ArticleScientific reports2020
Gene expression is stable in a complete CIB1 knockout keratinocyte model.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Deficiency inJournal of virology · 2024Article
- CRISPR-Cas9‒Based Genomic Engineering in Keratinocytes: From Technology to Application.JID innovations : skin science from molecules to population health · 2022Review
- Description of CRISPR-Cas9 development and its prospects in human papillomavirus-driven cancer treatment.Frontiers in immunology · 2022Review
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Authors and funding
8 authors at 4 institutions in 4 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Epidermodysplasia verruciformis (EV) is a genodermatosis characterized by the inability of keratinocytes to control cutaneous β-HPV infection and a high risk for non-melanoma skin cancer (NMSC). Bi-allelic loss of function variants in TMC6, TMC8, and CIB1 predispose to EV. The correlation between these proteins and β-HPV infection is unclear. Its elucidation will advance the understanding of HPV control in human keratinocytes and development of NMSC. We generated a cell culture model by CRISPR/Cas9-mediated deletion of CIB1 to study the function of CIB1 in keratinocytes. Nine CIB1 knockout and nine mock control clones were generated originating from a human keratinocyte line. We observed small changes in gene expression as a result of CIB1 knockout, which is consistent with the clearly defined phenotype of EV patients. This suggests that the function of human CIB1 in keratinocytes is limited and involves the restriction of β-HPV. The presented model is useful to investigate CIB1 interaction with β-HPV in future studies.
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