N terminus of ASPP2 binds to Ras and enhances Ras/Raf/MEK/ERK activation to promote oncogene-induced senescence-Reference-Cited by-同舟云学术

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N terminus of ASPP2 binds to Ras and enhances Ras/Raf/MEK/ERK activation to promote oncogene-induced senescence

Published:2012-12-17 Issue:1 Volume:110 Page:312-317
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Wang Z.,Liu Y.,Takahashi M.,Van Hook K.,Kampa-Schittenhelm K. M.,Sheppard B. C.,Sears R. C.,Stork P. J. S.,Lopez C. D.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference50 articles.

1. New insights into the expanding complexity of the tumor suppressor ASPP2

2. ASPP2 is a haploinsufficient tumor suppressor that cooperates with p53 to suppress tumor growth

3. Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholds

4. ASPP1 and ASPP2: Common Activators of p53 Family Members

5. Structure of the p53 Tumor Suppressor Bound to the Ankyrin and SH3 Domains of 53BP2

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4. Alternative splicing of Apoptosis Stimulating Protein of TP53-2 (ASPP2) results in an oncogenic isoform promoting migration and therapy resistance in soft tissue sarcoma (STS);BMC Cancer;2022-07-02

5. RDIVpSGP motif of ASPP2 binds to 14-3-3 and enhances ASPP2/k18/14-3-3 ternary complex formulation to promote BRAF/MEK/ERK signal inhibited cell proliferation in hepatocellular carcinoma;Cancer Gene Therapy;2022-05-03

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