| Gene Name | COMMD2 |
| HF Protein Name | COMM Domain Containing 2 |
| HF Function | |
| Uniprot ID | Q86X83 |
| Protein Sequence | View Fasta Sequence |
| NCBI Gene ID | 51122 |
| Host Factor (HF) Name in Paper | COMMD2 |
| Gene synonyms | N.A. |
| Ensemble Gene ID | ENSG00000114744 |
| Ensemble Transcript | ENST00000473414.6 [Q86X83-1] |
| KEGG ID | Go to KEGG Database |
| Gene Ontology ID(s) | GO:0005737, |
| MINT ID | N.A. |
| STRING | Click to see interaction map |
| GWAS Analysis | Click to see gwas analysis |
| OMIM ID | 616699 |
| PANTHER ID | PTHR15857;PTHR15857:SF0 |
| PDB ID(s) | 8F2R, 8F2U, 8P0W, |
| pfam ID | PF07258, PF21672, |
| Drug Bank ID | N.A., |
| ChEMBL ID | N.A. |
| Organism | Homo sapiens (Human) |
| Virus Name | Severe Acute Respiratory Syndrome Coronavirus 2 |
| Virus Short Name | SARS CoV-2 |
| Order | Nidovirales |
| Virus Family | Coronaviridae |
| Virus Subfamily | Coronavirinae |
| Genus | Betacoronavirus |
| Species | Betacoronavirus-1 |
| Host | Vertebrates |
| Cell Tropism | Epithelial cells of respiratory or enteric tracts, neurological tissues are also frequently infected |
| Associated Disease | Mainly respiratory diseases |
| Mode of Transmission | Sexual contact, blood, breast feeding |
| VIPR DB link | https://www.viprbrc.org/brc/vipr_search.do?species=Betacoronavirus |
| ICTV DB link | https://ictv.global/report/182/orthocoronavirinae |
| Virus Host DB link |
| Paper Title | Identification of Required Host Factors for SARS-CoV-2 Infection in Human Cells |
| Author's Name | Zharko Daniloski, Tristan X Jordan, Hans-Hermann Wessels, Daisy A Hoagland, Silva Kasela, Mateusz Legut , Silas Maniatis, Eleni P Mimitou, Lu Lu, Evan Geller, Oded Danziger, Brad R Rosenberg, Hemali Phatnani, Peter Smibert, Tuuli Lappalainen, Benjamin R tenOever, Neville E Sanjana |
| Journal Name | Cell |
| Pubmed ID | 33147445 |
| Abstract | To better understand host-virus genetic dependencies and find potential therapeutic targets for COVID-19, we performed a genome-scale CRISPR loss-of-function screen to identify host factors required for SARS-CoV-2 viral infection of human alveolar epithelial cells. Top-ranked genes cluster into distinct pathways, including the vacuolar ATPase proton pump, Retromer, and Commander complexes. We validate these gene targets using several orthogonal methods such as CRISPR knockout, RNA interference knockdown, and small-molecule inhibitors. Using single-cell RNA-sequencing, we identify shared transcriptional changes in cholesterol biosynthesis upon loss of top-ranked genes. In addition, given the key role of the ACE2 receptor in the early stages of viral entry, we show that loss of RAB7A reduces viral entry by sequestering the ACE2 receptor inside cells. Overall, this work provides a genome-scale, quantitative resource of the impact of the loss of each host gene on fitness/response to viral infection. |
| Used Model | Huh7.5ACE2 |
| DOI | 10.1016/j.cell.2020.10.030 |
