Naomi X. Jones
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Naomi X. Jones has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Aarthi Narayanan
Department of Biology, College of Science, George Mason University, Fairfax, VA 22030, USA
1 shared publication - Farhang Alem
Institute of Biohealth Innovation, George Mason University, Fairfax, VA 22030, USA
1 shared publication - Haseebullah Baha
School of Systems Biology, College of Science, George Mason University, Fairfax, VA 22030, USA
1 shared publication - Lorreta Aboagyewa Opoku
School of Systems Biology, College of Science, George Mason University, Manassas, VA 20110, USA
1 shared publication - Maame Konadu
School of Systems Biology, College of Science, George Mason University, Manassas, VA 20110, USA
1 shared publication - Michael D. Barrera
Biomedical Research Laboratory, George Mason University, Manassas, VA 20110, USA
1 shared publication
Latest Publications
- Open Access
Host-Driven Ubiquitination Events in Vector-Transmitted RNA Virus Infections as Options for Broad-Spectrum Therapeutic Intervention Strategies
Many vector-borne viruses are re-emerging as public health threats, yet our understanding of the virus–host interactions critical for productive infection remains limited. The ubiquitination of proteins, including host- and pathogen-derived proteins is a highly prominent and consistent post-translational modification that regulates protein function through signaling and degradation. Viral proteins are documented to hijack the host ubiquitination machinery to modulate multiple host processes including antiviral defense mechanisms. The engagement of the host ubiquitination machinery in the post-translational modification of viral proteins to support aspects of the viral life cycle including assembly and egress is also well documented. Exploring the role ubiquitination plays in the life cycle of vector-transmitted viral pathogens will increase the knowledge base pertinent to the impact of host-enabled ubiquitination of viral and host proteins and the consequences on viral pathogenesis. In this review, we explore E3 ligase-regulated ubiquitination pathways functioning as proviral and viral restriction factors in the context of acutely infectious, vector-transmitted viral pathogens and the potential for therapeutically targeting them for countermeasures development.
Open AccessHost-Driven Ubiquitination Events in Vector-Transmitted RNA Virus Infections as Options for Broad-Spectrum Therapeutic Intervention Strategies
Many vector-borne viruses are re-emerging as public health threats, yet our understanding of the virus–host interactions critical for productive infection remains limited. The ubiquitination of proteins, including host- and pathogen-derived proteins is a highly prominent and consistent post-translational modification that regulates protein function through signaling and degradation. Viral proteins are documented to hijack the host ubiquitination machinery to modulate multiple host processes including antiviral defense mechanisms. The engagement of the host ubiquitination machinery in the post-translational modification of viral proteins to support aspects of the viral life cycle including assembly and egress is also well documented. Exploring the role ubiquitination plays in the life cycle of vector-transmitted viral pathogens will increase the knowledge base pertinent to the impact of host-enabled ubiquitination of viral and host proteins and the consequences on viral pathogenesis. In this review, we explore E3 ligase-regulated ubiquitination pathways functioning as proviral and viral restriction factors in the context of acutely infectious, vector-transmitted viral pathogens and the potential for therapeutically targeting them for countermeasures development.