ArticleMolecular and cellular biology2003
BRCT domain-containing protein PTIP is essential for progression through mitosis.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- PAXIP1 is regulated by NRF1 and is a prognosis‑related biomarker in hepatocellular carcinoma.Biomedical reports · 2025Article
- Morphogenesis-coupled DNA repair - in mammalian embryogenesis, morphogenesis and DNA double strand break (DSB) repair are carried out simultaneously to ensure normal development.Journal of radiation research · 2024Article
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- The genomic stability regulator PTIP is required for proper chromosome segregation in mitosis.Cell division · 2022Article
- Temporal transcriptomic landscape of postnatal mouse ovaries reveals dynamic gene signatures associated with ovarian aging.Human molecular genetics · 2021Article
- Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance.Communications biology · 2021Article
- COMPASS and SWI/SNF complexes in development and disease.Nature reviews. Genetics · 2021Review
- Post-Translational Modifications of PCNA in Control of DNA Synthesis and DNA Damage Tolerance-the Implications in Carcinogenesis.International journal of biological sciences · 2021Review
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- Regeneration after acute kidney injury requires PTIP-mediated epigenetic modifications.JCI insight · 2020Article
- 53BP1 Enforces Distinct Pre- and Post-resection Blocks on Homologous Recombination.Molecular cell · 2020Article
- A Survey of Essential Genome Stability Genes Reveals That Replication Stress Mitigation Is Critical for Peri-Implantation Embryogenesis.Frontiers in cell and developmental biology · 2020Review
- Functional Impacts of the BRCA1-mTORC2 Interaction in Breast Cancer.International journal of molecular sciences · 2019Article
- Histone methylation regulator PTIP is required to maintain normal and leukemic bone marrow niches.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- PAXIP1 Potentiates the Combination of WEE1 Inhibitor AZD1775 and Platinum Agents in Lung Cancer.Molecular cancer therapeutics · 2016Article
- NOP14 suppresses breast cancer progression by inhibiting NRIP1/Wnt/β-catenin pathway.Oncotarget · 2015Article
- Evidence for intermediate mesoderm and kidney progenitor cell specification by Pax2 and PTIP dependent mechanisms.Developmental biology · 2015Article
- The Groucho-associated phosphatase PPM1B displaces Pax transactivation domain interacting protein (PTIP) to switch the transcription factor Pax2 from a transcriptional activator to a repressor.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The Pax transactivation domain-interacting protein (PTIP) is a large nuclear protein with multiple BRCT domains that was identified on the basis of its interaction with transcription factors of the Pax and Smad families. To address the function of PTIP during mouse development, we generated a constitutive null allele. Homozygous PTIP mutants are developmentally retarded, disorganized, and embryonic lethal by day 9.5 of embryonic development (E9.5). PTIP mutant cells appear to replicate DNA but show reduced levels of mitosis and widespread cell death by E8.5. DNA damage appears to precede nuclear condensation at E7.5, suggesting a defect in DNA repair. Neither embryonic fibroblast nor embryonic stem cells from PTIP mutants proliferate in culture, suggesting a fundamental defect in cell proliferation. Trophoblast cells from PTIP mutants are more sensitive to DNA-damaging agents. Condensation of chromatin and expression of phospho-histone H3 are also affected in PTIP mutants, and this may underlie the inability of PTIP mutants to progress through mitosis. Given the role of BRCT domain proteins in DNA repair and cell cycle control, we propose that PTIP is an essential element of the cell proliferation machinery, perhaps by functioning in the DNA repair pathways.
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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.