Research Topics
| Grazyna NowakSummaryAffiliation: University of Arkansas for Medical Sciences Country: USA Publications
Research Grants
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Detail Information
Publications
Protein kinase C-alpha and ERK1/2 mediate mitochondrial dysfunction, decreases in active Na+ transport, and cisplatin-induced apoptosis in renal cellsGrazyna Nowak
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
J Biol Chem 277:43377-88. 2002....
Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cellsGrazyna Nowak
Univ of Arkansas for Medical Sciences, Dept of Pharmaceutical Sciences, 4301 West Markham St, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 303:F515-26. 2012....
Protein kinase C-epsilon activation induces mitochondrial dysfunction and fragmentation in renal proximal tubulesGrazyna Nowak
University of Arkansas for Medical Sciences, Dept of Pharmaceutical Sciences, 4301 West Markham St, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 301:F197-208. 2011..These results show that in contrast to protective effects of PKC-ε activation in cardiomyocytes, sustained PKC-ε activation is detrimental to mitochondrial function and viability in RPTC...
Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cellsGrazyna Nowak
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, 4301 West Markham St, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 291:F840-55. 2006....
γ-Tocotrienol protects against mitochondrial dysfunction and renal cell deathGrazyna Nowak
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, 4301 West Markham St, MS 522 3, Little Rock, AR 72205, USA
J Pharmacol Exp Ther 340:330-8. 2012..Our data suggest that GT3 is superior to AT in protecting RPTCs against oxidant injury and may prove therapeutically valuable for preventing renal injury associated with oxidative stress...
Linoleic acid epoxide promotes the maintenance of mitochondrial function and active Na+ transport following hypoxiaGrazyna Nowak
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
Toxicol Lett 147:161-75. 2004....
Protein kinase C-epsilon modulates mitochondrial function and active Na+ transport after oxidant injury in renal cellsGrazyna Nowak
Dept of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 286:F307-16. 2004....
Lack of a functional p21WAF1/CIP1 gene accelerates caspase-independent apoptosis induced by cisplatin in renal cellsGrazyna Nowak
Dept of Pharmaceutical Sciences, Univ of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 285:F440-50. 2003....
Protein kinase C mediates repair of mitochondrial and transport functions after toxicant-induced injury in renal cellsGrazyna Nowak
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, 4301 West Markham St, MS 522 3, Little Rock, AR 72205, USA
J Pharmacol Exp Ther 306:157-65. 2003..These results suggest that the repair of renal functions is mediated through PKC-dependent mechanisms and that cysteine conjugates may inhibit renal repair, in part, through inhibition of PKC signaling...
Succinate ameliorates energy deficits and prevents dysfunction of complex I in injured renal proximal tubular cellsGrazyna Nowak
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, 4301 West Markham St, MS 522 3, Little Rock, AR 72205, USA
J Pharmacol Exp Ther 324:1155-62. 2008..Succinate 1) uses an alternate pathway of mitochondrial energy metabolism, 2) improves activity of complex I and oxidation of substrates through complex I, and 3) decreases oxidative stress and cell lysis in oxidant-injured RPTC...
Akt activation improves oxidative phosphorylation in renal proximal tubular cells following nephrotoxicant injuryZabeena P Shaik
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
Am J Physiol Renal Physiol 294:F423-32. 2008....
Protein kinase B/Akt modulates nephrotoxicant-induced necrosis in renal cellsZabeena P Shaik
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
Am J Physiol Renal Physiol 292:F292-303. 2007..We conclude that Akt activation plays a protective role against necrosis caused by nephrotoxic insult in RPTC. Furthermore, we identified mitochondria as a subcellular target of protective actions of Akt against necrosis...
Protein kinase C-alpha inhibits the repair of oxidative phosphorylation after S-(1,2-dichlorovinyl)-L-cysteine injury in renal cellsXiuli Liu
Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
Am J Physiol Renal Physiol 287:F64-73. 2004..This is the first report showing that PKC-alpha phosphorylates the catalytic subunit of F(1)F(0)-ATPase and that PKC-alpha plays an important role in regulating repair of mitochondrial function...
Dependence of cisplatin-induced cell death in vitro and in vivo on cyclin-dependent kinase 2Peter M Price
Department of Medicine, University of Arkansas for Medical Sciences, VA Medical Center Research Section, 4300 West 7th Street, Room GC 147, Little Rock, AR 72205, USA
J Am Soc Nephrol 17:2434-42. 2006..It also was demonstrated that this pathway of cisplatin-induced cell death can be interceded in vivo to prevent nephrotoxicity...
Research Grants
- Protein Kinase C in the Repair of Cellular FunctionsGrazyna Nowak; Fiscal Year: 2005..Completion of these aims will result in a better understanding of the role of PKC isozymes in the repair of RPTC functions and may help to identify agents that protect against ARF or accelerate recovery from ARF. ..
- Protein Kinase C in the Repair of Cellular FunctionsGrazyna Nowak; Fiscal Year: 2010....
