| First Author | Iwata TN | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 11 | Pages | e78841 |
| PubMed ID | 24250814 | Mgi Jnum | J:209688 |
| Mgi Id | MGI:5568315 | Doi | 10.1371/journal.pone.0078841 |
| Citation | Iwata TN, et al. (2013) The transcriptional co-regulator HCF-1 is required for INS-1 beta-cell glucose-stimulated insulin secretion. PLoS One 8(11):e78841 |
| abstractText | The transcriptional co-regulator host cell factor-1 (HCF-1) plays critical roles in promoting cell cycle progression in diverse cell types, and in maintaining self-renewal of embryonic stem cells, but its role in pancreatic beta-cell function has not been investigated. Immunhistochemistry of mouse pancreas revealed nuclear expression of HCF-1 in pancreatic islets. Reducing HCF-1 expression in the INS-1 pancreatic beta-cell line resulted in reduced cell proliferation, reduced glucose-stimulated insulin secretion, and reduced expression of the critical beta-cell transcription factor Pdx1. HCF-1 is a known co-activator of the E2F1 transcription factor, and loss of E2F1 results in pancreatic beta-cell dysfunction and reduced expression of Pdx1. Therefore we wondered whether HCF-1 might be required for E2F1 regulation of Pdx1. Chromatin immunoprecipitation experiments revealed that HCF-1 and E2F1 co-localize to the Pdx1 promoter. These results indicate that HCF-1 represents a novel transcriptional regulator required for maintaining pancreatic beta-cell function. |
