ArticleCell death and differentiation2011
MTBP plays a crucial role in mitotic progression and chromosome segregation.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Minor spliceosome inhibition via ablation of its U11 snRNA gene results in multiple defects in murine spermatogenesis.Nucleic acids research · 2026Article
- Targeting KIFC1 Promotes Senescence in Soft Tissue Sarcoma via FXR1-Dependent Regulation of MAD2L1 mRNA Stability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Characterization of anCancers · 2023Article
- Review
- The Role of MTBP as a Replication Origin Firing Factor.Biology · 2022Review
- MTBP phosphorylation controls DNA replication origin firing.Scientific reports · 2021Article
- The Cdk8/19-cyclin C transcription regulator functions in genome replication through metazoan Sld7.PLoS biology · 2019Article
- Article
- Haploinsufficiency of the Myc regulator Mtbp extends survival and delays tumor development in aging mice.Aging · 2016Article
- Murine double minute 2, a potential p53-independent regulator of liver cancer metastasis.Hepatoma research · 2016Article
- MTBP Promotes the Invasion and Metastasis of Hepatocellular Carcinoma by Enhancing the MDM2-Mediated Degradation of E-Cadherin.Digestive diseases and sciences · 2015Article
- MTBP inhibits migration and metastasis of hepatocellular carcinoma.Clinical & experimental metastasis · 2015Article
- MTBP is overexpressed in triple-negative breast cancer and contributes to its growth and survival.Molecular cancer research : MCR · 2014Article
- Oncogenic protein MTBP interacts with MYC to promote tumorigenesis.Cancer research · 2014Article
- Metastasis suppressors in breast cancers: mechanistic insights and clinical potential.Journal of molecular medicine (Berlin, Germany) · 2014Review
- Article
- Critical role of cyclin B1/Cdc2 up-regulation in the induction of mitotic prometaphase arrest in human breast cancer cells treated with 2-methoxyestradiol.Biochimica et biophysica acta · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Murine double minute 2 (MDM2) binding protein (MTBP) has been implicated in tumor cell proliferation, but the underlying mechanisms remain unclear. The results of MTBP expression analysis during cell cycle progression demonstrated that MTBP protein was rapidly degraded during mitosis. Immunofluorescence studies revealed that a portion of MTBP was localized at the kinetochores during prometaphase. MTBP overexpression delayed mitotic progression from nuclear envelope breakdown (NEB) to anaphase onset and induced abnormal chromosome segregation such as lagging chromosomes, chromosome bridges, and multipolar chromosome segregation. Conversely, MTBP downmodulation caused an abbreviated metaphase and insufficient mitotic arrest, resulting in abnormal chromosome segregation, aneuploidy, decreased cell proliferation, senescence, and cell death, similar to that of Mad2 (mitotic arrest-deficient 2) downmodulation. Furthermore, MTBP downmodulation inhibited the accumulation of Mad1 and Mad2, but not BubR1 (budding uninhibited by benzimidazoles related 1), on the kinetochores, whereas MTBP overexpression inhibited the release of Mad2 from the metaphase kinetochores. These results may imply that MTBP has an important role in recruiting and/or retaining the Mad1/Mad2 complex at the kinetochores during prometaphase, but its degradation is required for silencing the mitotic checkpoint. Together, this study indicates that MTBP has a crucial role in proper mitotic progression and faithful chromosome segregation, providing new insights into regulation of the mitotic checkpoint.
Indexed as
Identifiers
What OpenQuestion holds
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.