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Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats
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SYSNO ASEP 0365731 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Role of FAT/CD36 in novel PKC isoform activation in heart of spontaneously hypertensive rats Author(s) Klevstig, M. J. (CZ)
Marková, I. (CZ)
Burianová, J. (CZ)
Kazdová, L. (CZ)
Pravenec, Michal (FGU-C) RID, ORCID
Nováková, O. (CZ)
Novák, F. (CZ)Source Title Molecular and Cellular Biochemistry. - : Springer - ISSN 0300-8177
Roč. 357, 1-2 (2011), s. 163-169Number of pages 7 s. Language eng - English Country US - United States Keywords CD36 ; novel PKC ; spontaneously hypertensive rat ; insulin resistance Subject RIV FB - Endocrinology, Diabetology, Metabolism, Nutrition R&D Projects GD305/08/H037 GA ČR - Czech Science Foundation (CSF) ME08006 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) CEZ AV0Z50110509 - FGU-C (2005-2011) UT WOS 000295941500018 DOI 10.1007/s11010-011-0886-2 Annotation Searching for a possible role of novel protein kinase C (nPKC) in heart with disrupted energy balance, we compared the insulin-resistant spontaneously hypertensive rats (SHR), which carry a nonfunctional variant of the fatty acid transporter FAT/CD36, with the less insulin-resistant congenic strain SHR-4 that is genetically identical except for a segment on chromosome 4 including a wild-type gene for a functional FAT/CD36. Our results demonstrate that reduced insulin resistance in SHR-4 rats is associated with the insulin signaling pathway involving nPKCs Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2012
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