The deaf and the dumb: the biology of ErbB-2 and ErbB-3.

By A. Citri, Kochupurakkal Bose Skaria, Y. Yarden. Experimental Cell Research, 2003

628 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology and Allergy, Oncology

View Paper: https://www.semanticscholar.org/paper/5a1a3a6c29d63517bf26fbad4dc6101d4f22883f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. R. Roskoski
2. C. Der
3. P. Roberts

In Immunology and Allergy

1. R. Roskoski

In Oncology

1. R. Roskoski
2. William Pao
3. Adi F. Gazdar
4. Vincent A. Miller
5. D. Leahy
6. P. Dempsey
7. M. Sliwkowski
8. M. Lemmon

Citations in the corpus

• Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer (2007, background): “Additional EGFR-activated pathways include the PI3K and AKT serine/threonine kinase, signal transducer and activator of transcription (STAT), as well as protein kinase C and phospholipase D pathways (Citri et al., 2003).”
• Hyaluronan: from extracellular glue to pericellular cue (2004, neutral): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&list_uids=2066">ERBB4 (Ref”
• Epidermal growth factor receptor mutations, small-molecule kinase inhibitors, and non-small-cell lung cancer: current knowledge and future directions. (2005, background): “Mutations in non–small-cell lung cancers have been found in [1] epidermal growth factor receptor (EGFR) and ErbB2, [2] PIK3CA, [3] K-ras, and [4] BRAF.”
• An open-and-shut case? Recent insights into the activation of EGF/ErbB receptors. (2003, background): “When NRG-bound ErbB3 molecules are present in the cell membrane, ErbB2 preferentially forms heterooligomers with ErbB3, leading to receptor activation and mitogenic signaling (Citri et al., 2003).”
• The ErbB/HER family of protein-tyrosine kinases and cancer. (2014, background): “Such autophosphorylation was ascribed to endogenous insect cell protein kinases leading to the view that the ErbB3 protein kinase is inactive [58,59].”
• Somatic mutations of the HER2 kinase domain in lung adenocarcinomas. (2005, background): “However, the genes have distinct properties: HER2 has strong kinase activity but has no identified ligand and ERBB3 lacks kinase activity due to substitutions in critical TK domain residues (10).”
• ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “This is best exemplified in the case of ErbB2-ErbB3 heterodimers where heterodimerization of kinase-impaired ErbB3 with ligandless ErbB2 produces a potent receptor signaling complex (15).”