{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chen Y"],"funding":["Hubei Agricultural Science and Technology Innovation Action Project","Jiangsu Provincial Key Research and Development Program","Science and Technology Service Network Plan","Trans-gene Key Project of China","Key Technologies Research and Development Program of Anhui Province"],"pagination":["84"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10176748"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["<h4>Background</h4>ISGylation is a post-translational protein modification that regulates many life activities, including immunomodulation, antiviral responses, and embryo implantation. The exact contribution of ISGylation to folliculogenesis remains largely undefined.<h4>Results</h4>Here, Isg15 knockout in mice causes hyperfertility along with sensitive ovarian responses to gonadotropin, such as increases in cumulus expansion and ovulation rate. Moreover, ISG15 represses the expression of ovulation-related genes in an ISGylation-dependent manner. Mechanistically, ISG15 binds to ADAMTS1 via the ISG15-conjugating system (UBA7, UBE2L6, and HERC6), ISGylating ADAMTS1 at the binding sites Lys309, Lys593, Lys597, and Lys602, resulting in ADAMTS1 degradation via a 20S proteasome-dependent pathwa"],"journal":["Cell & bioscience"],"pubmed_title":["ISG15 suppresses ovulation and female fertility by ISGylating ADAMTS1."],"pmcid":["PMC10176748"],"funding_grant_id":["2018skjcx05","2018ZX08009-27B","2021YFF1000601","2020BBB069","2020ABA016"],"pubmed_authors":["Peng X","Li F","Wu S","Chen G","Mei S","Chen Y","Zhou J","Wang L","Chen D","Miao YL"],"additional_accession":[]},"is_claimable":false,"name":"ISG15 suppresses ovulation and female fertility by ISGylating ADAMTS1.","description":"<h4>Background</h4>ISGylation is a post-translational protein modification that regulates many life activities, including immunomodulation, antiviral responses, and embryo implantation. The exact contribution of ISGylation to folliculogenesis remains largely undefined.<h4>Results</h4>Here, Isg15 knockout in mice causes hyperfertility along with sensitive ovarian responses to gonadotropin, such as increases in cumulus expansion and ovulation rate. Moreover, ISG15 represses the expression of ovulation-related genes in an ISGylation-dependent manner. Mechanistically, ISG15 binds to ADAMTS1 via the ISG15-conjugating system (UBA7, UBE2L6, and HERC6), ISGylating ADAMTS1 at the binding sites Lys309, Lys593, Lys597, and Lys602, resulting in ADAMTS1 degradation via a 20S proteasome-dependent pathwa","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2025-04-26T17:21:00.442Z","creation":"2025-04-06T15:32:05.128Z"},"accession":"S-EPMC10176748","cross_references":{"pubmed":["37170317"],"doi":["10.1186/s13578-023-01024-4"]}}