ArticleBiochemical and biophysical research communications2004
Ku80 is required but not sufficient for Galpha13-mediated endodermal differentiation in P19 embryonic carcinoma cells.
Article in Biochemical and biophysical research communications, 2004. 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.
- Puromycin-resistant lentiviral control shRNA vector, pLKO.1 induces unexpected cellular differentiation of P19 embryonic stem cells.Biochemical and biophysical research communications · 2017Article
- DNA-PK Deficiency in Alzheimer's Disease.Journal of neurology & neuromedicine · 2016Article
- Tumor Suppressors and Endodermal Differentiation of P19 Embryonic Stem Cells.Cell & developmental biology · 2015Article
- DNA-dependent protein kinase and DNA repair: relevance to Alzheimer's disease.Alzheimer's research & therapy · 2013Review
- Menin induces endodermal differentiation in aggregated P19 stem cells by modulating the retinoic acid receptors.Molecular and cellular biochemistry · 2012Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We have shown that a constitutively active Galpha13 (Galpha13Q226L) induces differentiation in P19 embryonic carcinoma cells to an endodermal phenotype. In this report, we demonstrate that Ku, a heterodimer of p80 (Ku80) and p70 (Ku70), is upregulated in P19 cells overexpressing Galpha13Q226L. Ku is the regulatory subunit of the DNA-dependent protein kinase and is primarily involved in DNA repair and recombination. Ku80 also is a somatostatin receptor. We show that while overexpression of Ku80 drastically reduced P19 cell proliferation, it was not sufficient to induce endodermal differentiation. However, coexpression of Galpha13Q226L and an antisense Ku80 abrogated the retarded growth rate and endodermal differentiation observed in cells expressing only Galpha13Q226L. Overexpression of Galpha13Q226L or Ku80 downregulated RNA polymerase I-mediated transcriptional activity and overexpression of antisense Ku80 restored the activity to control level. These results suggest that Ku80 is required for Galpha13-mediated endodermal differentiation in P19 cells.
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