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Review
. 2022 Aug 8;15(1):69.
doi: 10.1186/s13041-022-00946-3.

Epigenetic signature of N-terminal acetyltransferases: a probable mediator of immune and neuropathogenesis in HIV infection

Affiliations
Review

Epigenetic signature of N-terminal acetyltransferases: a probable mediator of immune and neuropathogenesis in HIV infection

Vaishnavi Sundar et al. Mol Brain. .

Abstract

HIV is a major global public threat burdening society, yet the exact mechanism of HIV pathogenesis needs to be elucidated. In the era of epigenetic therapy, N-terminal acetylation (Nt-acetylation) changes induced by viral infection might play a critical role in virus-host interactions in HIV infection. The mitochondrial epigenetic mechanism, predominantly Nt acetylation, holds HIV immunopathogenesis and is vastly unexplored. The challenge is to single out the specific pathological role of NAT changes in HIV-associated neurodegeneration. Therefore, this nano review aims to shine light on Nt acetylation in HIV pathogenesis, which we believe can lead to effective future therapeutic strategies against HIV-associated neurodegeneration.

Keywords: Epigenetics; HIV; Neurodegeneration; Nt acetyltransferase; Nt-acetylation.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Proposed mechanisms of HIV disease progression influenced by the epigenetic signatures of N-terminal acetylation-impaired immunity and neuropathogenesis in microglial cells. HIV human immunodeficiency virus, NAT N-terminal acetylation, NAA N-alpha acetyltransferases, HYPK huntingtin interacting protein K

References

    1. Borjabad A, Morgello S, Chao W, Kim S-Y, Brooks AI, Murray J, et al. Significant effects of antiretroviral therapy on global gene expression in brain tissues of patients with HIV-1-associated neurocognitive disorders. PLoS Pathog. 2011;7(9):e1002213. doi: 10.1371/journal.ppat.1002213. - DOI - PMC - PubMed
    1. Aksnes H, Drazic A, Marie M, Arnesen T. First things first: vital protein marks by N-terminal acetyltransferases. Trends Biochem Sci. 2016;41(9):746–60. doi: 10.1016/j.tibs.2016.07.005. - DOI - PubMed
    1. Perrier J, Durand A, Giardina T, Puigserver A. Catabolism of intracellular N-terminal acetylated proteins: involvement of acylpeptide hydrolase and acylase. Biochimie. 2005;87(8):673–85. doi: 10.1016/j.biochi.2005.04.002. - DOI - PubMed
    1. Lee C-F, Ou DS-C, Lee S-B, Chang L-H, Lin R-K, Li Y-S, et al. hNaa10p contributes to tumorigenesis by facilitating DNMT1-mediated tumor suppressor gene silencing. J Clin Invest. 2010;120(8):2920–30. doi: 10.1172/JCI42275. - DOI - PMC - PubMed
    1. Doke M, Kashanchi F, Khan MA, Samikkannu T. HIV-1 Tat and cocaine impact astrocytic energy reservoir influence on miRNA epigenetic regulation. Genomics. 2021;113(6):3461–75. doi: 10.1016/j.ygeno.2021.08.013. - DOI - PMC - PubMed

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