Extensive conformational and physical plasticity protects HER2-HER3 tumorigenic signaling

This is the authors' abstract. We don't add key points for this paper.

Main text(Cell Reports 38, 110285; February 1, 2022)In the originally published version of this article, Methods S1 was missing from the supplemental information file due to a processing error. The complete supplemental information file now appears online with the article.Cell Press apologizes for this error. Main text(Cell Reports 38, 110285; February 1, 2022)In the originally published version of this article, Methods S1 was missing from the supplemental information file due to a processing error. The complete supplemental information file now appears online with the article.Cell Press apologizes for this error. (Cell Reports 38, 110285; February 1, 2022) In the originally published version of this article, Methods S1 was missing from the supplemental information file due to a processing error. The complete supplemental information file now appears online with the article. Cell Press apologizes for this error. Targetable HER3 functions driving tumorigenic signaling in HER2-amplified cancersCampbell et al.Cell ReportsFebruary 01, 2022In BriefCampbell et al. undertake a structure-function analysis of the HER2-HER3 kinase domains when HER2 is overexpressed in cancers. The analysis confirms the critical role of this kinase dimer in this cancer type and identifies multiple new opportunities for the design of first-in-class allosteric inhibitors for this disease.