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Human BCL2 Protein expressed in Wheat germ - ABIN1346542
Su, Guo, Qi: Threonine 56 phosphorylation of Bcl-2 is required for LRRK2 G2019S-induced mitochondrial depolarization and autophagy. in Biochimica et biophysica acta 2014
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.
The findings are consistent with rs539846 influencing chronic lymphocytic leukemia (CLL) susceptibility through differential RELA (show NFkBP65 Proteins) binding, with direct modulation of BMF (show BMF Proteins) expression impacting on anti-apoptotic BCL2, a hallmark of oncogenic dependency in CLL.
DR_MOMP delivers a system-based biomarker with significant potential as a prognostic tool for stage III CRC (show CALR Proteins) that significantly improves established histopathological risk factors. BCL-2-dependent signalling critically contributed to treatment responses in consensus molecular subtypes 1 and 3, linking for the first time specific molecular subtypes to apoptosis signalling.
Results show that expression level of mTOR (show FRAP1 Proteins) and BCL2 are regulated by miR497 and provide evidence for their role in the development of TMZ-resistance phenotype of glioma cells.
Data show that MYC (show MYC Proteins), BCL2 and BCL6 (show BCL6 Proteins) translocation had no prognostic impact with respect to progression free survival (PFS) or overall survival (OS).
Interaction of the N-Terminal Tandem Domains of hnRNP (show HNRNPC Proteins) LL with the BCL2 Promoter i-Motif DNA Sequence
MYC (show MYC Proteins)/BCL2 co-expression is associated with a poorer prognosis and is independent of cell-of-origin classification in diffuse large B-cell lymphoma in the CNS.
These findings provide new insights into MCL-1 (show MCL1 Proteins) ligands, and the interplay between DRP-1 (show CRMP1 Proteins) and the anti-apoptotic BCL-2 family members in the regulation of apoptosis
Our findings suggest that the molecular machinery and mechanisms for executing Bcl-2-mediated apoptosis as observed in mammals are evolutionary ancient, with early regulation of apoptotic machineries closely resembling their modern counterparts in mammals rather than Caenorhabditis elegans or drosophila.
Clinical utility for selective inhibition of specific anti-apoptotic Bcl-2 family proteins has recently been realized with the Food and Drug Administration (FDA) approval of venetoclax (formerly ABT-199/GDC (show SLC25A16 Proteins)-0199) in relapsed chronic lymphocytic leukemia (CLL) with 17p deletion.
E2 protects skeletal myoblasts against apoptosis induced by H2 O2 modulating p53 (show TP53 Proteins) and FoxO (show FOXO3 Proteins) transcription factors and then their target genes Bcl-2, Bim (show BCL2L11 Proteins), Puma (show BBC3 Proteins), PERP (show PERP Proteins), and MDM2 (show MDM2 Proteins), without affecting Noxa (show PMAIP1 Proteins) gene.
Bcl-2 expression has a significant impact on the mineralogical content of enamel crystals of tooth structure
The results suggest that CARP (show ANKRD1 Proteins) can protect against hypoxia-reperfusion induced cardiomyocyte apoptosis, possibly through increasing anti-apoptosis Bcl2 gene expression.
This study provides evidence from transgenic mouse models that Crebbp (show CREBBP Proteins) deletion results in deficits in B-cell development and can cooperate with Bcl2 overexpression to promote B-cell lymphoma.
an essential role for the binding of BCL2 to BIM (show BCL2L11 Proteins) in the survival of noncycling NK cells.
LIGHT signalling pathway combined with IFN-gamma (show IFNG Proteins) induces beta cells apoptosis via an NF-kappaB (show NFKB1 Proteins)/Bcl2-dependent mitochondrial pathway.
Bcl-2 was highly expressed in tubulointerstitial infiltrates in (NZB x NZW)F1 (NZB/NZW) lupus-prone mice.
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
the augmentation of endogenous MTA1 (show MTA1 Proteins) expression during neuronal ischemic injury acts additionally to an endocrinous cascade orchestrating intimate interactions between ERalpha (show ESR1 Proteins) and BCL2 pathways.
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.
Over-expression of STC-1 (show STC1 Proteins) up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 (show CASP3 Proteins) production in the damaged cells. Findings from this study suggest that STC-1 (show STC1 Proteins) plays a protective role in intestinal cells through an antioxidant mechanism.
BoHV-5 replication apparently modulates BCL-2 expression and gene transcription, enhancing production of virus progeny, but does not increase Bax (show BAX Proteins) expression.
G3139, a BCL-2 antisesnse oligonucleotide is a promising candidate for treatment of patients with imatinib-resistant Ph-positive leukemia.
role of vascular endothelial growth factor receptor-1 (show FLT1 Proteins) in Bcl-2 expression
apoptosis-inducing factor (show AIFM1 Proteins) was expressed in luminal alveolar cells and, in concert with a change in bax (show BAX Proteins) protein to bcl-2 protein ratio, might contribute to signalling of a change in the dynamic balance of the cell population as lactation progresses
mRNA expression of Bax (show BAX Proteins), Bcl-2, caspase-3 (show CASP3 Proteins) and-7 cannot be used as a reliable apoptosis detection method.
These results propose an additional mechanism whereby resveratrol may exert its cardioprotective effects and suggest a key role for Bcl-2 in the resveratrol anti-apoptotic action, especially in disrupting peroxynitrite-triggered mitochondrial pathway.
bcl-2 and bax (show BAX Proteins) were expressed strongly in denervated guinea-pig facial muscle. [bcl-2; bax (show BAX Proteins)]
excessive apoptosis does occur in acetabular cartilage with developmental dislocations of the hip, and is positively correlated with high caspase-3 (show CASP3 Proteins) expression as well as low Bcl-2 expression.
These results indicate that RI-PostC can ameliorate myocardial ischemia-reperfusion injury and increase the Bcl-2/Bax ratio through a mechanism involving protein kinase C.
Cinobufagin can remarkably inhibit the proliferation and induce the apoptosis of lens epithelial cells by increasing expression of bax (show BAX Proteins) and decreasing expression of bcl2.
Elevated local temperature of the testis buried in the inguinal pocket increases the apoptosis of spermatogenic cells, and the spermatogenic cell apoptosis is highly correlated with the decreased expression of Bcl-2 and increased expression of Bax (show BAX Proteins).
Our data indicate that exposure to rabbits to Pb(Ac)(2) caused a significant increase of apoptosis protein p53 (show TP53 Proteins) and decrease in the antiapoptotic BCl2 proteins.
Isoflurane delayed preconditioning can inhibit the apoptosis of myocardium by up-regulating the expression of Bcl-2 and down-regulating the activation of caspase-3 (show CASP3 Proteins).
Data show that the damaged electron transport chain leads to bcl-2 depletion and MPT opening.
This gene encodes 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. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends.
apoptosis regulator Bcl-2
, protein phosphatase 1, regulatory subunit 50
, B cell lymphoma 2 associated oncogene
, B-cell leukemia/lymphoma 2
, Bcl2-like protein
, BCL2B-cell CLL/lymphoma 2
, B-cell lymphoma protein 2
, B-cell CLL/lymphoma 2
, LOW QUALITY PROTEIN: apoptosis regulator Bcl-2
, Apoptosis regulator Bcl-2