{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lu C"],"funding":["Priority Academic Program Development of Jiangsu Higher Education Institutions","National Natural Science Foundation of China"],"pagination":["106670"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10165255"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["26(5)"],"pubmed_abstract":["Hypothalamic pro-opiomelanocortin (POMC) neuron development is considered to play an essential role in the development of obesity. However, the underlying mechanisms remain unclear. Casein kinase 1α (CK1α) was expressed in the embryonic mouse hypothalamus at high levels and colocalized with POMC neurons. CK1α deletion in POMC neurons caused weight gain, metabolic defects, and increased food intake. The number of POMC-expressing cells was considerably decreased in Csnk1a1<sup>fl/fl;</sup>POMC<sup>cre</sup> (PKO) mice from embryonic day 15.5 to postnatal day 60, while apoptosis of POMC neurons was not affected. Furthermore, unchanged POMC progenitor cells and a decreased POMC phenotype established CK1α function in hypothalamic POMC neuron development. CK1α deletion led to elevated Notch intr"],"journal":["iScience"],"pubmed_title":["Casein kinase 1α is required to maintain murine hypothalamic pro-opiomelanocortin expression."],"pmcid":["PMC10165255"],"funding_grant_id":["32102618","32130098"],"pubmed_authors":["Gao Q","Pei S","Li J","Zhang J","Wang B","Lu C","Ma K","Cui S"],"additional_accession":[]},"is_claimable":false,"name":"Casein kinase 1α is required to maintain murine hypothalamic pro-opiomelanocortin expression.","description":"Hypothalamic pro-opiomelanocortin (POMC) neuron development is considered to play an essential role in the development of obesity. However, the underlying mechanisms remain unclear. Casein kinase 1α (CK1α) was expressed in the embryonic mouse hypothalamus at high levels and colocalized with POMC neurons. CK1α deletion in POMC neurons caused weight gain, metabolic defects, and increased food intake. The number of POMC-expressing cells was considerably decreased in Csnk1a1<sup>fl/fl;</sup>POMC<sup>cre</sup> (PKO) mice from embryonic day 15.5 to postnatal day 60, while apoptosis of POMC neurons was not affected. Furthermore, unchanged POMC progenitor cells and a decreased POMC phenotype established CK1α function in hypothalamic POMC neuron development. CK1α deletion led to elevated Notch intr","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2025-04-21T16:36:46.834Z","creation":"2025-04-21T16:36:46.834Z"},"accession":"S-EPMC10165255","cross_references":{"pubmed":["37168577"],"doi":["10.1016/j.isci.2023.106670"]}}