Journal Article |
| Venkatesan B, Prabhu SD, Venkatachalam K, Mummidi S, Valente AJ, Clark RA, Delafontaine P, Chandrasekar B. WNT1-inducible signaling pathway protein-1 activates diverse cell survival pathways and blocks doxorubicin-induced cardiomyocyte death Cell Signal 2010 May;22(5):809-820.
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| El Jamali A, Valente AJ, Clark RA. Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca(2+)/c-Abl signaling pathway Free Radic Biol Med 2010 Jan;:798-810.
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| Venkatachalam K, Venkatesan B, Valente AJ, Melby PC, Nandish S, Reusch JE, Clark RA, Chandrasekar B. WISP1, a pro-mitogenic, pro-survival factor, mediates tumor necrosis factor-alpha (TNF-alpha)-stimulated cardiac fibroblast proliferation but inhibits TNF-alpha-induced cardiomyocyte death J Biol Chem 2009 May;284(21):14414-14427.
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| Shostakovich-Koretskaya L, Catano G, Chykarenko ZA, He W, Gornalusse G, Mummidi S, Sanchez R, Dolan MJ, Ahuja SS, Clark RA, Kulkarni H, Ahuja SK. Combinatorial content of CCL3L and CCL4L gene copy numbers influence HIV-AIDS susceptibility in Ukrainian children AIDS 2009 Mar;23(6):679-688.
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| Catano G, Kulkarni H, He W, Marconi VC, Agan BK, Landrum M, Anderson S, Delmar J, Telles V, Song L, Castiblanco J, Clark RA, Dolan MJ, Ahuja SK, Delmar JA. HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles PLoS ONE 2008 Nov;3(11):3636-3636.
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| Ahuja SK, Kulkarni H, Catano G, Agan BK, Camargo JF, He W, OConnell RJ, Marconi VC, Delmar J, Eron J, Clark RA, Frost S, Martin J, Ahuja SS, Deeks SG, Little S, Richman D, Hecht FM, Dolan MJ, Kulkarni HR. CCL3L1-CCR5 genotype influences durability of immune recovery during antiretroviral therapy of HIV-1-infected individuals Nat Med 2008 Apr;14(4):413-420.
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| El Jamali A, Valente AJ, Lechleiter JD, Gamez MJ, Pearson DW, Nauseef WM, Clark RA. Novel redox-dependent regulation of NOX5 by the tyrosine kinase c-Abl Free Radic Biol Med 2008 Mar;44(5):868-881.
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| Chandrasekar B, Patel DN, Mummidi S, Kim JW, Clark RA, Valente AJ. Interleukin-18 Suppresses Adiponectin Expression in 3T3-L1 Adipocytes via a Novel Signal Transduction Pathway Involving ERK1/2-dependent NFATc4 Phosphorylation J Biol Chem 2008 Feb;283(7):4200-4209.
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| Valente AJ, Zhou Q, Lu Z, He W, Qiang M, Ma W, Li G, Wang L, Banfi B, Steger K, Krause KH, Clark RA, Li S. Regulation of NOX1 expression by GATA, HNF-1alpha, and Cdx transcription factors Free Radic Biol Med 2008 Feb;44(3):430-443.
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| Habib SL, Michel D, Masliah E, Thomas B, Ko HS, Dawson TM, Abboud H, Clark RA, Imam SZ. Role of tuberin in neuronal degeneration Neurochemical Research 2008 Jan;33:1113-1116.
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| Kulkarni H, Marconi VC, Agan BK, McArthur C, Crawford G, Clark RA, Dolan MJ, Ahuja SK. Role of CCL3L1-CCR5 genotypes in the epidemic spread of HIV-1 and evaluation of vaccine efficacy PLoS ONE 2008 Jan;3(11).
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| Dolan MJ**, Kulkarni H**, Camargo JF, He W, Smith A, Anaya JM, Miura T, Hecht FM, Mamtani M, Pereyra F, Marconi V, Mangano A, Sen L, Bologna R, Clark RA, Anderson SA, Delmar J, OConnell RJ, Lloyd A, Martin J, Ahuja SS, Agan BK, Walker BD, Deeks SG, Ahuja SK (** These authors contributed equally as first authors. This article was accompanied by a commentary: Lederman MM, Sieg SF. CCR5 and its ligands: a new axis of evil? Nat Immunol. 2007;8(12):1283-5.). CCL3L1 and CCR5 influence cell-mediated immunity and affect HIV-AIDS pathogenesis via viral entry-independent mechanisms Nat Immunol 2007 Dec;8(12):1324-1336.
