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Titolo:
Co-assembly of polycystin-1 and-2 produces unique cation-permeable currents
Autore:
Hanaoka, K; Qian, F; Boletta, A; Bhumia, AK; Piontek, K; Tsiokas, L; Sukhatme, VP; Guggino, WB; Germino, GG;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 pt Med, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 hysiol, Baltimore, MD 21205 USA Univ Oklahoma, Hlth Sci Ctr, Dept Cell Biol, Oklahoma City, OK 73104 USA Univ Oklahoma Oklahoma City OK USA 73104 iol, Oklahoma City, OK 73104 USA Univ Oklahoma, Hlth Sci Ctr, Warren Med Res Inst, Oklahoma City, OK 73104 USA Univ Oklahoma Oklahoma City OK USA 73104 nst, Oklahoma City, OK 73104 USA Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Div Renal, Boston, MA 02215 USA Harvard Univ Boston MA USA 02215 Med Ctr, Div Renal, Boston, MA 02215 USA
Titolo Testata:
NATURE
fascicolo: 6815, volume: 408, anno: 2000,
pagine: 990 - 994
SICI:
0028-0836(200012)408:6815<990:COPAPU>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
KIDNEY-DISEASE; GENE-PRODUCT; CHANNEL; PKD2; RECEPTOR; IDENTIFICATION; ENCODES; PROTEIN; ATP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Physical, Chemical & Earth Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Guggino, WB Johns Hopkins Univ, Sch Med, Dept Med, 725 N Wolfe St, Baltimore, MD 21205USA Johns Hopkins Univ 725 N Wolfe St Baltimore MD USA 21205 05USA
Citazione:
K. Hanaoka et al., "Co-assembly of polycystin-1 and-2 produces unique cation-permeable currents", NATURE, 408(6815), 2000, pp. 990-994

Abstract

The human kidney is composed of roughly 1.2-million renal tubules that must maintain their tubular structure to function properly. In autosomal dominant polycystic kidney disease (ADPKD) cysts develop from renal tubules and enlarge independently, in a process that ultimately causes renal failure in50% of affected individuals(1,2). Mutations in either PKD1 or PKD2 are associated with ADPKD but the function of these genes is unknown. PKD1 is thought to encode a membrane protein, polycystin-1, involved in cell-cell or cell-matrix interactions(3-5), whereas the PKD2 gene product, polycystin-2, is thought to be a channel protein(6). Here we show that polycystin-1 and -2interact to produce new calcium-permeable non-selective cation currents. Neither polycystin-1 nor -2 alone is capable of producing currents. Moreover, disease-associated mutant forms of either polycystin protein that are incapable of heterodimerization do not result in new channel activity. We alsoshow that polycystin-2 is localized in the cell in the absence of polycystin-1, but is translocated to the plasma membrane in its presence. Thus, polycystin-1 and -2 co-assemble at the plasma membrane to produce a new channel and to regulate renal tubular morphology and function.

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Documento generato il 03/12/20 alle ore 15:04:30