Application | Comment | Organism |
---|---|---|
medicine | subunits Dpm1 and Dpm3 function as host dependency factors for Dengue virus and other related flaviviruses such as Zika virus. Mutation in the DXD motif of Dpm1, which is essential for its catalytic activity, abolishes DPMS-mediated Dengue virus infection. Genetic ablation of mannosyltransferase ALG3 renders cells poorly susceptible to Dengue virus. In cells deficient for DPMS activity, viral RNA amplification is hampered and truncated oligosaccharides are transferred to the viral precursor of the M protein and E glycoproteins, affecting their proper folding | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | O60762 and Q9P2X0 | O60762 i.e. subunit Dpm1, Q9P2X0 i.e. subunit Dpm3 | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HAP-1 cell | - |
Homo sapiens | - |
General Information | Comment | Organism |
---|---|---|
physiological function | subunits Dpm1 and Dpm3 function as host dependency factors for Dengue virus and other related flaviviruses such as Zika virus. Mutation in the DXD motif of Dpm1, which is essential for its catalytic activity, abolishes DPMS-mediated Dengue virus infection. Genetic ablation of mannosyltransferase ALG3 renders cells poorly susceptible to Dengue virus. In cells deficient for DPMS activity, viral RNA amplification is hampered and truncated oligosaccharides are transferred to the viral precursor of the M protein and E glycoproteins, affecting their proper folding | Homo sapiens |