ArticlePloS one2014
Loss of the HPV-infection resistance EVER2 protein impairs NF-κB signaling pathways in keratinocytes.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- The human CIB1-EVER1-EVER2 complex governs keratinocyte-intrinsic immunity to β-papillomaviruses.The Journal of experimental medicine · 2018Trial
- Elevated TMC8 expression correlates with CD8Translational cancer research · 2026Article
- TMC6/8-associated epidermodysplasia verruciformis: germline variants and a complex structural alteration in a skin cancer predisposition syndrome.European journal of human genetics : EJHG · 2026Article
- Review
- Gene expression is stable in a complete CIB1 knockout keratinocyte model.Scientific reports · 2020Article
- Human inborn errors of immunity to infection affecting cells other than leukocytes: from the immune system to the whole organism.Current opinion in immunology · 2019Review
- Cross-talk of cutaneous beta human papillomaviruses and the immune system: determinants of disease penetrance.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Review
- Epidermodysplasia Verruciformis: Inborn Errors of Immunity to Human Beta-Papillomaviruses.Frontiers in microbiology · 2018Article
- Transmembrane channel-like protein 8 as a potential biomarker for poor prognosis of hepatocellular carcinoma.Molecular and clinical oncology · 2017Article
- The EVER genes - the genetic etiology of carcinogenesis in epidermodysplasia verruciformis and a possible role in non-epidermodysplasia verruciformis patients.Postepy dermatologii i alergologii · 2016Review
- Cornoid Lamella-Like Structures in HIV-Associated Epidermodysplasia Verruciformis: A Unique Histopathologic Finding.The American Journal of dermatopathology · 2015Article
- HPV Type 16 Infection Switches Keratinocytes from Apoptotic to Proliferative Fate under TWEAK/Fn14 Interaction.The Journal of investigative dermatology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homozygous mutations in EVER genes cause epidermodysplasia verruciformis (EV), characterized by an immune defect and the development of skin cancers associated with β-human papillomavirus (HPV) infections. The effects of EVER protein loss on the keratinocyte immune response remain unknown. We show here that EVER2 plays a critical role in the interplay between the NF-κB and JNK/AP-1 signaling pathways. EVER2-deficient cells overproduce IL-6 following the upregulation of JNK activation. They respond poorly to phorbol ester and TNF via the NF-κB pathway. They have lower levels of IKKα subunit, potentially accounting for impairments of p100 processing and the alternative NF-κB pathway. The loss of EVER2 is associated with an unusual TRAF protein profile. We demonstrate that EVER2 deficiency sustains TRAF2 ubiquitination and decreases the pool of TRAF2 available in the detergent-soluble fraction of the cell. Finally, we demonstrate that EVER2 loss induces constitutive PKCα-dependent c-jun phosphorylation and facilitates activation of the HPV5 long control region through a JNK-dependent pathway. These findings indicate that defects of the EVER2 gene may create an environment conducive to HPV replication and the persistence of lesions with the potential to develop into skin cancer.
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