{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Iwamoto M"],"funding":["JST Core Research for Evolutional Science and Technology","Smoking Research Foundation","Takeda Science Foundation","Japan Agency for Medical Research and Development","Mochida Memorial Foundation for Medical and Pharmaceutical Research","Kyushu University Qdai-jump Research Program","Japan Science and Technology Agency","Yasuda Memorial Medical Foundation","Japan Society for the Promotion of Science"],"pagination":["800-807"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6970923"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["295(3)"],"pubmed_abstract":["Sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the surface of human hepatocytes and functions as an entry receptor of hepatitis B virus (HBV). Recently, we have reported that epidermal growth factor receptor (EGFR) is involved in NTCP-mediated viral internalization during the cell entry process. Here, we analyzed which function of EGFR is essential for mediating HBV internalization. In contrast to the reported crucial function of EGFR-downstream signaling for the entry of hepatitis C virus (HCV), blockade of EGFR-downstream signaling proteins, including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and signal transducer and activator of transcription (STAT), had no or only minor effects on HBV infection. Instead, deficiency of EGFR endocy"],"journal":["The Journal of biological chemistry"],"pubmed_title":["The machinery for endocytosis of epidermal growth factor receptor coordinates the transport of incoming hepatitis B virus to the endosomal network."],"pmcid":["PMC6970923"],"funding_grant_id":["JP19fk0310114j0003","MIRAI","JP19J21455","JP19fk0310103j0203","JP19fk0210036j0002","JP19fm0208019j0003","JP19fk0310101j1003","JP17H04085","JP19K16672"],"pubmed_authors":["Suzuki R","Iwamoto M","Iwami S","Ohashi H","Matano T","Aizaki H","Nishioka K","Park SY","Sureau C","Saso W","Yun JH","Sugiyama R","Muramatsu M","Ohshima T","Ryo A","Watashi K","Ohki M","Wakita T"],"additional_accession":[]},"is_claimable":false,"name":"The machinery for endocytosis of epidermal growth factor receptor coordinates the transport of incoming hepatitis B virus to the endosomal network.","description":"Sodium taurocholate cotransporting polypeptide (NTCP) is expressed at the surface of human hepatocytes and functions as an entry receptor of hepatitis B virus (HBV). Recently, we have reported that epidermal growth factor receptor (EGFR) is involved in NTCP-mediated viral internalization during the cell entry process. Here, we analyzed which function of EGFR is essential for mediating HBV internalization. In contrast to the reported crucial function of EGFR-downstream signaling for the entry of hepatitis C virus (HCV), blockade of EGFR-downstream signaling proteins, including mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and signal transducer and activator of transcription (STAT), had no or only minor effects on HBV infection. Instead, deficiency of EGFR endocy","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jan","modification":"2025-04-26T18:55:41.985Z","creation":"2021-02-20T22:08:53Z"},"accession":"S-EPMC6970923","cross_references":{"pubmed":["31836663"],"doi":["10.1074/jbc.AC119.010366","10.1074/jbc.ac119.010366"]}}