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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2023,11,7]]},"abstract":"<jats:p>\n                    L-type voltage-gated calcium (Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ) channels (L-VGCC) dysfunction is implicated in several neurological and psychiatric diseases. While a popular therapeutic target, it is unknown whether molecular mechanisms leading to disrupted L-VGCC across neurodegenerative disorders are conserved. Importantly, L-VGCC integrate synaptic signals to facilitate a plethora of cellular mechanisms; however, mechanisms that regulate L-VGCC channel density and subcellular compartmentalization are understudied. Herein, we report that in disease models with overactive mammalian target of rapamycin complex 1 (mTORC1) signaling (or mTORopathies), deficits in dendritic L-VGCC activity are associated with increased expression of the RNA-binding protein (RBP) Parkinsonism-associated deglycase (DJ-1). DJ-1 binds the mRNA coding for the alpha and auxiliary Ca\n                    <jats:sup>2+<\/jats:sup>\n                    channel subunits Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2 and \u03b12\u03b42, and represses their mRNA translation, only in the disease states, specifically preclinical models of tuberous sclerosis complex (TSC) and Alzheimer\u2019s disease (AD). In agreement, DJ-1-mediated repression of Ca\n                    <jats:sub>V<\/jats:sub>\n                    1.2\/\u03b12\u03b42 protein synthesis in dendrites is exaggerated in mouse models of AD and TSC, resulting in deficits in dendritic L-VGCC calcium activity. Finding of DJ-1-regulated L-VGCC activity in dendrites in TSC and AD provides a unique signaling pathway that can be targeted in clinical mTORopathies.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2301534120","type":"journal-article","created":{"date-parts":[[2023,10,30]],"date-time":"2023-10-30T15:09:20Z","timestamp":1698678560000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":15,"title":["Aberrant DJ-1 expression underlies L-type calcium channel hypoactivity in dendrites in tuberous sclerosis complex and Alzheimer\u2019s disease"],"prefix":"10.1073","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0287-0889","authenticated-orcid":false,"given":"Farr","family":"Niere","sequence":"first","affiliation":[{"name":"Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157"},{"name":"Department of Biology, North Carolina Agricultural and Technical State 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