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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 ELISA Kits) expression promotes survival of immature B cells, expression of BCL-2 (show BCL2 ELISA Kits) 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 ELISA Kits)-32/MCL-1 pathway members were identified as key early genetic events driving melanoma progression.
GSK3B (show GSK3b ELISA Kits)-MCL1 signaling to regulate axonal autophagy might be important for the successful completion of Wallerian degeneration.
Specific downregulation of Mcl-1 significantly increases apoptosis of peritoneal macrophages and that the MAPK (show MAPK1 ELISA Kits) signaling pathway is the primary mediator of Mcl-1 expression.
MCL1 plays a pivotal role in Leydig-cell steroidogenesis, and might provide novel insights into metabolic regulation in this cell
Although loss of one Mcl-1 allele did not noticeably impair the survival of normal B lymphoid cells, it markedly diminished the survival of Proto-Oncogene (show RAB1A ELISA Kits) Proteins c-myc (show MYC ELISA Kits) overexpressing B cell progenitors.
MCL-1 loss in early B-lymphoid progenitors delayed MYC (show MYC ELISA Kits)-driven lymphomagenesis.
High Mcl-1 levels enhanced mTOR (show FRAP1 ELISA Kits) phosphorylation and augmented the differentiation of terminal effector cells and effector memory CD8 (show CD8A ELISA Kits) T cells.
HB-EGF (show HBEGF ELISA Kits) is implicated in DNA double strand breaks repair as silencing of HB-EGF (show HBEGF ELISA Kits) increased gammaH2AX (show H2AFX ELISA Kits) foci half-life as well as USP9X (show USP9X ELISA Kits) expression, two features that could be linked to the observed effect on Mcl-1.
Augmentation of proteasome activity had a critical role in downregulation of Mcl-1 and c-FLIP (show CFLAR ELISA Kits) expression at the post-translational level.
These findings provide new insights into MCL-1 ligands, and the interplay between DRP-1 (show CRMP1 ELISA Kits) and the anti-apoptotic BCL-2 (show BCL2 ELISA Kits) family members in the regulation of apoptosis
the c-FLIP (show CFLAR ELISA Kits) and NOXA (show PMAIP1 ELISA Kits)/Mcl-1 axis participated in the synergistic effect of pemetrexed plus cisplatin in human choroidal melanoma cells
that inhibition of Mcl-1 expression by siRNA considerably enhanced Pevonedistat-triggered the activation of caspase-3 (show CASP3 ELISA Kits), PARP (show COL11A2 ELISA Kits) cleavage and apoptosis
Targeted Mcl-1 blockade using RNAi increased caspase (show CASP3 ELISA Kits)-mediated cell death in ERalpha (show ESR1 ELISA Kits)(+) breast cancer cells, resulting in sustained growth inhibition.
Expression level of MCL-1 is upregulated in renal cell carcinoma.
Study indicates that two distinct micro-environmental factors, CD40L (show CD40LG ELISA Kits) and Mphis, signal via CCR1 to induce AKT (show AKT1 ELISA Kits) activation resulting in translational stabilization of MCL-1, and hence can contribute to CLL cell survival.
High MCL1 expression is associated with cisplatin-resistance in breast cancer.
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