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observed that knockout (KO) of PMEPA1 in human breast cancer cell line MDA-MB-231 using a CRISPR-Cas9 system resulted in reduction of in vivo tumour growth and lung metastasis but not of in vitro monolayer growth capacity of these KO cell lines
This study highlights that TMEPAI decreases c-Maf stability by recruiting the ubiquitin ligase NEDD4 to c-Maf for proteasomal degradation in myeloma cells.
JHY-A007-50 mediates the downregulation of TMEPAI expression.
describe recent progresses in the understanding of how the TMEPAI family physiologically contributes to cellular functions and diseases
binding of SMAD2/3, the intracellular effectors of activin signaling, was significantly enriched at the Pmepa1 gene, which encodes a negative feedback regulator of TGF-beta signaling in cancer cells, and at the Kdm6b gene, which encodes an epigenetic regulator promoting transcriptional plasticity.
study showed that the inhibition of autophagy induced by the depletion of TMEPAI is involved in regulation of Beclin-1.
these findings indicated that PMEPA1 participates in TGF-beta- and hypoxia-regulated gene expression networks in solid tumors and thereby may contribute to tumor progression.
the present study suggest that the upregulation of miR19a3p expression levels contributes to tumor progression and that one of its underlying mechanisms involves inhibition of PMEPA1 expression.
Sp1 up-regulated TMEPAI protein expression, as well as Sp1 promoting TMEPAI-induced cell proliferation.
PMEPA1 was upregulated in breast cancer cell lines as well as in a set of clinical invasive breast ductal carcinomas. Interestingly, depletion of PMEPA1 decreased breast cancer stem cell (CSC)-enriched populations, while ectopic overexpression of PMEPA1 increased breast CSC-enriched populations.
these data elaborated on the diverse activity among TCF/LEF family members with respect to the transcriptional regulation of the TMEPAI gene.
Data show that over-expressed transmembrane prostate androgen-induced protein 1 (PMEPA1) can promote cell migration and maintain the mesenchymal-like morphology of breast cancer cells.
Data show that silencing of PMEPA1 protein facilitates the growth of prostate cancer cells and modulates androgen receptor (AR) through NEDD4 ubiquitin protein ligase and PTEN protein.
Downregulation of PMEPA1 may result in increased androgen receptor protein levels and function in cancer of the prostate cells, contributing to prostate tumorigenesis.
EGF signaling collaboratively regulates TGF-beta-induced TMEPAI expression.
TMEPAI is translocated on the lysosome and late endosome, and that association with Nedd4 is required for the transport of TMEPAI to the lysosome.
TMEPAI promotes tumorigenic activities in lung cancer cells.
The levels of TMEPAI in lung tumor tissues are very high.
Differentially expressed genes were identified, including E-cadherin, IL-8 and STAG1/PMEPA1 in an androgen-independent prostate cancer PC3 subclone.
Results suggest that TMEPAI functions in breast cancer as a molecular switch that converts TGF-beta from a tumor suppressor to a tumor promoter.
Pmepa1 is induced by RANK-p38 MAPK pathway signaling.
Wnt/beta-catenin/TCF7L2 pathway is preferentially able to alter the transcriptional regulation of the TGF-beta-target gene, TMEPAI.
This gene encodes a transmembrane protein that contains a Smad interacting motif (SIM). Expression of this gene is induced by androgens and transforming growth factor beta, and the encoded protein suppresses the androgen receptor and transforming growth factor beta signaling pathways though interactions with Smad proteins. Overexpression of this gene may play a role in multiple types of cancer. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
transmembrane prostate androgen-induced protein
, transmembrane, prostate androgen induced RNA
, prostate transmembrane protein, androgen induced 1
, solid tumor-associated 1 protein
, NEDD4 WW domain-binding protein 4
, Nedd4 WW binding protein 4