ArticleMolecular and cellular biology2007
Cooperation between p27 and p107 during endochondral ossification suggests a genetic pathway controlled by p27 and p130.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- The Tumor Suppressor p53 Downregulates p107 (International journal of molecular sciences · 2025Article
- p27Cells · 2025Article
- C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer.Nature communications · 2024Article
- RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation.Nucleic acids research · 2019Article
- Up-regulated expression of E2F2 is necessary for p16INK4a-induced cartilage injury.BMC musculoskeletal disorders · 2018Article
- PP2A: more than a reset switch to activate pRB proteins during the cell cycle and in response to signaling cues.Cell cycle (Georgetown, Tex.) · 2015Review
- Article
- p16INK4a and its regulator miR-24 link senescence and chondrocyte terminal differentiation-associated matrix remodeling in osteoarthritis.Arthritis research & therapy · 2014Article
- Article
- Activation of p107 by fibroblast growth factor, which is essential for chondrocyte cell cycle exit, is mediated by the protein phosphatase 2A/B55α holoenzyme.Molecular and cellular biology · 2013Article
- p27Kip1 represses transcription by direct interaction with p130/E2F4 at the promoters of target genes.Oncogene · 2012Article
- p27kip1 protein levels reflect a nexus of oncogenic signaling during cell transformation.The Journal of biological chemistry · 2012Article
- p107 in the public eye: an Rb understudy and more.Cell division · 2010Article
- PP2A-mediated dephosphorylation of p107 plays a critical role in chondrocyte cell cycle arrest by FGF.PloS one · 2008Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Pocket proteins and cyclin-dependent kinase (CDK) inhibitors negatively regulate cell proliferation and can promote differentiation. However, which members of these gene families, which cell type they interact in, and what they do to promote differentiation in that cell type during mouse development are largely unknown. To identify the cell types in which p107 and p27 interact, we generated compound mutant mice. These mice were null for p107 and had a deletion in p27 that prevented its binding to cyclin-CDK complexes. Although a fraction of these animals survived into adulthood and looked similar to single p27 mutant mice, a larger number of animals died at birth or within a few weeks thereafter. These animals displayed defects in chondrocyte maturation and endochondral bone formation. Proliferation of chondrocytes was increased, and ectopic ossification was observed. Uncommitted mouse embryo fibroblasts could be induced into the chondrocytic lineage ex vivo, but these cells failed to mature normally. These results demonstrate that p27 carries out overlapping functions with p107 in controlling cell cycle exit during chondrocyte maturation. The phenotypic similarities between p107(-/-) p27(D51/D51) and p107(-/-) p130(-/-) mice and the cells derived from them suggest that p27 and p130 act in an analogous pathway during chondrocyte maturation.
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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.