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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.
Data suggest Leishmania donovani exploits host anti-apoptotic protein MCL-1 to prevent apoptosis of host macrophages upon treatment with antiparasitic agents; thus, L. donovani protects its host, a factor in progression of visceral leishmaniasis.
Data demonstrate that soluble factors from MM cells are able to generate MDSC through Mcl-1 upregulation.
a mechanism of inverse coregulation between BECN1 (show BECN1 ELISA Kits) and MCL1 significantly contributes to their opposing roles in tumorigenesis
There is a non-redundant pathway linking IL-15 (show IL15 ELISA Kits) to Mcl1 in the maintenance of NK cells and innate immune responses in vivo.
Authors recognize MCL-1 as the essential survival factor required for conservation of the postnatal PMF (show PRB1 ELISA Kits) pool, growing follicle survival and effective oocyte mitochondrial function.
knockdown of MCL-1 in MRT cell lines induced apoptosis and increased DOX sensitivity in malignant rhabdoid tumor cells
there was minimal effect of HDAC (show HDAC3 ELISA Kits) inhibition on H3/H4 acetylation and H3K4me3 levels along the MCL1 gene and no change in pre-mRNA splicing choice
The mechanisms by which silencing Mcl-1 sensitizes hepatoma cells towards chemotherapy may be not attributed to the upregulated expression of p53 (show TP53 ELISA Kits) but the dysfunction of p53 (show TP53 ELISA Kits) through Mcl-1/p53 (show TP53 ELISA Kits) interaction. Mcl-1 may be a potential target of gene therapy for Hepatocellular carcinoma (HCC (show FAM126A ELISA Kits))
BAG3 (show BAG3 ELISA Kits) was found to positively regulate Mcl-1 levels by binding to and inhibiting USP9X (show USP9X ELISA Kits). Our data show that BAG3 (show BAG3 ELISA Kits) and Mcl-1 are key mediators of resistance to chemotherapy in ovarian cancer
demonstrate that downregulation of PHD3 (show EGLN3 ELISA Kits) augments metastatic spread in human colorectal cancer and identify MCL-1 as a novel downstream effector of oxygen sensing
addition of imperatorin significantly reversed the resistance to cisplatin in cisplatin-resistant HCC (show FAM126A ELISA Kits) cells, which was Mcl-1 dependent
In particular, the treatment with the cocrystal MetH(2 (show ADAMTS8 ELISA Kits))(++)*2DCA(-) induced a synergistic apoptotic cell death coupled to a marked down-modulation of the anti-apoptotic Mcl-1 protein.
these findings provided that in lung cancer cells, tumor suppressor miR (show MLXIP ELISA Kits)-451 enhanced DPP (show DSPP ELISA Kits) sensitivity via regulation of Mcl-1 expression, which could be served as a novel therapeutic target for the treatment of chemotherapy resistant in lung cancer.
This review covers findings on how the mitochondrial fission and fusion machinery may intersect apoptotic pathways focusing on recent advances on the key role played by Mcl-1. [review]
However, because mitotic degradation of Mcl-1 appears not to be under the control of an E3 ligase, we suggest that the notion of network crosstalk is used with caution.
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