ArticleOncogene2005
p38alpha MAPK is required for contact inhibition.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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
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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Novel genetic variants in the P38MAPK pathway gene ZAK and susceptibility to lung cancer.Molecular carcinogenesis · 2018Pooled it
- Same same but different? How blood and lymphatic vessels induce cell contact inhibition.Biochemical Society transactions · 2025Review
- Cell-cell contacts prevent t-BuOOH-triggered ferroptosis and cellular damage in vitro by regulation of intracellular calcium.Archives of toxicology · 2024Article
- Article
- L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2022Article
- Stress Relief Techniques: p38 MAPK Determines the Balance of Cell Cycle and Apoptosis Pathways.Biomolecules · 2021Review
- Ferroptosis Meets Cell-Cell Contacts.Cells · 2021Review
- Together we stand, apart we fall: how cell-to-cell contact/interplay provides resistance to ferroptosis.Cell death & disease · 2020Review
- Novel Nanocomposite Inhibiting Caries at the Enamel Restoration Margins in an In Vitro Saliva-Derived Biofilm Secondary Caries Model.International journal of molecular sciences · 2020Article
- Novel CaFJournal of functional biomaterials · 2020Article
- Distinct and sequential re-replication barriers ensure precise genome duplication.PLoS genetics · 2020Article
- Downregulation ofAnnals of translational medicine · 2019Article
- Dynamics of transcriptome changes during subcutaneous preadipocyte differentiation in ducks.BMC genomics · 2019Article
- Sleeping Beauty and the Microenvironment Enchantment: Microenvironmental Regulation of the Proliferation-Quiescence Decision in Normal Tissues and in Cancer Development.Frontiers in cell and developmental biology · 2018Review
- p38α MAPK regulates proliferation and differentiation of osteoclast progenitors and bone remodeling in an aging-dependent manner.Scientific reports · 2017Article
- Matrix Stiffness Enhances VEGFR-2 Internalization, Signaling, and Proliferation in Endothelial Cells.Convergent science physical oncology · 2017Article
- Differences and Similarities in TRAIL- and Tumor Necrosis Factor-Mediated Necroptotic Signaling in Cancer Cells.Molecular and cellular biology · 2016Article
- Deciphering fact from artifact when using reporter assays to investigate the roles of host factors on L1 retrotransposition.Mobile DNA · 2016Article
- Endosomal regulation of contact inhibition through the AMOT:YAP pathway.Molecular biology of the cell · 2015Article
- Gerosuppression in confluent cells.Aging · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proliferation of nontransformed cells is regulated by cell-cell contacts, which are referred to as contact-inhibition. Despite its generally accepted importance for cell cycle control, knowledge about the intracellular signalling pathways involved in contact inhibition is scarce. In the present work we show that p38alpha mitogen-activated protein kinase (MAPK) is involved in the growth-inhibitory signalling cascade of contact inhibition in fibroblasts. p38alpha activity is increased in confluent cultures of human fibroblasts compared to proliferating cultures. Time course studies show a sustained activation of p38alpha in response to cell-cell contacts in contrast to a transient activation after serum stimulation. The induction of contact inhibition by addition of glutaraldehyde-fixed cells is impaired by pharmacological inhibition of p38 as well as in p38alpha-/- fibroblasts. Further evidence for a central role of p38alpha in contact inhibition comes from the observation that p38alpha-/- fibroblasts show a higher saturation density compared to wild-type (wt) fibroblasts, which is reversed by reconstituted expression of p38alpha. In agreement with a defect in contact inhibition, p27(Kip1) accumulation is impaired in p38alpha-/- fibroblasts compared to wt fibroblasts. Hence, our work shows a new role for p38alpha in contact inhibition and provides a mechanistic basis for the recently proposed tumour suppressive function of this MAPK pathway.
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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.