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Ashok Kulkarni, Ph.D.

Ashok Kulkarni, Ph.D.
Senior Investigator
Functional Genomics Section

NIH/NIDCR
Building 30, Room 130
30 Convent Dr. MSC 4395
Bethesda, MD 20892-4395
United States

(301) 435-2887
ashok.kulkarni@nih.gov
Research Interests

Dr. Ashok Kulkarni's research focuses on understanding the cellular mechanisms that promote pain hypersensitivity using both mouse models and human clinical samples. The ability to perform genetic engineering in mice has allowed for the identification of pain genes that modulate pain signaling. As such, his group demonstrated that the activity of the neuronal enzyme CDK5 has a key role in regulating pain perception. A needed advancement beyond the traditional use of rodent models in pain research has recently occurred as human sensory ganglia have become available from organ transplant donors for scientific study. Dr. Kulkarni's lab has thereby been able to complement his rodent pain models with multi-omic analysis of human dorsal root ganglia from donors with chronic pain conditions like rheumatoid arthritis, diabetic painful neuropathy, and fibromyalgia, which are examples of chronic inflammatory pain, neuropathic pain, and nociplastic pain respectively. Such studies are important as 1 in 5 adults in the U.S. experience chronic pain, where women are more frequently affected than men. Principally, a better understanding of human nociception is vitally needed in order to better design targeted pain drugs that lack the side effects of current treatments, such as with opioids. Work with mouse models and with limited but critically important human neuronal samples will be conducted in the lab with the goal of finding new therapeutic targets to control and alleviate pain hypersensitivity.

Biographical Sketch

Dr. Kulkarni received his Ph.D. from Maharaja Sayajirao University in Baroda, India. He was a postdoctoral fellow at Columbia University, New York, from 1982 to 1987, and then a senior staff fellow at the National Institute of Neurological Disorders and Stroke at NIH from 1987 to 1995. In 1995, he joined NIDCR as a tenure-track investigator to head the Functional Genomics Unit and the Gene Transfer Facility. In 2000, he was tenured as a senior investigator and appointed chief of the Functional Genomics Section at NIDCR. His laboratory studies the molecular mechanisms involved in chronic pain affecting the oral and craniofacial areas. He is a member of the American Association for Dental, Oral, and Craniofacial Research; the International Association for Dental, Oral, and Craniofacial Research; the Society for Neuroscience; and the International Association for the Study of Pain. He currently serves as a reviewer for numerous scientific journals and as an editorial board member for Nature Scientific Reports.

Selected Publications
  • Rozas P, Lazcano P, Pina R, Cho A, Terse A, Pertusa M, Madrid R, Gonzales-Billault C, Kulkarni AB, Utreras, E. Targeted overexpression of Tumor Necrosis Factor-α increases Cdk5 activity and TRPV1-dependent Ca+ influx in trigeminal neurons. Pain. 2016 Jun;157(6):1346-62. doi: 10.1097/j.pain.0000000000000527.
  • Jendryke T, Prochazkova M, Hall BE, Nordmann GC, Schladt M, Milenkovic VM, Kulkarni AB, Wetzel, CH. TRPV1 function is modulated by Cdk5-mediated phosphorylation: Insights into the molecular mechanism of nociception. Sci Rep. 2016 Feb 23;6:22007. doi: 10.1038/srep22007.
  • Hall BE, Zhang L, Sun ZJ, Utreras E, Prochazkova M, Cho A, Terse A, Dolan JC, Schmidt BL, Kulkarni AB. Conditional TNF-a overexpression in the tooth and alveolar bone results in painful pulpitis and osteitis. J Dent Res. 2016 Feb;95(2):188-95. doi: 10.1177/0022034515612022. Epub 2015 Oct 26.
  • Prochazkova M, Terse A, Amin ND, Hall B, Utreras E, Pant HC, Kulkarni AB. Activation of cyclin-dependent 5 mediates orofacial mechanical hyperalgesia. Mol Pain. 2013 Dec 21;9: 66. 2013 Dec 21;9:66. doi: 10.1186/1744-8069-9-66.
  • Utreras E, Keller J, Terse A, Prochazkova M, Iadarola MJ, Kulkarni AB. Transforming Growth Factor-β1 Regulates Cdk5 Activity in Primary Sensory Neurons. J. Biol. Chem. 2012 May 11;287(20): 16917-29. doi: 10.1074/jbc.M111.329979. Epub 2012 Mar 28.
  • Utreras E, Terse A, Keller J, Iadarola M, Kulkarni AB. Resveratrol inhibits Cdk5 activity through regulation of p35 expression. Mol Pain. 2011 Jul 7;7:49. doi: 10.1186/1744-8069-7-49.
  • Utreras E, Futatsugi A, Rudrabhatla P, Keller J, Iadarola MJ, Pant HC, Kulkarni AB. Tumor necrosis factor-alpha regulates cyclin-dependent kinase 5 activity during pain signaling through transcriptional activation of p35. J Biol Chem. 2009 Jan 23;284(4):2275-84. doi: 10.1074/jbc.M805052200. Epub 2008 Dec 2.
  • Nandula SR, Amarnath S, Molinolo A, Bandyopadhyay BC, Hall B, Goldsmith CM, et al. Female mice are more susceptible to developing inflammatory disorders due to impaired transforming growth factor beta signaling in salivary glands. Arthritis Rheum. 2007 Jun;56(6):1798-1805. doi: 10.1002/art.22715.
  • Pareek TK, Keller J, Kesavapany S, Pant HC, Iadarola MJ, Brady RO, Kulkarni AB. Cyclin-dependent kinase 5 activity regulates pain signaling. Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):791-796. doi: 10.1073/pnas.0510405103. Epub 2006 Jan 9.
Last Reviewed
March 2025
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