findings suggest that the expression of Shh (show SHH Proteins) may inhibit cell death by activating Bcl-2 through a GRP78 (show HSPA5 Proteins)-dependent pathway.
Knockdown of NF-kappaB (show NFKB1 Proteins) p65 (show NFkBP65 Proteins) 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 Proteins) were expressed strongly in denervated guinea-pig facial muscle. [bcl-2; bax (show BAX Proteins)]
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