HER2 recruits AKT1 to disrupt STING signalling and suppress antiviral defence and antitumour immunity - Wu, Shiying; Zhang, Qian; Zhang, Fei; Meng, Fansen; Liu, Shengduo; Zhou, Ruyuan; Wu, Qingzhe; Li, Xinran; Shen, Li; Huang, Jun; Qin, Jun; Ouyang, Songying; et al. (Nature cell biology, 2019)
Keywords: 13/1; 13/2; 13/21; 13/51; 13/89; 13/95; 14/19; 38/77; 631/67; 631/67/395; 631/80/509; 631/80/86; 64/116; 64/60; 82/47; 82/58; 82/83; AKT1 protein; Antiviral drugs; Apoptosis; Biomedical and Life Sciences; Cancer Research; Carcinogenesis; Cell Biology; Cell research; Cytokines; Damage; Deoxyribonucleic acid; Developmental Biology; DNA; Epidermal growth factor receptors; ErbB protein; ErbB-2 protein; Genetic aspects; Health aspects; Host-Pathogen Interactions; Humans; Immune response; Immunity; Immunity, Innate - immunology; Immunoregulation; Kinases; Life Sciences; Membrane proteins; Membrane Proteins - immunology; Membrane Proteins - metabolism; Microorganisms; Negative feedback; Phosphorylation; Physiological aspects; Protein kinases; Protein-tyrosine kinase receptors; Proto-Oncogene Proteins c-akt - immunology; Proto-Oncogene Proteins c-akt - metabolism; Receptor, ErbB-2 - immunology; Receptor, ErbB-2 - metabolism; Senescence; Signal transduction; Signaling; Stem Cells; Surveillance; Tumorigenesis; Tyrosine; Ubiquitination; Ubiquitination - immunology; China