{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ilbay O"],"funding":["National Institutes of Health","NIGMS NIH HHS"],"pagination":["dev183111"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6857590"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["146(21)"],"pubmed_abstract":["MicroRNAs target complementary mRNAs for degradation or translational repression, reducing or preventing protein synthesis. In <i>Caenorhabditis elegans</i>, the transcription factor HBL-1 (Hunchback-like 1) promotes early larval (L2)-stage cell fates, and the <i>let-7</i> family microRNAs temporally downregulate HBL-1 to enable the L2-to-L3 cell-fate progression. In parallel to <i>let-7</i>-family microRNAs, the conserved RNA-binding protein LIN-28 and its downstream gene <i>lin-46</i> also act upstream of HBL-1 in regulating the L2-to-L3 cell-fate progression. The molecular function of LIN-46, and how the <i>lin-28-lin-46</i> pathway regulates HBL-1, are not understood. Here, we report that the regulation of HBL-1 by the <i>lin-28-lin-46</i> pathway is independent of the <i>let-7</i>/<i>"],"journal":["Development (Cambridge, England)"],"pubmed_title":["Regulation of nuclear-cytoplasmic partitioning by the <i>lin-28</i>-<i>lin-46</i> pathway reinforces microRNA repression of HBL-1 to confer robust cell-fate progression in <i>C. elegans</i>."],"pmcid":["PMC6857590"],"funding_grant_id":["R01GM088365","R01 GM088365","R35 GM131741","R01 GM034028"],"pubmed_authors":["Ilbay O","Ambros V"],"additional_accession":[]},"is_claimable":false,"name":"Regulation of nuclear-cytoplasmic partitioning by the <i>lin-28</i>-<i>lin-46</i> pathway reinforces microRNA repression of HBL-1 to confer robust cell-fate progression in <i>C. elegans</i>.","description":"MicroRNAs target complementary mRNAs for degradation or translational repression, reducing or preventing protein synthesis. In <i>Caenorhabditis elegans</i>, the transcription factor HBL-1 (Hunchback-like 1) promotes early larval (L2)-stage cell fates, and the <i>let-7</i> family microRNAs temporally downregulate HBL-1 to enable the L2-to-L3 cell-fate progression. In parallel to <i>let-7</i>-family microRNAs, the conserved RNA-binding protein LIN-28 and its downstream gene <i>lin-46</i> also act upstream of HBL-1 in regulating the L2-to-L3 cell-fate progression. The molecular function of LIN-46, and how the <i>lin-28-lin-46</i> pathway regulates HBL-1, are not understood. Here, we report that the regulation of HBL-1 by the <i>lin-28-lin-46</i> pathway is independent of the <i>let-7</i>/<i>","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Nov","modification":"2025-04-04T11:52:35.117Z","creation":"2020-11-03T08:02:46Z"},"accession":"S-EPMC6857590","cross_references":{"pubmed":["31597658"],"doi":["10.1242/dev.183111"]}}