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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

p38α: A Suppressor of Cell Proliferation and Tumorigenesis

Open access
Hui, Lijian, Bakiri, Latifa, Stepniak, Ewa, Wagner, Erwin F.·2007·Cell Cycle

Abstract

The mitogen-activated protein kinase (MAPK) p38alpha is involved in numerous biological processes and is a drug target for inflammation-associated diseases. Genetic analysis in mice demonstrated that fetuses lacking p38alpha are embryonic lethal owing to impaired placental development. The function of p38alpha in mice after birth remained unclear until conditional alleles of p38alpha were used. It was found that p38alpha is essential for lung function in both neonatal and adult mice. Increased proliferation and impaired differentiation are the hallmarks of p38alpha-deficient cells. Moreover, mice deficient in p38alpha are prone to cancer development using carcinogen or oncogene-induced cancer models. p38alpha can suppress cell proliferation by antagonizing the JNK/c-Jun pathway, which is an important regulator of proliferation and apoptosis. These findings suggest that therapeutic inhibition of p38 might lead to unwanted proliferation. Therefore, a combined inhibition of p38 and other pathways, such as the JNK pathway, should be considered for targeting cancer inflammation.

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Metadata

Authors
Hui, L., Bakiri, L., Stepniak, E., & Wagner, E. F.
Venue
Cell Cycle
Published
2007-10-15
Volume
6
Issue
20
Pages
2429-2433
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W1986735026
Cited by
183
References
2
FWCI
3.95
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: p38α: A Suppressor of Cell Proliferation and Tumorigenesis. https://app.cochat.ai/papers/10.4161/cc.6.20.4774
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Hui, L., Bakiri, L., Stepniak, E., & Wagner, E. F. (2007). p38α: A Suppressor of Cell Proliferation and Tumorigenesis. Cell Cycle. https://doi.org/10.4161/cc.6.20.4774

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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