1
Views
10
CrossRef citations to date
0
Altmetric
Cell Growth and Development

The Transforming Potential of the c-erbB-2 Protein Is Regulated by Its Autophosphorylation at the Carboxyl-Terminal Domain

, , , , &
Pages 833-842 | Received 19 Jun 1990, Accepted 31 Oct 1990, Published online: 31 Mar 2023

Keep up to date with the latest research on this topic with citation updates for this article.

Read on this site (6)

Milos Dokmanovic, Yun Wu, Yi Shen, Jieqing Chen, Dianne S Hirsch & Wen Jin Wu. (2014) Trastuzumab-induced recruitment of Csk-homologous kinase (CHK) to ErbB2 receptor is associated with ErbB2-Y1248 phosphorylation and ErbB2 degradation to mediate cell growth inhibition. Cancer Biology & Therapy 15:8, pages 1029-1041.
Read now
Wendy Béguelin, María Celeste Díaz Flaqué, Cecilia J. Proietti, Florencia Cayrol, Martín A. Rivas, Mercedes Tkach, Cinthia Rosemblit, Johanna M. Tocci, Eduardo H. Charreau, Roxana Schillaci & Patricia V. Elizalde. (2010) Progesterone Receptor Induces ErbB-2 Nuclear Translocation To Promote Breast Cancer Growth via a Novel Transcriptional Effect: ErbB-2 Function as a Coactivator of Stat3. Molecular and Cellular Biology 30:23, pages 5456-5472.
Read now
Gregory J. Tsongalis & Andrew Ricci Jr.. (2001) HER2: The Neu Prognostic Marker for Breast Cancer. Critical Reviews in Clinical Laboratory Sciences 38:2, pages 167-182.
Read now
David L. Dankort, Zhixiang Wang, Valerie Blackmore, Michael F. Moran & William J. Muller. (1997) Distinct Tyrosine Autophosphorylation Sites Negatively and Positively Modulate Neu-Mediated Transformation. Molecular and Cellular Biology 17:9, pages 5410-5425.
Read now
Hideshi Ishii, Teruhiko Yoshida, Hakumei Oh, Sho Yoshida & Masaaki Terada. (1995) A Truncated K-sam Product Lacking the Distal Carboxyl-Terminal Portion Provides a Reduced Level of Autophosphorylation and Greater Resistance against Induction of Differentiation. Molecular and Cellular Biology 15:7, pages 3664-3671.
Read now
Peter M. Siegel, David L. Dankort, William R. Hardy & William J. Muller. (1994) Novel Activating Mutations in the neu Proto-oncogene Involved in Induction of Mammary Tumors. Molecular and Cellular Biology 14:11, pages 7068-7077.
Read now

Articles from other publishers (4)

Paula J. Whittington, Marie P. Piechocki, Henry H. Heng, Jennifer B. Jacob, Richard F. Jones, Jessica B. Back & Wei-Zen Wei. (2008) DNA Vaccination Controls Her-2+ Tumors that Are Refractory to Targeted Therapies. Cancer Research 68:18, pages 7502-7511.
Crossref
Torsten Trowe, Sotiria Boukouvala, Keith Calkins, Richard E. CutlerJr.Jr., Ryan Fong, Roel Funke, Steven B. Gendreau, Yong D. Kim, Nicole Miller, John R. Woolfrey, Valentina Vysotskaia, Jing Ping Yang, Mary E. Gerritsen, David J. Matthews, Peter Lamb & Timothy S. Heuer. (2008) EXEL-7647 Inhibits Mutant Forms of ErbB2 Associated with Lapatinib Resistance and Neoplastic Transformation. Clinical Cancer Research 14:8, pages 2465-2475.
Crossref
Ming Tan, Ping Li, Kristine S. Klos, Jing Lu, Keng-Hsueh Lan, Yoichi Nagata, Dexing Fang, Tong Jing & Dihua Yu. (2005) ErbB2 Promotes Src Synthesis and Stability: Novel Mechanisms of Src Activation That Confer Breast Cancer Metastasis. Cancer Research 65:5, pages 1858-1867.
Crossref
Satoru Yamasaki, Keigo Nishida, Yuichi Yoshida, Motoyuki Itoh, Masahiko Hibi & Toshio Hirano. (2003) Gab1 is required for EGF receptor signaling and the transformation by activated ErbB2. Oncogene 22:10, pages 1546-1556.
Crossref

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.