ArticleMolecular and cellular biology2004
Failure to proliferate and mitotic arrest of CDK11(p110/p58)-null mutant mice at the blastocyst stage of embryonic cell development.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 85 citations in OpenAlex.
- CDK7, CDK9, or CDK11 inhibition reduces neutrophil-driven inflammation and tissue damage in experimental autoimmune models.Cell communication and signaling : CCS · 2026Article
- Phase Separation of SF3B1 Serves as a Critical Post-Transcriptional Regulator During Early Mouse Embryogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CDK11 facilitates centromeric transcription to maintain centromeric cohesion during mitosis.Molecular biology of the cell · 2024Article
- Cyclin-dependent kinases: Masters of the eukaryotic universe.Wiley interdisciplinary reviews. RNA · 2023Review
- CMGC Kinases in Health and Cancer.Cancers · 2023Review
- Review
- CDK11 Promotes Cytokine-Induced Apoptosis in Pancreatic Beta Cells Independently of Glucose Concentration and Is Regulated by Inflammation in the NOD Mouse Model.Frontiers in immunology · 2021Article
- A cyclin-dependent kinase, CDK11/p58, represses cap-dependent translation during mitosis.Cellular and molecular life sciences : CMLS · 2020Article
- The Role of CDKs and CDKIs in Murine Development.International journal of molecular sciences · 2020Review
- CDK11 negatively regulates Wnt/β-catenin signaling in the endosomal compartment by affecting microtubule stability.Cancer biology & medicine · 2020Article
- CDK11 is required for transcription of replication-dependent histone genes.Nature structural & molecular biology · 2020Article
- Transcriptional activation of CBFβ by CDK11Cell communication and signaling : CCS · 2019Article
- CDK11 Loss Induces Cell Cycle Dysfunction and Death of BRAF and NRAS Melanoma Cells.Pharmaceuticals (Basel, Switzerland) · 2019Article
- CDK-11-Cyclin L is required for gametogenesis and fertility in C. elegans.Developmental biology · 2018Article
- Mettl3-mediated mCell research · 2017Article
- Kinases Involved in Both Autophagy and Mitosis.International journal of molecular sciences · 2017Review
- Checkpoints of apicomplexan cell division identified in Toxoplasma gondii.PLoS pathogens · 2017Article
- Identification and characterization of the BmCyclin L1-BmCDK11A/B complex in relation to cell cycle regulation.Cell cycle (Georgetown, Tex.) · 2017Article
- The emerging roles and therapeutic potential of cyclin-dependent kinase 11 (CDK11) in human cancer.Oncotarget · 2016Review
- Targeting CDK11 in osteosarcoma cells using the CRISPR-Cas9 system.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The CDK11(p110) protein kinases are part of large-molecular-weight complexes that also contain RNA polymerase II, transcriptional elongation factors, and general pre-mRNA splicing factors. CDK11(p110) isoforms may therefore couple transcription and pre-mRNA splicing by their effect(s) on certain proteins required for these processes. The CDK11(p58) kinase isoform is generated from the CDK11(p110) mRNA through the use of an internal ribosome entry site in a mitosis-specific manner, suggesting that this kinase may regulate the cell cycle during mitosis. The in vivo role and necessity of CDK11(p110/p58) kinase function during mammalian development were examined by generating CDK11(p110/p58)-null mice through targeted disruption of the corresponding gene using homologous recombination. While heterozygous mice develop normally, disruption of both CDK11(p110/p58) alleles results in early embryonic lethality due to apoptosis of the blastocyst cells between 3.5 and 4 days postcoitus. Cells within these embryos exhibit both proliferative defect(s) and a mitotic arrest. These results are consistent with the proposed cellular functions of the CDK11(p110/p58) kinases and confirm that the CDK11(p110/p58) kinases are essential for cellular viability as well as normal early embryonic development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.