{"doi":"10.1073/pnas.98.1.194","title":"Deletion of the\n                    <i>p27</i>\n                    <sup>Kip1</sup>\n                    gene restores normal development in cyclin D1-deficient mice","abstract":"<jats:p>\n                    D-type cyclins (cyclins D1, D2, and D3) are key components of cell\n cycle machinery in mammalian cells. These proteins are believed to\n drive cell cycle progression by associating with their kinase partners,\n cyclin-dependent kinases, and by directing phosphorylation of critical\n cellular substrates. In addition, D-cyclins play a kinase-independent\n role by sequestering cell cycle inhibitors p27\n                    <jats:sup>Kip1</jats:sup>\n                    and\n p21\n                    <jats:sup>Cip1</jats:sup>\n                    . In the past, we and others generated cyclin\n D1-deficient mice and have shown that these mice display developmental\n abnormalities, hypoplastic retinas, and pregnancy-insensitive mammary\n glands. To test the significance of cyclin D1–p27\n                    <jats:sup>Kip1</jats:sup>\n                    interaction within a living mouse, we crossed cyclin D1-deficient mice\n with mice lacking p27\n                    <jats:sup>Kip1</jats:sup>\n                    , and we generated double-mutant\n cyclin D1\n                    <jats:sup>−/−</jats:sup>\n                    p27\n                    <jats:sup>−/−</jats:sup>\n                    animals. Here we report\n that ablation of\n                    <jats:italic>p27</jats:italic>\n                    <jats:sup>Kip1</jats:sup>\n                    restores\n essentially normal development in cyclin D1-deficient mice. Our results\n provide genetic evidence that p27\n                    <jats:sup>Kip1</jats:sup>\n                    functions downstream\n of cyclin D1.\n                  </jats:p>","journal":"Proceedings of the National Academy of Sciences","year":2001,"id":641761,"datarank":0.7555428903620446,"base_score":5.0369526024136295,"endowment":5.0369526024136295,"self_citation_contribution":0.7555428903620446,"citation_network_contribution":0.0,"self_endowment_contribution":0.7555428903620446,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":153,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1527091,"name":"Qunyan Yu","orcid":null,"position":1,"is_corresponding":false},{"id":869526,"name":"Ewa Sicinska","orcid":null,"position":2,"is_corresponding":false},{"id":318812,"name":"Manjusri Das","orcid":null,"position":3,"is_corresponding":false},{"id":39878,"name":"Roderick T. Bronson","orcid":"0000-0003-3725-2511","position":4,"is_corresponding":false},{"id":1527095,"name":"Piotr Sicinski","orcid":null,"position":5,"is_corresponding":false},{"id":626391,"name":"Yan Geng","orcid":"0009-0008-2658-7598","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Deletion of the\n                    <i>p27</i>\n                    <sup>Kip1</sup>\n                    gene restores normal development in cyclin D1-deficient mice","abstract":"<jats:p>\n                    D-type cyclins (cyclins D1, D2, and D3) are key components of cell\n cycle machinery in mammalian cells. These proteins are believed to\n drive cell cycle progression by associating with their kinase partners,\n cyclin-dependent kinases, and by directing phosphorylation of critical\n cellular substrates. In addition, D-cyclins play a kinase-independent\n role by sequestering cell cycle inhibitors p27\n                    <jats:sup>Kip1</jats:sup>\n                    and\n p21\n                    <jats:sup>Cip1</jats:sup>\n                    . In the past, we and others generated cyclin\n D1-deficient mice and have shown that these mice display developmental\n abnormalities, hypoplastic retinas, and pregnancy-insensitive mammary\n glands. To test the significance of cyclin