HIV co-opts a cellular antiviral mechanism, activation of stress kinase PKR by its RNA, to enable splicing of rev/tat mRNA.

Namer, Lise Sarah; Harwig, Alex; Heynen, Stephan P; Das, Atze T; Berkhout, Ben; Kaempfer, Raymond

Namer, Lise Sarah; Harwig, Alex; Heynen, Stephan P; Das, Atze T; Berkhout, Ben; Kaempfer, Raymond.

Afiliación

Namer LS; Department of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, 9112102, Jerusalem, Israel.
Harwig A; Laboratory of Experimental Virology, Department of Medical Microbiology, Amsterdam UMC, 1105 AZ, Amsterdam, The Netherlands.
Heynen SP; Laboratory of Experimental Virology, Department of Medical Microbiology, Amsterdam UMC, 1105 AZ, Amsterdam, The Netherlands.
Das AT; Laboratory of Experimental Virology, Department of Medical Microbiology, Amsterdam UMC, 1105 AZ, Amsterdam, The Netherlands.
Berkhout B; Laboratory of Experimental Virology, Department of Medical Microbiology, Amsterdam UMC, 1105 AZ, Amsterdam, The Netherlands.
Kaempfer R; Department of Biochemistry and Molecular Biology, Institute of Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, 9112102, Jerusalem, Israel. kaempfer@hebrew.edu.

Cell Biosci ; 13(1): 28, 2023 Feb 11.

Article en En | MEDLINE | ID: mdl-36774495

Palabras clave

Cellular antiviral response; HIV; PKR activation; Phylogenetic conservation of RNA structure; RNA pseudoknot; Viral RNA; eIF2alpha phosphorylation; mRNA splicing

Texto completo

Añadir a Mi BVS

Imprimir

XML

PubMed Links

Buscar en Google

Texto completo: 1 Bases de datos: MEDLINE Idioma: En Revista: Cell Biosci Año: 2023 Tipo del documento: Article País de afiliación: Israel