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Biochemistry, Biophysics, and Structural Biology Commons

Open Access. Powered by Scholars. Published by Universities.®

Physiology

2011

Animals; Apoptosis; Cadherins; Cell Proliferation; Cell Transformation, Neoplastic; Contact Inhibition; Fibroblasts; JNK Mitogen-Activated Protein Kinases; Lung Neoplasms; Mice; Precancerous Conditions; Proto-Oncogene Proteins p21(ras); Signal Transduction; Stress, Physiological; Tumor Stem Cell Assay; Tumor Suppressor Protein p53

Articles 1 - 1 of 1

Full-Text Articles in Biochemistry, Biophysics, and Structural Biology

Requirement Of C-Jun Nh(2)-Terminal Kinase For Ras-Initiated Tumor Formation, Cristina Arrigo Cellurale, Guadalupe Sabio, Norman J. Kennedy, Madhumita Das, Marissa Bylsma, Peter Sandy, Tyler Jacks, Roger J. Davis Apr 2011

Requirement Of C-Jun Nh(2)-Terminal Kinase For Ras-Initiated Tumor Formation, Cristina Arrigo Cellurale, Guadalupe Sabio, Norman J. Kennedy, Madhumita Das, Marissa Bylsma, Peter Sandy, Tyler Jacks, Roger J. Davis

Davis Lab Publications

The c-Jun NH(2)-terminal kinase (JNK) signal transduction pathway causes increased gene expression mediated, in part, by members of the activating transcription factor protein (AP1) group. JNK is therefore implicated in the regulation of cell growth and cancer. To test the role of JNK in Ras-induced tumor formation, we examined the effect of compound ablation of the ubiquitously expressed genes Jnk1 plus Jnk2. We report that JNK is required for Ras-induced transformation of p53-deficient primary cells in vitro. Moreover, JNK is required for lung tumor development caused by mutational activation of the endogenous KRas gene in vivo. Together, these ...