Journal Article |
| Murray DR, Mummidi S, Valente AJ, Yoshida T, Somanna NK, Delafontaine P, Dinarello CA, Chandrasekar B. 2 adrenergic activation induces the expression of IL-18 binding protein, a potent inhibitor of isoproterenol induced cardiomyocyte hypertrophy in vitro and myocardial hypertrophy in vivo J Mol Cell Cardiol 2012 Jan;52(1):206-218.
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| Jiang D, Mummidi S, Ahuja SK, Jarrett HW. CCR5 Promoter Haplotype Transcription Complex Characterization J Health Care Poor Underserved 2011 Nov;22(4 Sup):73-90.
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| Bonello GB, Pham MH, Begum K, Sigala J, Sataranatarajan K, Mummidi S. An Evolutionarily Conserved TNF-{alpha}-Responsive Enhancer in the Far Upstream Region of Human CCL2 Locus Influences Its Gene Expression J Immunol 2011 Jun;186(12):7025-7038.
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| Mamtani M, Mummidi S, Ramsuran V, Pham MH, Maldonado R, Begum K, Valera MS, Sanchez R, Castiblanco J, Kulkarni H, Ndungu T, He W, Anaya JM, Ahuja SK. Influence of Variations in CCL3L1 and CCR5 on Tuberculosis in a Northwestern Colombian Population J Infect Dis 2011 Jun;203(11):1590-1594.
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| Reddy VS, Prabhu SD, Mummidi S, Valente AJ, Venkatesan B, Shanmugam P, Delafontaine P, Chandrasekar B. Interleukin-18 induces EMMPRIN expression in primary cardiomyocytes via JNK/Sp1 signaling and MMP-9 in part via EMMPRIN and through AP-1 and NF-kappaB activation Am J Physiol Heart Circ Physiol 2010 Oct;299(4):1242-1254.
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| 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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| 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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| Camargo JF, Quinones MP, Mummidi S, Srinivas S, Gaitan AA, Begum K, Jimenez F, VanCompernolle S, Unutmaz D, Ahuja SS, Ahuja SK. CCR5 expression levels influence NFAT translocation, IL-2 production, and subsequent signaling events during T lymphocyte activation J Immunol 2009 Jan;182(1):171-182.
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| Gornalusse G, Mummidi S, He W, Silvestri G, Bamshad M, Ahuja SK. CCL3L Copy number variation and the co-evolution of primate and viral genomes PLoS Genet 2009 Jan;5(1):1000359-1000359.
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| Mummidi S, Bonello GB, Ahuja SK. Confirmation of differential binding of Interferon Regulatory Factor-1 (IRF-1) to the functional and HIV disease-influencing -2578 A/G polymorphism in CCL2 Genes Immun 2008 Oct;.
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| Venkatachalam K, Mummidi S, Cortez DM, Prabhu SD, Valente AJ, Chandrasekar B. Resveratrol inhibits high glucose-induced PI3K/Akt/ERK-dependent interleukin-17 expression in primary mouse cardiac fibroblasts Am J Physiol Heart Circ Physiol 2008 May;294(5):2078-2087.
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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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| Quinones MP, Kalkonde Y, Estrada CA, Jimenez F, Ramirez R, Mahimainathan L, Mummidi S, Choudhury GG, Martinez H, Adams L, Mack M, Reddick RL, Maffi S, Haralambous S, Probert L, Ahuja SK, Ahuja SS. Role of astrocytes and chemokine systems in acute TNFalpha induced demyelinating syndrome: CCR2-dependent signals promote astrocyte activation and survival via NF-kappaB and Akt Mol Cell Neurosci 2008 Jan;37(1):96-109.
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| Cortez DM, Feldman MD, Mummidi S, Valente AJ, Steffensen B, Vincenti M, Barnes JL, Chandrasekar B. Interleukin-17 stimulates MMP-1 expression in primary human cardiac fibroblasts via p38 MAPK- and ERK 1/2-dependent C/EBP-beta , NF-kappaB, and AP-1 activation Am J Physiol Heart Circ Physiol 2007 Dec;293(6):H3356-H3365.
