Effect of Cdc42 and salt-tolerant protein on hypertension and ischemia
| Project/Area Number |
14570705
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Fukuoka University |
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Principal Investigator |
TSUJI Emiko Fukoka University, School of Medicine, Lecturer, 医学部, 講師 (10248495)
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| Co-Investigator(Kenkyū-buntansha) |
辻 祐治 福岡大学, 医学部, 助教授 (10188534)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | salt-sensitivity / hypertension / molecular biology / small G protein / actin cytoskeleton |
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| Research Abstract |
Human hypertension is a multifactorial disease which is complicated by genetic and environmental factors. Excessive dietary sodium intake is an important factor in hypertension ; however, the molecular basis of the salt sensitivity in hypertension is not yet fully understood. Recently, we isolated a novel rat cDNA named salt-tolerant protein (STP), using functional complementation to improve the growth of the yeast S.cervisiae HAL1-deficient strain under high salt conditions (Tsuji et al. 1996). To determine the physiological function of this gene, we examined whether intracellular cation content is affected by STP. The intracellular [Na^+]/[K^+] ratio in STP-transfected cells was higher than that in control cells, suggesting that STP somehow affects intracellular cation homeostasis. This protein might increase sodium influx and/or decrease sodium efflux by modulating Na^+,K^+-ATPase, Na^+,K^+-cotransport and other membranous ion-transport systems. The STP gene may increase renal sodium reabsorption in proximal tubules, and thus be an important determinant of hypertension associated with excess salt intake (Tsuji et al. 1998).
HSTP contains predicted coiled-coil domains and an SH3 domain, and identical with human Cdc42 interacting protein-4 (CIP4) (Aspenstrom, 1997). Cdc42 is known to have many cell biological activities such as rearrangement of actin cytoskeleton and vesicular transport. Hirano et al. reported to associate between this molecule and lipid transport. They raised a novel hypothesis that this type of small G protein may play a role in some steps of cholesterol efflux. We suggest that HSTP may play a role in cholesterol transport and contribute to atherosclerosis. We are testing if HSTP affect on cholesterol efflux. We confirm that HSTP is critical for cell-cell adhesion by defective intracellular trafficking of β-catenin
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Report
(3 results)
Research Products
(4 results)
