ArticleBiotechnology journal2013
Molecular modeling of ErbB4/HER4 kinase in the context of the HER4 signaling network helps rationalize the effects of clinically identified HER4 somatic mutations on the cell phenotype.
Article in Biotechnology journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Establishment of a patient-derived mucoepidermoid carcinoma cell line with theMolecular and clinical oncology · 2022Article
- The role of ERBB4 mutations in the prognosis of advanced non-small cell lung cancer treated with immune checkpoint inhibitors.Molecular medicine (Cambridge, Mass.) · 2021Article
- PET and SPECT Imaging of the EGFR Family (RTK Class I) in Oncology.International journal of molecular sciences · 2021Review
- The role of ErbB4 in cancer.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Computational algorithms for in silico profiling of activating mutations in cancer.Cellular and molecular life sciences : CMLS · 2019Review
- Insights into evolutionary interaction patterns of the 'Phosphorylation Activation Segment' in kinase.Bioinformation · 2019Article
- A comprehensive review of heregulins, HER3, and HER4 as potential therapeutic targets in cancer.Oncotarget · 2017Review
- Cervical small cell neuroendocrine tumor mutation profiles via whole exome sequencing.Oncotarget · 2017Article
- Computational delineation of tyrosyl-substrate recognition and catalytic landscapes by the epidermal growth factor receptor tyrosine kinase domain.Molecular bioSystems · 2014Article
- Article
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Authors and funding
3 authors.
Funding
Abstract
In the ErbB/HER family of receptor tyrosine kinases, the deregulation of the EGFR/ErbB1/HER1, HER2/ErbB2, and HER3/ErbB3 kinases is associated with several cancers, while the HER4/ErbB4 kinase has been shown to play an anti-carcinogenic role in certain tumors. We present molecular and network models of HER4/ErbB4 activation and signaling in order to elucidate molecular mechanisms of activation and rationalize the effects of the clinically identified HER4 somatic mutants. Our molecular-scale simulations identify the important role played by the interactions within the juxtamembrane region during the activation process. Our results also support the hypothesis that the HER4 mutants may heterodimerize but not activate, resulting in blockage of the HER4-STAT5 differentiation pathway, in favor of the proliferative PI3K/AKT pathway. Translating our molecular simulation results into a cellular pathway model of wild type versus mutant HER4 signaling, we are able to recapitulate the major features of the PI3K/AKT and JAK/STAT activation downstream of HER4. Our model predicts that the signaling downstream of the wild type HER4 is enriched for the JAK-STAT pathway, whereas downstream of the mutant HER4 is enriched for the PI3K/AKT pathway. HER4 mutations may hence constitute a cellular shift from a program of differentiation to that of proliferation.
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