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Titolo:
THE POLYCYSTIC KIDNEY-DISEASE-1 GENE-PRODUCT MEDIATES PROTEIN-KINASE-C ALPHA-DEPENDENT AND C-JUN N-TERMINAL KINASE-DEPENDENT ACTIVATION OF THE TRANSCRIPTION FACTOR AP-1
Autore:
ARNOULD T; KIM E; TSIOKAS L; JOCHIMSEN F; GRUNING W; CHANG JD; WALZ G;
Indirizzi:
HARVARD UNIV,SCH MED,BETH ISRAEL DEACONESS MED CTR,DEPT MED,RENAL DIV,330 BROOKLINE AVE BOSTON MA 02215 HARVARD UNIV,SCH MED,BETH ISRAEL DEACONESS MED CTR,DEPT MED,RENAL DIVBOSTON MA 02215 HARVARD UNIV,SCH MED,BETH ISRAEL DEACONESS MED CTR,DEPT MED,CARDIOL DIV BOSTON MA 02215 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,LAB MOL & DEV NEUROSCI BOSTON MA 02114
Titolo Testata:
The Journal of biological chemistry
fascicolo: 11, volume: 273, anno: 1998,
pagine: 6013 - 6018
SICI:
0021-9258(1998)273:11<6013:TPKGMP>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
JNK/SAPK SIGNALING PATHWAY; SYSTEM EFFECTOR FUNCTION; RECEPTOR ZETA-CHAIN; T-CELL; DIFFERENTIAL ACTIVATION; EPITHELIAL-CELLS; DOMAINS; EXPRESSION; PROLIFERATION; TRANSDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
65
Recensione:
Indirizzi per estratti:
Citazione:
T. Arnould et al., "THE POLYCYSTIC KIDNEY-DISEASE-1 GENE-PRODUCT MEDIATES PROTEIN-KINASE-C ALPHA-DEPENDENT AND C-JUN N-TERMINAL KINASE-DEPENDENT ACTIVATION OF THE TRANSCRIPTION FACTOR AP-1", The Journal of biological chemistry, 273(11), 1998, pp. 6013-6018

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is a common hereditary disorder that accounts far 8-10% of end stage renal disease, PKD1, one of two recently isolated ADPKD gene products, has been implicated in cell-cell and cell-matrix interactions, However, the signaling pathway of PKD1 remains undefined, We found that the C-terminal 226 amino acids of PKD1 transactivate an AP-1. promoter construct in human embryonic kidney cells (293T). PKD1-induced transcription is specific for AP-1; promoter constructs containing cAMP response element-binding protein, c-Fos, c-Myc, or NF kappa B-binding sites are unaffected by PKD1. In vitro kinase assays revealed that PKD1 triggers the activationof c-Jun N-terminal kinase (JNK), but not of mitogen-activated protein kinases p38 or p44, Dominant-negative Rac-1 and Cdc42 mutations abrogated PKD1-mediated JNK and AP-1 activation, suggesting a critical role for small GTP-binding proteins in PKD1-mediated signaling. Several protein kinase C (PRC) inhibitors decreased PKD1-mediated AP-1 activation, Conversely, expression of the C-terminal domain of PKD1 increased PRC activity in 293T cells, A dominant-negative PKC alpha, but not a dominant-negative PKC beta or delta, abrogated PKD1-mediated AP-1 activation, These findings indicate that small GTP-binding proteins and PKCalpha mediate PKD1-induced JNK/AP-1 activation, together comprising asignaling cascade that may regulate renal tubulogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/12/20 alle ore 15:55:21