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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 (show PSG1 Proteins) up-regulated TMEPAI protein expression, as well as Sp1 (show PSG1 Proteins) 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 (show HNF4A Proteins)/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 (show AR Proteins)) through NEDD4 (show NEDD4 Proteins) ubiquitin protein ligase (show UBE2K Proteins) and PTEN protein.
Downregulation of PMEPA1 may result in increased androgen receptor (show AR Proteins) protein levels and function in cancer of the prostate cells, contributing to prostate tumorigenesis.
EGF (show EGF Proteins) signaling collaboratively regulates TGF-beta (show TGFB1 Proteins)-induced TMEPAI expression.
TMEPAI is translocated on the lysosome and late endosome, and that association with Nedd4 (show NEDD4 Proteins) is required for the transport of TMEPAI to the lysosome.
TMEPAI promotes tumorigenic activities in lung cancer cells.
Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins)/TCF7L2 (show TCF7L2 Proteins) pathway is preferentially able to alter the transcriptional regulation of the TGF-beta (show TGFB1 Proteins)-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