Genetic inactivation of Par4 results in hyperactivation of NF‐κB and impairment of JNK and p38-Reference-Cited by-同舟云学术

Genetic inactivation of Par4 results in hyperactivation of NF‐κB and impairment of JNK and p38

Published:2003-02-07 Issue:3 Volume:4 Page:307-312
ISSN:1469-221X
Container-title:EMBO reports
language:en
Short-container-title:EMBO Rep

Author:

Garcia‐Cao Isabel¹,Lafuente María José²,Criado Luis M¹,Diaz‐Meco María Teresa²,Serrano Manuel¹,Moscat Jorge²

Affiliation:

1. Department of Immunology and Oncology, Centro Nacional de Biotecnología, Universidad Autonoma de Madrid, Canto Blanco 28049 Madrid Spain

2. Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autonoma de Madrid, Canto Blanco 28049 Madrid Spain

Publisher

EMBO

Subject

Genetics,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1038/sj.embor.embor769

Reference19 articles.

1. The downregulation of the pro-apoptotic protein Par-4 is critical for Ras-induced survival and tumor progression

2. Evidence for a role of MEK and MAPK during signal transduction by protein kinase C zeta.

3. Positioning atypical protein kinase C isoforms in the UV-induced apoptotic signaling cascade

4. Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling

5. The Product of par-4, a Gene Induced during Apoptosis, Interacts Selectively with the Atypical Isoforms of Protein Kinase C

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