DNA Damage Meets Neurotrophin Signaling: A Delicate Balancing AKT to Maintain Virus Latency

Anna R Cliffe

doi:10.1016/j.molcel.2019.04.015

DNA Damage Meets Neurotrophin Signaling: A Delicate Balancing AKT to Maintain Virus Latency

Mol Cell. 2019 May 2;74(3):411-413. doi: 10.1016/j.molcel.2019.04.015.

Author

Anna R Cliffe¹

Affiliation

¹ Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, VA 22908, USA. Electronic address: [email protected].

PMID: 31051136
DOI: 10.1016/j.molcel.2019.04.015

Abstract

In this issue of Molecular Cell, Hu et al. (2019) discover that coordinated regulation of AKT activity emanating from neurotrophic-factor stimulation and endogenous DNA damage maintains HSV latency. These studies provide novel insights into the role of AKT in integrating multiple signals to maintain neuronal homeostasis.

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MeSH terms

DNA Damage
Nerve Growth Factors
Phosphorylation
Proto-Oncogene Proteins c-akt*
Virus Latency*

Substances

Nerve Growth Factors
Proto-Oncogene Proteins c-akt