| Gene Name | PACSIN3 |
| HF Protein Name | Protein kinase C and casein kinase substrate in neurons protein 3 |
| HF Function | Helps in virus budding |
| Uniprot ID | Q9UKS6 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 29763 |
| Host Factor (HF) Name in Paper | PACSIN3 |
| Gene synonyms | N.A. |
| Ensemble Gene ID | N.A. |
| Ensemble Transcript | ENST00000298838;ENST00000539589 |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0005737, GO:0005768, GO:0005829, GO:0005886, GO:0006897, GO:0008092, GO:0008289, GO:0019855, GO:0030100, GO:0045806, GO:0051044, GO:0051926, GO:0070062, GO:0097320, |
| MINT ID | Q9UKS6 |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 606513 |
| PANTHER ID | PTHR23065:SF18 |
| PDB ID(s) | N.A., |
| pfam ID | PF00611, PF14604, |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Hepatitis C virus |
| Virus Short Name | HCV |
| Order | Unassigned |
| Virus Family | Flaviviridae |
| Virus Subfamily | N.A. |
| Genus | Hepacivirus |
| Species | Hepatitis C virus |
| Host | Human |
| Cell Tropism | Hepatocytes |
| Associated Disease | Hepatitis, hepatocellular carcinoma |
| Mode of Transmission | Sexual contact, blood |
| VIPR DB link | http://www.viprbrc.org/brc/home.spg?decorator=flavi |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_online_report/positive-sense-rna-viruses/w/flaviviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Flaviviridae |
| Paper Title | Molecular Determinants and Dynamics of Hepatitis C |
| Author's Name | Coller KE, Heaton NS, Berger KL, Cooper JD, Saunders JL, Randall G. |
| Journal Name | PLoS Pathogens |
| Pubmed ID | 22241992 |
| Abstract | The current model of hepatitis C virus (HCV) production involves the assembly of virions on or near the surface of lipid droplets, envelopment at the ER in association with components of VLDL synthesis, and egress via the secretory pathway. However, the cellular requirements for and a mechanistic understanding of HCV secretion are incomplete at best. We combined an RNA interference (RNAi) analysis of host factors for infectious HCV secretion with the development of live cell imaging of HCV core trafficking to gain a detailed understanding of HCV egress. RNAi studies identified multiple components of the secretory pathway, including ER to Golgi trafficking, lipid and protein kinases that regulate budding from the trans-Golgi network (TGN), VAMP1 vesicles and adaptor proteins, and the recycling endosome. Our results support a model wherein HCV is infectious upon envelopment at the ER and exits the cell via the secretory pathway. We next constructed infectious HCV with a tetracysteine (TC) tag insertion in core (TC-core) to monitor the dynamics of HCV core trafficking in association with its cellular cofactors. In order to isolate core protein movements associated with infectious HCV secretion, only trafficking events that required the essential HCV assembly factor NS2 were quantified. TC-core traffics to the cell periphery along microtubules and this movement can be inhibited by nocodazole. Sub-populations of TC-core localize to the Golgi and co-traffic with components of the recycling endosome. Silencing of the recycling endosome component Rab11a results in the accumulation of HCV core at the Golgi. The majority of dynamic core traffics in association with apolipoprotein E (ApoE) and VAMP1 vesicles. This study identifies many new host cofactors of HCV egress, while presenting dynamic studies of HCV core trafficking in infected cells. |
| Used Model | Huh-7.5 cells |
| DOI | 10.1371/journal.ppat.1002466 |
