{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T08:06:46Z","timestamp":1788941206773,"version":"build-2803163510"},"reference-count":132,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"731","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Sci. Signal."],"published-print":{"date-parts":[[2022,4,26]]},"abstract":"<jats:p>\n            Chronic pain is a major health issue, and the search for new analgesics has become increasingly important because of the addictive properties and unwanted side effects of opioids. To explore potentially new drug targets, we investigated mutations in the\n            <jats:italic>NTRK1<\/jats:italic>\n            gene found in individuals with congenital insensitivity to pain with anhidrosis (CIPA).\n            <jats:italic>NTRK1<\/jats:italic>\n            encodes tropomyosin receptor kinase A (TrkA), the receptor for nerve growth factor (NGF) and that contributes to nociception. Molecular modeling and biochemical analysis identified mutations that decreased the interaction between TrkA and one of its substrates and signaling effectors, phospholipase C\u03b3 (PLC\u03b3). We developed a cell-permeable phosphopeptide derived from TrkA (TAT-pQYP) that bound the Src homology domain 2 (SH2) of PLC\u03b3. In HEK-293T cells, TAT-pQYP inhibited the binding of heterologously expressed TrkA to PLC\u03b3 and decreased NGF-induced, TrkA-mediated PLC\u03b3 activation and signaling. In mice, intraplantar administration of TAT-pQYP decreased mechanical sensitivity in an inflammatory pain model, suggesting that targeting this interaction may be analgesic. The findings demonstrate a strategy to identify new targets for pain relief by analyzing the signaling pathways that are perturbed in CIPA.\n          <\/jats:p>","DOI":"10.1126\/scisignal.abm6046","type":"journal-article","created":{"date-parts":[[2022,4,26]],"date-time":"2022-04-26T17:56:36Z","timestamp":1650995796000},"source":"Crossref","is-referenced-by-count":13,"title":["Structural analysis of TrkA mutations in patients with congenital insensitivity to pain reveals PLC\u03b3 as an analgesic drug target"],"prefix":"10.1126","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5639-0050","authenticated-orcid":true,"given":"Beatriz C.","family":"Moraes","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Chemistry Institute, University of S\u00e3o Paulo, SP 05508-000, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8471-207X","authenticated-orcid":true,"given":"Helder V.","family":"Ribeiro-Filho","sequence":"additional","affiliation":[{"name":"Brazilian Center for Research in Energy and Materials (CNPEM), Brazilian Biosciences National Laboratory (LNBio) Campinas, SP 13083-100, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3429-7872","authenticated-orcid":true,"given":"Allan P.","family":"Rold\u00e3o","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Chemistry Institute, University of S\u00e3o Paulo, SP 05508-000, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0074-2640","authenticated-orcid":true,"given":"Elaine F.","family":"Toniolo","sequence":"additional","affiliation":[{"name":"Laboratory of Neuromodulation of Experimental Pain (LaNed), Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, SP 05508-000, Brazil."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7776-6256","authenticated-orcid":true,"given":"Gustavo P. 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