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Federal |
| Funding Agency |
National Institutes of Health |
| Title |
CCR5 regulation and promoter variants in HIV-1 |
| Status |
Active |
| Period |
8/2003 - 9/2015 |
| Role |
Co-Principal Investigator |
| Grant Detail |
An absolute requirement for HIV-1 infection is expression of CCR5 on the cell surface of specific leukocyte subsets. Delineating the molecular mechanisms that control the expression of CCR5 is of importance to our understanding HIV-1 pathogenesis, and this fact along with our quest to elucidate how genetic variation in the CCR5 gene influence its transcriptional/epigenetic machinery, and eventually its expression and coreceptor efficiency is the major focus of this competing renewal. |
| Funding Agency |
Department of Veterans Affairs |
| Title |
Transcriptional Mechanisms Regulating the HIV-1 Coreceptor CCR5 |
| Status |
Active |
| Period |
4/2011 - 3/2015 |
| Role |
Principal Investigator |
| Grant Detail |
CCR5 expression levels are a critical determinant of HIV-1 susceptibility and progression rate to AIDS. There is strong evidence indicating that these differences could be ascribed to genetic variation in the CCR5 locus. Genetic variability in CCR5 also has been implicated in susceptibility to other infectious and systemic diseases that are relevant to the veteran population. Delineating the mechanisms that modulate intersubject differences in CCR5 expression levels is thus of indisputable importance and significance for understanding pathogenesis of HIV-1 infection and other diseases such as diabetes. There is strong in vitro and in vivo evidence that the polymorphic residues at positions -2135 and -2459 in the CCR5 cis-regulatory region have a dominant effect on its expression. Our studies in this proposal are designed to elucidate the mechanisms by which differential binding of transcription factors to these polymorphisms leads to allele-specific modulation of gene expression resulting in variable CCR5 levels. Specific Aim 1 will test the hypothesis that disease-modifying CCR5 alleles exhibit variable transcription factor binding repertoire. Specific Aim 2 will determine whether the TFs that bind differentially to CCR5 SNPs also influence variable CCR5 expression. We will employ state-of-the art and innovative proteomic and molecular techniques to dissect the complex interactions between the TF binding to CCR5 polymorphisms which lead to variability in CCR5 expression levels. These studies have translational (benchAEbedside) utility as they will identify mechanisms of variable CCR5 expression that may impact on susceptibility to HIV-1/AIDS and other diseases. These molecular studies will capitalize on the vast experience of the PI in transcriptional gene regulation and collaborative efforts with Dr. Jarrett, a leading authority in transcriptional proteomics. There are several down-stream, value-added features of this application: (a) although the studies outlined |
| Funding Agency |
National Institute of Health |
| Title |
Redox signaling in osteoblast differentiation. |
| Status |
Active |
| Period |
9/2005 - 8/2012 |
| Role |
Consultant |
| Grant Detail |
In this proposal, using preosteoblast cell line and primary fetal rat calvarial cells, we will test the hypothesis that concerted action of redox and PI 3 K/Akt signaling regulates BMP-2 expression via NFKappaB and MEF-2A to induce osteoblast differentiation. In the first specific aim, we plan to investigate the role of PI 3 K/Akt signaling cascade in the regulation of NFKappaB and MEF-2A transcription factors. In the second specific aim, we will examine the role of ROS, a downstream mediator of PI 3 K, in osteoblast differentiation in response to BMP-2. In the specific aim 3, we will study the PI 3 K/Akt signaling pathway as mechanism for statin-induced BMP-2 expression and osteoblast differentiation. Understanding the signal transduction pathways of osteoblast differentiation may result in the development of therapeutic modalities for the human diseases where lack of bone formation is the pathology. |
| Funding Agency |
Veterans Affairs |
| Title |
Mechanisms Underlying the Disease-modulating Effects of CCL2 Variants |
| Status |
Complete |
| Period |
10/2007 - 9/2010 |
| Role |
Principal Investigator |
| Grant Detail |
This grant proposed the molecular mechanisms by which SNPs in the CCL2 locus modulate its expression. |
