Proteomics

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The Protein Composition of Human Adenovirus Replication Compartments.


ABSTRACT: Human adenoviruses are double–stranded DNA viruses that replicate in the cell nucleus and induce the formation of replication compartments (RCs) that are critical in viral replication and control of virus-host interactions. RCs are specialized virus-induced subnuclear microenvironments in which viral genome replication and expression are orchestrated, but also where host proteins known to restrict viral replication are co-opted and subverted. However, the protein composition of these RCs remains largely unexplored. In this study, we isolated adenovirus RC-enriched fractions from infected cells at different times post-infection and employed a tandem mass tag-based quantitative mass spectrometry approach to identify proteins associated with RCs. To validate the RC-protein components identified by mass spectrometry, we employed immunofluorescence and western blotting techniques. Proteins previously described to colocalize in RCs in infected cells were identified in the isolated subnuclear fractions. Moreover, we were able to validate previously unidentified RC-associated proteins, including the High Mobility Group Box 1, the SET nuclear proto-oncogene, the Structure Specific Recognition Protein 1 and the CCCTC-binding protein. These findings reveal an elaborate network of host and viral proteins potentially relevant for RC formation and function. The results also suggest potential candidate targets for therapeutic intervention and further mechanistic insights into the molecular basis of virus-host interactions

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Foreskin Fibroblast

DISEASE(S): Upper Respiratory Tract Disease

SUBMITTER: Ramón A. González  

LAB HEAD: Ileana M.

PROVIDER: PXD051745 | Pride | 2024-11-20

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
20180418_Exp1_Fr.msf Msf
20180418_Exp1_Fr1.raw Raw
20180418_Exp1_Fr2.raw Raw
20180418_Exp1_Fr3.raw Raw
20180418_Exp1_Fr4.raw Raw
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