‘Arc’-hitecture of normal cognitive aging

Myrum, Craig; Moreno-Castilla, Perla; Rapp, Peter R.

doi:10.1016/j.arr.2022.101678

Cited by 5 publications

(1 citation statement)

References 130 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fv1 orthologues have been identified in a wide range of rodent species [ 98 , 99 ] and some Fv1 homologues restrict non-MuLV retroviruses [ 100 ], suggesting that Fv1 does not recognize conserved amino acid motifs but may instead detect structurally conserved spatial patterns in the hexameric lattice typical of retroviral capsid cores [ 97 , 101 ]. Notably, the neuronal Arc protein, which evolved from a Ty3/Gypsy retrotransposon Gag domain and has retained the topology of a retroviral Gag protein [ 102 ], is able to self-assemble into virus-like capsids that encapsulate RNA [ 103 ]. The Arc protein is released from neurons in extracellular vesicles and transfer the Arc mRNA into new target cells, where it can undergo activity-dependent translation, suggesting that Gag retroelements have been repurposed during evolution to mediate intercellular communication in the nervous system [ 103 ].…”

Section: Transcriptional Dysregulation Of Ervs In Human Diseasesmentioning

confidence: 99%

Transcriptional Regulation of Endogenous Retroviruses and Their Misregulation in Human Diseases

Zhang

Pan

Cong

et al. 2022

IJMS

View full text Add to dashboard Cite

Endogenous retroviruses (ERVs), deriving from exogenous retroviral infections of germ line cells occurred millions of years ago, represent ~8% of human genome. Most ERVs are highly inactivated because of the accumulation of mutations, insertions, deletions, and/or truncations. However, it is becoming increasingly apparent that ERVs influence host biology through genetic and epigenetic mechanisms under particular physiological and pathological conditions, which provide both beneficial and deleterious effects for the host. For instance, certain ERVs expression is essential for human embryonic development. Whereas abnormal activation of ERVs was found to be involved in numbers of human diseases, such as cancer and neurodegenerative diseases. Therefore, understanding the mechanisms of regulation of ERVs would provide insights into the role of ERVs in health and diseases. Here, we provide an overview of mechanisms of transcriptional regulation of ERVs and their dysregulation in human diseases.

show abstract