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Titolo:
VHL tumor suppressor regulates Cl-/HCO3- exchange and Na+/H+ exchange activities in renal carcinoma cells
Autore:
Karumanchi, SA; Jiang, LW; Knebelmann, B; Stuart-Tilley, AK; Alper, SL; Sukhatme, VP;
Indirizzi:
Beth Israel Deaconess Med Ctr, Div Renal, Boston, MA 02215 USA Beth IsraelDeaconess Med Ctr Boston MA USA 02215 l, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr, Ctr Canc, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 c, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr, Mol Med Unit, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 t, Boston, MA 02215 USA Harvard Univ, Sch Med, Dept Med, Boston, MA 02215 USA Harvard Univ BostonMA USA 02215 Sch Med, Dept Med, Boston, MA 02215 USA Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02215 USA Harvard Univ Boston MA USA 02215 ed, Dept Cell Biol, Boston, MA 02215 USA
Titolo Testata:
PHYSIOLOGICAL GENOMICS
fascicolo: 3, volume: 5, anno: 2001,
pagine: 119 - 128
SICI:
1094-8341(20010402)5:3<119:VTSRCE>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSFORMING-GROWTH-FACTOR; XENOPUS-LAEVIS OOCYTES; HIPPEL-LINDAU PROTEIN; NA-H EXCHANGE; GENE-PRODUCT; ANION-EXCHANGER; CHROMOSOMAL LOCALIZATION; PROXIMAL TUBULE; MESSENGER-RNA; ISOFORMS;
Keywords:
von Hippel-Lindau disease; AE2; NHE3; renal cell carcinoma; intracellular pH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Alper, SL Beth Israel Deaconess Med Ctr, Mol Med Unit RW 763, 330 Brookline Ave, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr 330 Brookline AveBoston MA USA 02215
Citazione:
S.A. Karumanchi et al., "VHL tumor suppressor regulates Cl-/HCO3- exchange and Na+/H+ exchange activities in renal carcinoma cells", PHYSIOL GEN, 5(3), 2001, pp. 119-128

Abstract

Mutations in the von Hippel-Lindau (VHL) tumor suppressor gene are thoughtto play a critical role in the pathogenesis of both sporadic and VHL disease-associated clear-cell renal carcinomas (RCC). Differential display-PCR identified the AE2 anion exchanger as a candidate VHL target gene. AE2 mRNA and polypeptide levels were approximately threefold higher in 786-O VHL cells than in 786-O Neo cells. In contrast, Cl-/HCO3- exchange activity in 786-O VHL cells was 50% lower than in 786-O Neo cells. Since resting intracellular pH (pH(i)) values were indistinguishable, we postulated that Na+/H+ exchange activity (NHE) might be similarly reduced in 786-O VHL cells. NHE-mediated pH(i) recovery from acid load was less than 50% that in 786-O Neo cells, whereas hypertonicity-stimulated, amiloride-sensitive NHE was indistinguishable in the two cell lines. The NHE3 mRNA level was higher in 786-O VHL than 786-O Neo cells, but NHE1 mRNA levels did not differ. AE2 and NHE3 are the first transcripts reported to be upregulated by pVHL. Elucidation ofmechanisms responsible for downregulation of both ion exchange activities will require further investigation.

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Documento generato il 19/01/20 alle ore 00:57:31