Kimberly Gomez, PhD, MS

Assistant Professor
Contact
Biomedical Sciences
3302 Gaston Ave.
Dallas,
TX
75246
kimberly.gomez@tamu.edu
Biography
Education and Post-Graduate Training
Postdoctoral Fellow, Neurobiology of Pain.
- Department of Pharmacology, College of Medicine, The University of Arizona (2020 – 2021)
- Pain Research Center, Department of Molecular Pathobiology, College of Dentistry, New York University (2022 – 2023)
- Department of Pharmacology & Therapeutics, College of Medicine, The University of Florida (2024 – 2025)
Ph.D., Cellular and Molecular Neurobiology.
- Department of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies (CINVESTAV) of the National Polytechnic Institute, Mexico City, Mexico (2015 – 2019).
M.S., Neuropharmacology and Experimental Therapeutics.
- Department of Pharmacobiology, Center for Research and Advanced Studies (CINVESTAV) of the National Polytechnic Institute, Mexico City, Mexico (2013 – 2015).
Career History
- Assistant Professor, Department of Biomedical Sciences, College of Dentistry, Texas A&M University (2025 – Present).
- Research Assistant, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego (2011 – 2013).
Teaching Interests
Dr. Gomez’s teaching interests span pharmacology, neuroscience, and physiology, with a focus on ion channel biology, neuropharmacology, and the mechanisms of pain at the molecular and cellular level.
Research Interests
Dr. Gomez’s research seeks to uncover the molecular and cellular mechanisms that drive pain, with particular attention to the regulation of voltage-gated sodium and calcium channels in nociceptors by accessory and regulatory proteins. Her work integrates electrophysiology, molecular biology, and animal models to identify novel, non-opioid targets and develop new strategies for the treatment of chronic pain.
Grants
- NIH/NINDS and HEAL Initiative K99NS134965 (Career Transition Award): “Lymphocyte Antigen 6 (Ly6) Proteins: New Players in Chronic Pain” (09/2023 – 08/2025).
- NIH/NINDS 3R01NS120663-01A1S1 (Research Supplement to Promote Diversity): “Sentrin proteases, CRMP2 deSUMOylation, and Chronic Pain” (01/2022 – 07/2024).
Selected Publications
- Martin L, Stratton HJ, Salih LY, Dumaire N, Gomez K, Do LD, Loya-Lopez S, Tang C, Calderon-Rivera A, Ran D, Nunna V, Bellampalli SS, François-Moutal L, Luo S, Porreca F, Ibrahim M, Rogemond V, Honnorat J, Khanna R, Moutal A. Anti-CV2/CRMP5 autoantibodies drive sensory neuron excitability and pain in rats. Nat Commun. 2025;16:7311. doi:10.1038/s41467-025-62380-y
- Tang C*, Gomez K*, Chen Y*, Allen HN, Hestehave S, Rodríguez-Palma EJ, Loya-Lopez S, Calderon-Rivera A, Duran P, Nelson TS, Kanumuri SRR, Shah B, Panigrahi NR, Perez-Miller S, Schackmuth MK, Ruparel S, Patwardhan A, Price TJ, Arora PS, Sharma RK, Sharma A, Yu J, Korczeniewska OA, Khanna R. C2230, a use- and state-dependent CaV2.2 channel blocker, mitigates pain behaviors across multiple models. J Clin Invest. 2024;e177429. doi:10.1172/JCI177429
- Peach CJ, Tonello R, Damo E, Gomez K, Calderon-Rivera A, Bruni R, Bansia H, Maile L, Manu AM, Hahn H, Thomsen AR, Schmidt BL, Davidson S, des Georges A, Khanna R, Bunnett NW. Neuropilin-1 inhibition suppresses nerve growth factor signaling and nociception. J Clin Invest. 2024;135:e183873. doi:10.1172/JCI183873
- Gomez K*, Santiago U*, Nelson TS, Allen HN, Calderon-Rivera A, Hestehave S, Rodríguez Palma EJ, Zhou Y, Duran P, Loya-Lopez S, Zhu E, Kumar U, Shields R, Koseli E, McKiver B, Giuvelis D, Zuo W, Inyang KE, Dorame A, Chefdeville A, Ran D, Perez-Miller S, Lu Y, Liu X, Handoko, Arora PS, Patek M, Moutal A, Khanna M, Hu H, Laumet G, King T, Wang J, Damaj MI, Korczeniewska OA, Camacho CJ, Khanna R. A peptidomimetic modulator of CaV2.2 N-type calcium channels for chronic pain. PNAS. 2023;120:e2305215120. doi:10.1073/pnas.2305215120
- Gomez K*, Stratton HJ*, Duran P, Loya S, Tang C, Calderon-Rivera A, François-Moutal L, Khanna M, Madura CL, Luo S, McKiver B, Choi E, Ran D, Boinon L, Perez-Miller S, Damaj MI, Moutal A, Khanna R. Identification of a unique NaV1.7 domain driving chronic pain. PNAS. 2023;120:e2217800120. doi:10.1073/pnas.2217800120
- Gomez K, Allen HN, Duran P, Loya-Lopez S, Calderon-Rivera A, Moutal A, Tang C, Nelson TS, Perez-Miller S, Khanna R. CRISPR activation of SENP1 enhances deSUMOylation pathways to elicit antinociception. Pain. 2024;165:866–883. doi:10.1097/j.pain.0000000000003080
- Gomez K, Duran P, Tonello R, Allen HN, Boinon L, Calderon-Rivera A, Loya-López S, Nelson TS, Ran D, Moutal A, Bunnett NW, Khanna R. Neuropilin-1 is essential for VEGF-A–mediated sensory neuron activity and pain-like behaviors. Pain. 2023;164:2696–2710. doi:10.1097/j.pain.0000000000002970
- Cai S, Moutal A, Yu J, Chew LA, Isensee J, Chawla R, Gomez K, Luo S, Zhou Y, Chefdeville A, Madura C, Perez-Miller S, Bellampalli SS, Dorame A, Scott DD, François-Moutal L, Shan Z, Woodward T, Gokhale V, Hohmann AG, Vanderah TW, Patek M, Khanna M, Hucho T, Khanna R. Selective targeting of NaV1.7 via inhibition of CRMP2-Ubc9 interaction reduces pain in rodents. Sci Transl Med. 2021;13:eabh1314. doi:10.1126/scitranslmed.abh1314
- Moutal A, Martin LF, Boinon L, Gomez K, Ran D, Zhou Y, Stratton HJ, Cai S, Luo S, Gonzalez KB, Perez-Miller S, Patwardhan A, Ibrahim MM, Khanna R. SARS-CoV-2 spike protein co-opts VEGF-A/neuropilin-1 signaling to induce analgesia. Pain. 2021;162:243–252. doi:10.1097/j.pain.0000000000002097
- Gomez K*, Calderón-Rivera A*, Sandoval A, González-Ramírez R, Vargas-Parada A, Ojeda-Alonso J, Granados-Soto V, Delgado-Lezama R, Felix R. Cdk5-dependent phosphorylation of CaV3.2 T-type channels: role in neuropathic allodynia. J Neurosci. 2020;40:283–296. doi:10.1523/JNEUROSCI.0181-19.2019