The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Heterogeneous nuclear ribonucleoprotein C proteins interact with the human papillomavirus type 16 (HPV16) early 3'-untranslated region and alleviate suppression of HPV16 late L1 mRNA splicing.

Author

Summary, in English

In order to identify cellular factors that regulate human papillomavirus type 16 (HPV16) gene expression, cervical cancer cells permissive for HPV16 late gene expression were identified and characterized. These cells either contained a novel spliced variant of the L1 mRNAs that bypassed the suppressed HPV16 late, 5'-splice site SD3632, produced elevated levels of RNA-binding proteins SRSF1 (ASF/SF2), SRSF9 (SRp30c) and HuR that are known to regulate HPV16 late gene expression, or were shown by a gene expression array analysis to overexpress the RALYL RNA-binding protein of the heterogeneous nuclear ribonucleoprotein C (hnRNP C)-family. Overexpression of RALYL or hnRNP C1 induced HPV16 late gene expression from HPV16 subgenomic plasmids and from episomal forms of the full-length HPV16 genome. This induction was dependent on the HPV16 early untranslated region. Binding of hnRNP C1 to the HPV16 early, untranslated region activated HPV16 late 5'-splice site SD3632 and resulted in production of HPV16 L1 mRNAs. Our results suggested that hnRNP C1 controls HPV16 late gene expression.

Publishing year

2015

Language

English

Pages

13354-13371

Publication/Series

Journal of Biological Chemistry

Volume

290

Issue

21

Document type

Journal article

Publisher

American Society for Biochemistry and Molecular Biology

Topic

  • Microbiology in the medical area
  • Infectious Medicine

Status

Published

Research group

  • Experimental Infection Medicine, Malmö
  • Molecular virology

ISBN/ISSN/Other

  • ISSN: 1083-351X