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| Valente AJ, El Jamali A, Epperson TK, Gamez MJ, Pearson DW, Clark RA. NOX1 NADPH oxidase regulation by the NOXA1 SH3 domain Free Radic Biol Med 2007 Aug;43(3):384-396.
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Book Chapter |
| Nauseef WM and Clark RA. Granulocytic Phagocytes. In: Mandell GL, Bennett JE, and Dolin R. Principles and Practice of Infectious Diseases (7th edition). Philadelphia: Churchill Livingstone / Elsevier; 2009. p. 99-127.
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Review Article |
| Jaquet V, Scapozza L, Clark RA, Krause K-H, Lambeth JD. Small molecule NOX Inhibitors: ROS-generating NADPH oxidases as therapeutic targets Antioxidants & Redox Signaling 2009 Jan;11(10):2535-2552.
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| Lambeth JD, Krause K-H, Clark RA. NOX enzymes as novel targets for drug development Seminars in Immunopathology 2008 Jan;30:339-363.
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Federal |
| Funding Agency |
Department of Veterans Affairs |
| Title |
Redox Regulation of Phagocyte NOX2 in Inflammation and Aging |
| Status |
Active |
| Period |
7/2010 - 6/2014 |
| Role |
Principal Investigator |
| Grant Detail |
The goals of this project are to characterize the molecular signaling pathways by which hydrogen peroxide activates superoxide generation by phagocyte NOX2 and assess the aberrant regulation of this pathway associated with aging. |
| Funding Agency |
NIH / NCRR |
| Title |
Institute for Integration of Medicine & Science: A Partnership to Improve Health (CTSA KL2) |
| Status |
Active |
| Period |
5/2008 - 4/2013 |
| Role |
Principal Investigator |
| Grant Detail |
This research career development award represents the KL2 component of the Clinical and Translational Science Award. The goal is to support the career development of promising young clinical / translational investigators. |
| Funding Agency |
NIH / NCRR |
| Title |
Institute for Integration of Medicine & Science: A Partnership to Improve Health |
| Status |
Active |
| Period |
5/2008 - 4/2013 |
| Role |
Principal Investigator |
| Grant Detail |
This Clinical and Translational Science Award (CTSA) provides a broad range of infrastructure support across the institution and its CTSA partners. |
| Funding Agency |
NIH / NHLBI |
| Title |
Pathobiology of Occlusive Vascular Disease |
| Status |
Complete |
| Period |
9/2007 - 8/2012 |
| Role |
Co-Investigator |
| Grant Detail |
This NIH training grant supports postdoctoral training in the area of occlusive cardiovascular disease, inflammation, and degenerative disorders of cardiovascular tissues. |
| Funding Agency |
NIH / NCRR |
| Title |
Institute for Integration of Medicine & Science (CTSA Administrative Supplements) |
| Status |
Active |
| Period |
9/2009 - 9/2011 |
| Role |
Co-Investigator |
| Grant Detail |
This CTSA Administrative Supplement supports four individual supplemental projects. The first, comprising Collaborative Community Engagement Research, uses community health priorities to identify curricular needs, create novel teaching materials to address those needs, and effectively improve health science education in public schools, focusing on community health needs per se, as well as scientific processes of community health assessments and community-based research.
The second project, Enhancing Pilot Projects, represents an exciting opportunity to accelerate the pace of translational research through the funding of carefully selected competitive pilot projects, capitalizing on a group of highly meritorious proposals that have already passed rigorous peer review and are poised for immediate implementation.
The third project in Translational Research will build on our primary care Practice-Based Research Networks (PBRNs) to accelerate the translation of clinical research into practice. We will enhance the ability of PBRN investigators to conduct research by implementing the NIH/NCRR Roadmap-funded ePCRN (electronic Primary Care Research Network) in 20 clinics within our primary care PBRN, including ten that primarily serve uninsured populations.
The fourth project in Translational Research will accelerate programs being supported by the CTSA Imaging Core, which is operated by the Research Imaging Center (RIC). The supplement will expand the number of translational imaging experts supporting the Imaging Core functions and enhance funding for the developmental project funding program. |
| Funding Agency |
NIH / NINDS |
| Title |
Macrophage Gene Therapy of Neurodegenerative Diseases |
| Status |
Complete |
| Period |
7/2004 - 6/2010 |
| Role |
Co-Investigator |
| Grant Detail |
The goal of this project is to develop gene therapy strategies for neurodegenerative diseases using ex vivo transduction of hematopoietic stem cells with lentiviral vectors expressing therapeutic genes driven by highly active macrophage-selective synthetic promoters. |