{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:12:03Z","timestamp":1787022723862,"version":"build-2736575974"},"reference-count":48,"publisher":"Society for Neuroscience","issue":"6","license":[{"start":{"date-parts":[[2006,8,8]],"date-time":"2006-08-08T00:00:00Z","timestamp":1154995200000},"content-version":"vor","delay-in-days":181,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2006,2,8]]},"abstract":"<jats:p>\n                    The serotonin-1A (5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    ) receptor is the primary somatodendritic autoreceptor that inhibits the activity of serotonergic raphe neurons and is also expressed in nonserotonergic cortical and limbic neurons. Alterations in 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    receptor levels are implicated in mood disorders, and a functional C(-1019)G 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    promoter polymorphism has been associated with depression, suicide, and panic disorder. We examined the cell-specific activity of identified transcription factors, human nuclear deformed epidermal autoregulatory factor-1 (DEAF-1)-related (NUDR)\/Deaf-1 and Hes5, at the 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    C(-1019) site. In serotonergic raphe RN46A cells, Deaf-1 and Hes5 repressed the 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    receptor gene at the C(-1019)-allele but not the G(-1019)-allele. However, in nonserotonergic cells that express 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    receptors (septal SN48, neuroblastoma SKN-SH, and neuroblastoma\/glioma NG108\u201315 cells), Deaf-1 enhanced 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    promoter activity at the C(-1019)-allele but not the G-allele, whereas Hes5 repressed in all cell types. The enhancer activity of Deaf-1 was orientation independent and competed out Hes5 repression. To test whether Deaf-1 activity is intrinsic, the activity of a Gal4DBD (DNA binding domain)-Deaf-1 fusion protein at a heterologous Gal4 DNA element was examined. Gal4DBD-Deaf-1 repressed transcription in RN46A cells but enhanced transcription in SN48 cells, indicating that these opposite activities are intrinsic to Deaf-1. Repressor or enhancer activities of Deaf-1 or Gal4DBD-Deaf-1 were blocked by histone deacetylase inhibitor trichostatin A. Thus, the intrinsic activity of Deaf-1 at the 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    promoter is opposite in presynaptic versus postsynaptic neuronal cells and requires deacetylation. Cell-specific regulation by Deaf-1 could underlie region-specific alterations in 5-HT\n                    <jats:sub>1A<\/jats:sub>\n                    receptor expression in different mood disorders.\n                  <\/jats:p>","DOI":"10.1523\/jneurosci.2643-05.2006","type":"journal-article","created":{"date-parts":[[2006,2,8]],"date-time":"2006-02-08T16:27:56Z","timestamp":1139416076000},"page":"1864-1871","source":"Crossref","is-referenced-by-count":118,"title":["Cell-Specific Repressor or Enhancer Activities of Deaf-1 at a Serotonin 1A Receptor Gene Polymorphism"],"prefix":"10.1523","volume":"26","author":[{"given":"Margaret","family":"Czesak","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvie","family":"Lemonde","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erica 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