ArticleCell reports2017
Citron Kinase Deficiency Leads to Chromosomal Instability and TP53-Sensitive Microcephaly.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
- Citron Kinase, a mitotic kinase with increasing significance in cancer.Cell cycle (Georgetown, Tex.) · 2026Review
- Rare genetic causes of primary microcephaly in two Saudi families identified via whole-exome sequencing: Genomic and phenotypic delineation of pathogenicMolecular genetics and metabolism reports · 2026Article
- Microcephaly-associated genes asp and Sas4 influence chromatin organization and nuclear lamina structure in Drosophila melanogaster.Development (Cambridge, England) · 2026Article
- CITK modulates BRCA1 recruitment at DNA double strand breaks sites through HDAC6.Cell death & disease · 2025Article
- Interneuron migration impairment and brain region-specific DNA damage response following irradiation during early neurogenesis in mice.Cellular and molecular life sciences : CMLS · 2025Article
- A human-specific, concerted repression of microcephaly genes contributes to radiation-induced growth defects in cortical organoids.iScience · 2025Article
- CIT kinase phosphorylation as significant regulatory node for cellular checkpoints.Frontiers in bioinformatics · 2025Article
- Modeling primary microcephaly with human brain organoids reveals fundamental roles of CIT kinase activity.The Journal of clinical investigation · 2024Article
- Mcph1, mutated in primary microcephaly, is also crucial for erythropoiesis.EMBO reports · 2024Article
- Aberrant generation of dentate gyrus granule cells is associated with epileptic susceptibility in p53 conditional knockout mice.Frontiers in neuroscience · 2024Article
- Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase.Cancer research · 2023Article
- P53 independent pathogenic mechanisms contribute to BubR1 microcephaly.Frontiers in cell and developmental biology · 2023Article
- DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023Review
- The impact of TP53 activation and apoptosis in primary hereditary microcephaly.Frontiers in neuroscience · 2023Review
- Lestaurtinib inhibits Citron kinase activity and medulloblastoma growth through induction of DNA damage, apoptosis and cytokinesis failure.Frontiers in oncology · 2023Article
- Evolutionary conserved relocation of chromatin remodeling complexes to the mitotic apparatus.BMC biology · 2022Article
- Molecular and functional heterogeneity in dorsal and ventral oligodendrocyte progenitor cells of the mouse forebrain in response to DNA damage.Nature communications · 2022Article
- Non-Structural Protein 5 of Zika Virus Interacts with p53 in Human Neural Progenitor Cells and Induces p53-Mediated Apoptosis.Virologica Sinica · 2021Article
- Cytokinetic Abscission Regulation in Neural Stem Cells and Tissue Development.Current stem cell reports · 2021Article
- Time is of the essence: the molecular mechanisms of primary microcephaly.Genes & development · 2021Review
Corrections and comments
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Authors and funding
22 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in citron (CIT), leading to loss or inactivation of the citron kinase protein (CITK), cause primary microcephaly in humans and rodents, associated with cytokinesis failure and apoptosis in neural progenitors. We show that CITK loss induces DNA damage accumulation and chromosomal instability in both mammals and Drosophila. CITK-deficient cells display "spontaneous" DNA damage, increased sensitivity to ionizing radiation, and defective recovery from radiation-induced DNA lesions. In CITK-deficient cells, DNA double-strand breaks increase independently of cytokinesis failure. Recruitment of RAD51 to DNA damage foci is compromised by CITK loss, and CITK physically interacts with RAD51, suggesting an involvement of CITK in homologous recombination. Consistent with this scenario, in doubly CitK and Trp53 mutant mice, neural progenitor cell death is dramatically reduced; moreover, clinical and neuroanatomical phenotypes are remarkably improved. Our results underscore a crucial role of CIT in the maintenance of genomic integrity during brain development.
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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.