D1–p27\n                    <jats:sup>Kip1</jats:sup>\n                    interaction within a living mouse, we crossed cyclin D1-deficient mice\n with mice lacking p27\n                    <jats:sup>Kip1</jats:sup>\n                    , and we generated double-mutant\n cyclin D1\n                    <jats:sup>−/−</jats:sup>\n                    p27\n                    <jats:sup>−/−</jats:sup>\n                    animals. Here we report\n that ablation of\n                    <jats:italic>p27</jats:italic>\n                    <jats:sup>Kip1</jats:sup>\n                    restores\n essentially normal development in cyclin D1-deficient mice. Our results\n provide genetic evidence that p27\n                    <jats:sup>Kip1</jats:sup>\n                    functions downstream\n of cyclin D1.\n                  </jats:p>","is_dataset_classified":null,"base_score":5.0369526024136295,"endowment":5.0369526024136295,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"11134518","pmcid":"PMC14567","openalex_id":"https://openalex.org/W1993616699","authors":[],"funders":[{"funder_name":"NCI NIH HHS","grant_id":"CA83688-01","title":null},{"funder_name":"NCI NIH HHS","grant_id":"R01 CA083688","title":null}],"total_grants":2,"fwci":6.1042,"citation_percentile":0.96931464,"influential_citations":0,"citation_trend":[{"year":2012,"count":5},{"year":2013,"count":5},{"year":2014,"count":6},{"year":2015,"count":4},{"year":2016,"count":6},{"year":2017,"count":4},{"year":2018,"count":3},{"year":2019,"count":3},{"year":2020,"count":3},{"year":2021,"count":3},{"year":2022,"count":2},{"year":2023,"count":1},{"year":2024,"count":2}],"oa_status":"green","license":null,"oa_locations":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/14567","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/14567","host_type":"repository"},{"url":"https://pnas.org/doi/pdf/10.1073/pnas.98.1.194","host_type":"publisher"},{"url":"https://doi.org/10.1073/pnas.98.1.194","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/11134518","host_type":"repository"},{"url":"https://mouseion.jax.org/stfb2000_2009/201","host_type":"repository"}],"fields_of_study":["Cancer-related Molecular Pathways","Cancer Research and Treatments","Epigenetics and DNA Methylation","Animals","Animals, Newborn","Body Weight","CDC2-CDC28 Kinases","Cell Cycle Proteins","Crosses, Genetic","Cyclin D1","Cyclin-Dependent Kinase 2","Cyclin-Dependent Kinase 4","Cyclin-Dependent Kinase Inhibitor p27","Cyclin-Dependent Kinases","Epistasis, Genetic","Female","Gene Deletion","Growth","Histocytochemistry","Male","Mammary Glands, Animal","Mice","Mice, Knockout","Microtubule-Associated Proteins","Organ Size","Phenotype","Phosphorylation","Pituitary Gland","Protein Serine-Threonine Kinases","Proto-Oncogene Proteins","Retina","Retinoblastoma Protein","Suppression, Genetic","Tumor Suppressor Proteins"],"mesh_terms":["Animals","Animals, Newborn","Body Weight","Crosses, Genetic","Epistasis, Genetic","Female","Growth","Histocytochemistry","Male","Mammary Glands, Animal","Microtubule-Associated Proteins","Organ Size","Phenotype","Phosphorylation","Pituitary Gland","Proto-Oncogene Proteins","Retina","Suppression, Genetic","Retinoblastoma Protein","Protein Serine-Threonine Kinases","Gene Deletion","Mice, Knockout","Cell Cycle Proteins","Cyclin-Dependent Kinases","Cyclin D1","Tumor Suppressor Proteins","CDC2-CDC28 Kinases","Cyclin-Dependent Kinase Inhibitor p27","Cyclin-Dependent Kinase 2","Cyclin-Dependent Kinase 4","Mice"],"keywords":["Cyclin D1","Cyclin","Biology","Cell biology","Cyclin A","Cyclin D","Cell cycle","Cyclin A2","Cyclin B","Cyclin-dependent kinase complex","Cyclin E","Cyclin-dependent kinase","Cyclin D3","Kinase","Cancer research","Genetics","Gene"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-07T20:11:11.826617Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}