Zobrazeno 1 - 10
of 19
pro vyhledávání: '"Helen M. Belalcazar"'
Publikováno v:
eLife, Vol 10 (2021)
Mutations in the lysine demethylase 5 (KDM5) family of transcriptional regulators are associated with intellectual disability, yet little is known regarding their spatiotemporal requirements or neurodevelopmental contributions. Utilizing the mushroom
Externí odkaz:
https://doaj.org/article/a04043ac6cdd40deac4e64dbb57e7db6
Autor:
Oscar Maldonado, Alexandra Jenkins, Helen M Belalcazar, Helena Hernandez-Cuervo, Katelynn M Hyman, Giannina Ladaga, Lucia Padilla, Gabriel A de Erausquin
Publikováno v:
PLoS ONE, Vol 15, Iss 7, p e0223633 (2020)
BackgroundSmall conductance, calcium-activated (SK3) potassium channels control the intrinsic excitability of dopaminergic neurons (DN) in the midbrain and modulate their susceptibility to toxic insults during development.MethodsWe evaluated the age-
Externí odkaz:
https://doaj.org/article/ca43b0b4acdf4cc1bea9de34e9ad4afc
Publikováno v:
Cell Reports, Vol 22, Iss 9, Pp 2359-2369 (2018)
Summary: Mutations in KDM5 family histone demethylases cause intellectual disability in humans. However, the molecular mechanisms linking KDM5-regulated transcription and cognition remain unknown. Here, we establish Drosophila as a model to understan
Externí odkaz:
https://doaj.org/article/b187904b04464079aec529b3a1b5186a
Publikováno v:
eLife
eLife, Vol 10 (2021)
eLife, Vol 10 (2021)
Mutations in the lysine demethylase 5 (KDM5) family of transcriptional regulators are associated with intellectual disability, yet little is known regarding their spatiotemporal requirements or neurodevelopmental contributions. Utilizing the mushroom
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::35ed156328260e1d8b3816586e7003ef
https://doi.org/10.7554/elife.63886
https://doi.org/10.7554/elife.63886
SummaryMutations in the genes encoding the KDM5 family of histone demethylases are observed in individuals with intellectual disability (ID). Despite clear evidence linking KDM5 function to neurodevelopmental pathways, how this family of proteins imp
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::2c5603199ea5ff9cefb94fbef6c2c9ac
https://doi.org/10.1101/2020.10.12.335711
https://doi.org/10.1101/2020.10.12.335711
Mutations in the lysine demethylase 5 (KDM5) family of transcriptional regulators are associated with intellectual disability, yet little is known regarding the spatiotemporal requirements or neurodevelopmental contributions of KDM5 proteins. Utilizi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::56bb0e4b7416758979f6859b1888bee5
https://doi.org/10.1101/2020.10.09.324939
https://doi.org/10.1101/2020.10.09.324939
Publikováno v:
SSRN Electronic Journal.
Mutations in the genes encoding the KDM5 family of histone demethylases are observed in individuals with intellectual disability (ID). Despite clear evidence linking KDM5 function to neurodevelopmental pathways, how this family of proteins impacts tr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7f67228efaa9477a575b143677f79a2b
https://doi.org/10.2139/ssrn.3717160
https://doi.org/10.2139/ssrn.3717160
Publikováno v:
Development (Cambridge, England)
In Drosophila, the larval prothoracic gland integrates nutritional status with developmental signals to regulate growth and maturation through the secretion of the steroid hormone ecdysone. While the nutritional signals and cellular pathways that reg
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::50d00573de33243d14161b8ad6aa879a
https://doi.org/10.1242/dev.182568
https://doi.org/10.1242/dev.182568
Publikováno v:
Genetics
Regulated gene expression is necessary for developmental and homeostatic processes. The KDM5 family of proteins are histone H3 lysine 4 demethylases that can regulate transcription through both demethylase-dependent and independent mechanisms. While
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fe7b5110a540b91e527ec73ae00363de
https://doi.org/10.1534/genetics.118.301004
https://doi.org/10.1534/genetics.118.301004