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The findings support a model in which survival is determined by quantitative participation of multiple anti-apoptotic proteins, BCL2 (show BCL2 Proteins), Mcl1, and BCL2A1 (show BCL2A1 Proteins), rather than by a single anti-apoptotic protein.
This dynamic change in B cell survival mechanisms is unique to Epstein-Barr virus-infected cells and relies on regulation of MCL-1 mitochondrial localization and BFL-1 transcription by the viral EBNA3A protein.
Overexpression of Mcl-1 via the hemopoietic cell specific vavP-Mcl-1 transgene markedly exacerbates and accelerates the lpr (show FAS Proteins) phenotype. The progressive splenomegaly and lymphadenopathy displayed by lpr (show FAS Proteins) mice was far more severe in Mcl (show CLEC4D Proteins)-1tg/lpr (show FAS Proteins) littermates
Endothelial cell -specific deletion of Mcl1 resulted in a dose-dependent increase in endothelial cell apoptosis in the angiogenic vasculature and a corresponding decline in vessel density.
Our findings indicate that MCL-1 expression is an important biomarker of TEC survival
These results identify MCL-1 as a critical prosurvival protein for preventing beta-cell death and clarify the mechanisms behind its downregulation by proinflammatory cytokines.
These data show that Mcl-1 is dispensable for the regulation of apoptosis during infection with different large DNA viruses.Bcl-XL, on the other hand, can be important to maintain survival of virus-infected cells
BCL-XL (show BCL2L1 Proteins) expression promotes survival of immature B cells, expression of BCL-2 (show BCL2 Proteins) is important for survival of mature B cells and long-lived plasma cells (PC), and expression of MCL-1 is important for survival throughout B-cell development.
miR (show MLXIP Proteins)-32/MCL-1 pathway members were identified as key early genetic events driving melanoma progression.
GSK3B-MCL1 signaling to regulate axonal autophagy might be important for the successful completion of Wallerian degeneration.
Data suggest that FBXW7, MCL1 and PLK1 may be relevant predictive markers of tumor progression and response to paclitaxel treatment.
Synthesis of MCL1, an antiapoptotic protein known to play a role in cancer cell survival during cell division, depends on the function of MELK (show MELK Proteins)-elF4B signaling.
Immunohistochemical analysis showed that the MCL-1 positive rate among myelodysplastic syndromes (MDSs) bone marrow CD34 (show CD34 Proteins) positive cells significantly increased during transformation to overt leukaemia (OL). Additionally, MCL-1 positive cells were negative for cleaved caspase 3 (show CASP3 Proteins), which indicated that these cells avoided apoptosis.
sequestration of Bim (show BCL2L11 Proteins) 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 (show RUNX1 Proteins).
Quinacrine and sorafenib inhibited expression of prosurvival MCL1.
Mcl-1 suppression was determined to play a critical role in mediating this enhancing effect.
The authors identified the apoptosis regulator Mcl-1 as a target that interacts with Chlamydia trachomatis Cdu1 and is stabilized by deubiquitination at the chlamydial inclusion.
geraniin retarded ovarian cancer growth and reduced expression of phospho-p65 (show GORASP1 Proteins) and Mcl-1. Collectively, geraniin elicits growth suppression in ovarian cancer through inhibition of NF-kappaB (show NFKB1 Proteins) and Mcl-1 and may provide therapeutic benefits for this malignancy.
Data show that Noxa (show PMAIP1 Proteins)-mediated MCL-1 phosphorylation and degradation is regulated by CDK2 (show CDK2 Proteins).
UMI-77 alone or in combination with TRAIL untethered pro-apoptotic Bcl-2 (show BCL2 Proteins) proteins Bim (show BCL2L11 Proteins) and Bak (show BAK1 Proteins) from the sequestration of Mcl-1 and promoted the conformational activation of Bak (show BAK1 Proteins).
This gene encodes an anti-apoptotic protein, which is a member of the Bcl-2 family. Alternative splicing results in multiple transcript variants. The longest gene product (isoform 1) enhances cell survival by inhibiting apoptosis while the alternatively spliced shorter gene products (isoform 2 and isoform 3) promote apoptosis and are death-inducing.
bcl-2-related protein EAT/mcl1
, induced myeloid leukemia cell differentiation protein Mcl-1 homolog
, bcl-2-like protein 3
, induced myeloid leukemia cell differentiation protein Mcl-1
, myeloid cell leukemia ES
, myeloid cell leukemia protein 1