Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 20, Issue 1, Pages 41-47Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2008020238
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Funding
- National Institutes of Health [R01DK42921, T32DK07257]
- FRM [FRMDEQ20061107958]
- UT Southwestern O'Brien Kidney Research Core Center [P30DK079328]
- PKD Foundation fellowship
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R37DK042921, R01DK042921, T32DK007257, P30DK079328] Funding Source: NIH RePORTER
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Hepatocyte nuclear factor-1 beta (HNF-1 beta) is a transcription factor that regulates gene expression in the kidney, liver, pancreas, and other epithelial organs. Mutations of HNF-1 beta lead to a syndrome of inherited renal cysts and diabetes and are also a common cause of sporadic renal dysplasia. The full complement of target genes responsible for the functions of HNF-1 beta, however, is incompletely defined. Using a functional genomics approach involving chromatin immunoprecipitation and promoter arrays, combined with gene expression profiling, we found that an HNF-1 beta target gene in the kidney is kinesin family member 12 (Kif12), a gene previously identified as a candidate modifier gene in the cpk mouse model of polycystic kidney disease. Mutations of HNF-1 beta inhibited Kif12 transcription in both cultured cells and knockout mice by altering co-factor recruitment and histone modification. Because kinesin-12 family members participate in orienting cell division, downregulation of Kif12 may underlie the abnormal planar cell polarity observed in cystic kidney diseases.
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