ArticleMolecular and cellular biology2008
p27kip1 deficiency impairs G2/M arrest in response to DNA damage, leading to an increase in genetic instability.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 64 citations in OpenAlex.
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- Suppressive cancer nonstop extension mutations increase C-terminal hydrophobicity and disrupt evolutionarily conserved amino acid patterns.Nature communications · 2024Article
- Nrg1 Regulates Cardiomyocyte Migration and Cell Cycle in Ventricular Development.Circulation research · 2023Article
- Coinhibition of topoisomerase 1 and BRD4-mediated pause release selectively kills pancreatic cancer via readthrough transcription.Science advances · 2023Article
- Bortezomib Is Effective in the Treatment of T Lymphoblastic Leukaemia by Inducing DNA Damage, WEE1 Downregulation, and Mitotic Catastrophe.International journal of molecular sciences · 2023Article
- CELF1 Selectively Regulates Alternative Splicing of DNA Repair Genes Associated With Cataract in Human Lens Cell Line.Biochemical genetics · 2023Article
- p27Cells · 2021Review
- CDKN1B mutation and copy number variation are associated with tumor aggressiveness in luminal breast cancer.The Journal of pathology · 2021Article
- Upregulation of fibronectin following loss of p53 function is a poor prognostic factor in ovarian carcinoma with a unique immunophenotype.Cell communication and signaling : CCS · 2020Article
- Anti-Cancer Potential ofMolecules (Basel, Switzerland) · 2020Article
- WIP1 dephosphorylation of p27Cell cycle (Georgetown, Tex.) · 2020Article
- Upregulation of miR-130b Contributes to Risk of Poor Prognosis and Racial Disparity in African-American Prostate Cancer.Cancer prevention research (Philadelphia, Pa.) · 2019Article
- Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability.Cell death & disease · 2019Article
- Notch1 activation enhances proliferation via activation of cdc2 and delays differentiation of myeloid progenitors.Leukemia research · 2018Article
- Article
- Loss of p27Scientific reports · 2017Article
- Constitutional t(8;22)(q24;q11.2) that mimics the variant Burkitt-type translocation in Philadelphia chromosome-positive chronic myeloid leukemia.International journal of hematology · 2017Article
- Frequently mutated genes/pathways and genomic instability as prevention targets in liver cancer.Carcinogenesis · 2017Review
- The non-canonical functions of p27(Kip1) in normal and tumor biology.Cell cycle (Georgetown, Tex.) · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
p27(kip1) is a cyclin-dependent kinase inhibitor and a tumor suppressor. In some tumors, p27 suppresses tumor growth by inhibition of cell proliferation. However, this is not universally observed, implying additional mechanisms of tumor suppression by p27. p27-deficient mice are particularly susceptibility to genotoxin-induced tumors, suggesting a role for p27 in the DNA damage response. To test this hypothesis, we measured genotoxin-induced mutations and chromosome damage in p27-deficient mice. Both p27(+/-) and p27(-/-) mice displayed a higher N-ethyl-N-nitrosourea-induced mutation frequency in the colon than p27(+/+) littermates. Furthermore, cells from irradiated p27-deficient mice exhibited a higher number of chromatid breaks and showed modestly increased micronucleus formation compared to cells from wild-type littermates. To determine if this mutator phenotype was related to the cell cycle-inhibitory function of p27, we measured cell cycle arrest in response to DNA damage. Both normal and tumor cells from p27-deficient mice showed impaired G(2)/M arrest following low doses of ionizing radiation. Thus, p27 may inhibit tumor development through two mechanisms. The first is by reducing the proliferation of cells that have already sustained an oncogenic lesion. The second is by transient inhibition of cell cycle progression following genotoxic insult, thereby minimizing chromosome damage and fixation of mutations.
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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.