Dr. Ashok Kulkarni’s research focuses on characterizing the molecular role of Cdk5 in orofacial pain. His laboratory has shown that the activity of Cdk5 is upregulated due to inflammation that, in turn, modulates peripheral pain signaling. Current research efforts are centered on delineating how Cdk5 and its two activators, p35 and p39, affect pain signaling specifically in the orofacial region. Orofacial pain differs from peripheral pain because the dense innervation of facial structures leads to increased sensitivity to pain, which makes orofacial pain difficult to diagnose and treat. His group uses an array of approaches to investigate the molecular mechanisms involved in how Cdk5 activity modulates orofacial pain signaling. Their research approaches include using genetically engineered mouse models for behavioral, genomic and proteomic analyses. Their current studies will contribute to a greater understanding of the molecular roles of Cdk5 in pain signaling, and also help future efforts to effectively treat pain.
Dr. Kulkarni received his PhD from M.S. University in Baroda, India. He served as a postdoctoral fellow at Columbia University, NY, from 1982 -1987, and then as a senior staff fellow in NINDS at NIH from 1987-1995. In 1995, he joined NIDCR as a tenure track investigator to head the Functional Genomics Unit and the Gene Transfer Facility, and in 2000 he was tenured as a senior investigator and appointed chief of the Functional Genomics Section in the NIDCR. His laboratory studies the molecular mechanisms involved in cancer and pain affecting the oral and craniofacial areas. He continues to serve as manager of the Gene Transfer Facility, which provides research and technical services to generate and preserve genetically engineered mouse models for the investigators in the Division of Intramural Research of NIDCR. He is a member of the American Association of Dental Research, the International Association of Dental 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 The Journal of Dental Research and Neurochemical Research.
- Kulkarni AB, Huh CG, Becker D, Geiser A, Lyght M, Flanders KC, Roberts AB, Sporn MB, Ward JM, Karlsson S. Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death. Proc Natl Acad Sci U S A. 1993;90(2):770-4.
- Ohshima T, Ward JM, Huh CG, Longenecker G, Veeranna, Pant HC, Brady RO, Martin LJ, Kulkarni AB. Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death. Proc Natl Acad Sci U S A. 1996;93(20):11173-8.
- Hu M, Doyle AD, Yamada KM, Kulkarni AB. Visualization of trigeminal ganglion sensory neuronal signaling regulated by Cdk5. Cell Rep. 2022;38(10):110458.
- Pareek TK, Keller J, Kesavapany S, Agarwal N, Kuner R, Pant HC, Iadarola MJ, Brady RO, Kulkarni AB. Cyclin-dependent kinase 5 modulates nociceptive signaling through direct phosphorylation of transient receptor potential vanilloid 1. Proc Natl Acad Sci U S A. 2007;104(2):660-5.
- Hall BE, Macdonald E, Cassidy M, Yun S, Sapio MR, Ray P, Doty M, Nara P, Burton MD, Shiers S, Ray-Chaudhury A, Mannes AJ, Price TJ, Iadarola MJ, Kulkarni AB. Transcriptomic analysis of human sensory neurons in painful diabetic neuropathy reveals inflammation and neuronal loss. Sci Rep. 2022;12(1):4729.
Related Scientific Focus Areas
Molecular Biology and Biochemistry
View additional Principal Investigators in Molecular Biology and Biochemistry
Genetics and Genomics
View additional Principal Investigators in Genetics and Genomics
View additional Principal Investigators in Health Disparities
This page was last updated on Thursday, August 4, 2022