Evolution of the viral genomes of SARS-CoV-2 in association with the changes in local condition: a genomic epidemiological study of a suburban city of Japan.

Understanding the factors driving the spread and evolution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at the local, regional, national, and international levels is important in protecting against future pandemics. By exploring their viral genomes, we attempted to analyse the spread of SARS-CoV-2 and its evolutionary convergence in Kashiwa City, as an example of a representative commuter town in Japan. From September 2020 to January 2023, a total of 47,134 nasopharyngeal swab and saliva specimens were collected from patients in 47 local clinics and hospitals, covering the vast majority of healthcare facilities.

Specific Activation of Yamanaka Factors via HSF1 Signaling in the Early Stage of Zebrafish Optic Nerve Regeneration.

In contrast to the case in mammals, the fish optic nerve can spontaneously regenerate and visual function can be fully restored 3-4 months after optic nerve injury (ONI). However, the regenerative mechanism behind this has remained unknown. This long process is reminiscent of the normal development of the visual system from immature neural cells to mature neurons.

Cyclosporine A and PSC833 inhibit ABCA1 function via direct binding.

ATP-binding cassette protein A1 (ABCA1) plays a key role in generating high-density lipoprotein (HDL). However, the detailed mechanism of HDL formation remains unclear; in order to reveal it, chemicals that specifically block each step of HDL formation would be useful. Cyclosporine A inhibits ABCA1-mediated cholesterol efflux, but it is not clear whether this is mediated via inhibition of calcineurin.

The COP9 signalosome controls ubiquitinylation of ABCA1.

ATP-binding cassette protein A1 (ABCA1) mediates the transfer of cellular free cholesterol and phospholipids to apolipoprotein A-I (apoA-I), an extracellular acceptor in plasma, to form high-density lipoprotein (HDL). ABCA1 has been suggested to be degraded by proteasome in cholesterol-loaded macrophages, however, the mechanism and regulation of proteasomal degradation of ABCA1 remain unclear. In this study, we analyzed the putative interaction between ABCA1 and COP9 signalosome (CSN), a key molecule in controlling protein ubiquitination and deubiquitination.