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Titolo:
ABNORMAL REGULATION OF THE KE-6 GENE, A NEW 17-BETA-HYDROXYSTEROID-DEHYDROGENASE IN THE CPK MOUSE KIDNEY
Autore:
RAMIREZ S; FOMITCHEVA I; AZIZ N;
Indirizzi:
HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT MED,NEPHROL DIV,ENDERS 1251,300 LONGWOOD AVE BOSTON MA 02115 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT MED,NEPHROL DIV BOSTON MA 02115 HARVARD UNIV,SCH MED,DEPT PEDIAT BOSTON MA 02115
Titolo Testata:
Molecular and cellular endocrinology
fascicolo: 1-2, volume: 143, anno: 1998,
pagine: 9 - 22
SICI:
0303-7207(1998)143:1-2<9:AROTKG>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROMOTER REGION; DISEASE; PROTEIN; CELLS; RAT;
Keywords:
KE 6 GENE; PROMOTER ACTIVITY; CPK CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
S. Ramirez et al., "ABNORMAL REGULATION OF THE KE-6 GENE, A NEW 17-BETA-HYDROXYSTEROID-DEHYDROGENASE IN THE CPK MOUSE KIDNEY", Molecular and cellular endocrinology, 143(1-2), 1998, pp. 9-22

Abstract

The function encoded by the Ke 6 gene has been recently determined tobe 17 beta-hydroxysteroid dehydrogenase. Previously, the abnormal expression of the Ke 6 gene has been intimately associated with development of recessive polycystic kidney disease. The Ke 6 gene is normally expressed at very high levels in the kidney and liver and is severely down regulated in all recessive murine models of polycystic kidney disease that have been examined to date. Here, we report a detailed examination of the promoter region of the Ke 6 gene in normal mouse kidney cells (CTA) and in cells derived from mouse kidneys homozygous for the cpk (congenital polycystic kidney) mutation, using transfection analysis and DNA-protein gel shift assays. The minimal promoter region, P1 (1 to -96), and a putative enhancer site, P3 (-165 to -256), within the Ke 6 gene 5' flanking sequence have been identified. We have also identified another region, P2 (-97 to -165), that may be responsible forthe lower promoter activity of the Ke 6 gene in cpk cells. Furthermore, absence of binding of a 38 kDa nuclear protein to a 16 bp sequence element (P1A) within the minimal promoter of the Ke 6 gene suggests that the P1A element could be responsible for the overall reduction in promoter function in cpk cells. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:03:35