ArticleMolecular and cellular biochemistry2013
INMAP, a novel truncated version of POLR3B, represses AP-1 and p53 transcriptional activity.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Whole Exome Sequencing of Highly Aggregated Lung Cancer Families Reveals Linked Loci for Increased Cancer Risk on Chromosomes 12q, 7p, and 4q.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020Article
- regQTLs: Single nucleotide polymorphisms that modulate microRNA regulation of gene expression in tumors.PLoS genetics · 2018Article
- INMAP overexpression inhibits cell proliferation, induces genomic instability and functions through p53/p21 pathways.PloS one · 2015Article
- A regulatory effect of INMAP on centromere proteins: antisense INMAP induces CENP-B variation and centromeric halo.PloS one · 2014Article
- Human TTC5, a novel tetratricopeptide repeat domain containing gene, activates p53 and inhibits AP-1 pathway.Molecular biology reports · 2013Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
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Abstract
INMAP was first identified as an interphase nucleus and mitotic apparatus-associated protein that plays essential roles in the formation of the spindle and cell-cycle progression. Here, we report that INMAP might be conserved from prokaryotes to humans, is a truncated version of the RNA polymerase III subunit B POLR3B, and is up-regulated in several human cancer cell lines including HeLa, Bel-7402, HepG2 and BGC-823. Deletion analysis revealed that the 209-290 amino-acid region is necessary for the punctate distribution of INMAP in the nucleus. Furthermore, over-expression of INMAP inhibited the transcriptional activities of p53 and AP-1 in a dose-dependent manner. These results suggest that INMAP may function through the p53 and AP-1 pathways, thus providing a possible link of its activity with tumourigenesis. Integrating our data and those in previous studies, it can be concluded that INMAP plays dual functional roles in the coordination of mitotic kinetics with gene expression as well as in cell-fate determination and proliferation.
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