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Yet, its putative roles in immune cell functions or in infections have remained elusive. Here, using primary dendritic cells (DCs) in an infection model with the protozoan Toxoplasma gondii, we show that two pathways activated by infection converge on Ras-Erk MAPK signaling to promote migration of parasitized DCs. We report that signaling through the receptor tyrosine kinase Met (also known as HGFR) contributes to T. gondii-induced DC hypermotility. Further, voltage-gated Ca2+ channel (VGCC, subtype CaV1.3) signaling impacted the migratory activation of DCs via calmodulin-calmodulin kinase II. We show that convergent VGCC signaling and Met signaling activate Ras GTPase to drive Erk1\/2 phosphorylation and hypermotility of T. gondii-infected DCs. The data provide a molecular basis for the hypermigratory mesenchymal-to-amoeboid transition (MAT) of parasitized DCs. The emerging concept suggests that parasitized DCs acquire metastasis-like migratory properties to promote infection-related dissemination.<\/jats:p>","DOI":"10.1242\/jcs.241752","type":"journal-article","created":{"date-parts":[[2020,3,11]],"date-time":"2020-03-11T13:45:27Z","timestamp":1583934327000},"source":"Crossref","is-referenced-by-count":19,"title":["Convergent Met and voltage-gated Ca2+ channel signaling drives hypermigration of <i>Toxoplasma<\/i>-infected dendritic cells"],"prefix":"10.1242","author":[{"given":"Einar B.","family":"\u00d3lafsson","sequence":"first","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arne L.","family":"ten Hoeve","sequence":"additional","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoze","family":"Li Wang","sequence":"additional","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda","family":"Westermark","sequence":"additional","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5857-4793","authenticated-orcid":false,"given":"Manuel","family":"Varas-Godoy","sequence":"additional","affiliation":[{"name":"Cancer Cell Biology Laboratory, Center for Cell Biology and Biomedicine (CEBICEM), Faculty of Medicine and Science, Universidad San Sebastian, Santiago, Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7746-9964","authenticated-orcid":false,"given":"Antonio","family":"Barragan","sequence":"additional","affiliation":[{"name":"Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2020,1,1]]},"reference":[{"key":"2021042623304927900_JCS241752C1","doi-asserted-by":"publisher","first-page":"649","DOI":"10.1016\/S0898-6568(02)00007-4","article-title":"Modulation of the Ras\/Raf\/MEK\/ERK pathway by Ca2+, and calmodulin","volume":"14","author":"Agell","year":"2002","journal-title":"Cell. 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