A clone of 7.1kb corresponding to the mouse L1 interspersed repeat family was selected for homology to a human interspersed repeat. This clone fairly represents mouse genomic members. Mapping of the clone revealed one common element at both the 5' and 3' ends in a head to tail arrangement, suggesting that at least some long L1 family members are tandemly arranged; genomic studies confirmed the unexpected tandem arrangement of a minor proportion of L1 members. A short SmaI tandem repeat appears to define the 5' end of most L1 family members. SmaI repeats may maintain, via a recursive regulatory function, the transcriptional viability of L1 members after retroposition events. A 2.5kb portion of the mouse L1 repeat that has not been previously sequenced is presented. It is 55-70% homologous to a corresponding portion of the human KpnI repeat family. Comparative sequence analysis revealed that one common open reading frame may conserve potential coding function across species. A second open reading frame bears an asymmetric distribution of codon replacements unlike both genes and pseudogenes. This latter feature could be consistent with a proposed chromosome organization function that is unrelated to peptide expression.
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http://dx.doi.org/10.1093/nar/14.7.3119 | DOI Listing |
World J Gastrointest Oncol
January 2025
Department of Clinical Laboratory, Affiliated Hospital of North Sichuan Medical College, Nanchong 637000, Sichuan Province, China.
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Department of Critical Care Medicine and Department of Anaesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China, 710032.
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CIRI, Centre International de Recherche en Infectiologie, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, Ecole Normale Supérieure de Lyon, Lyon, France.
We have assessed antiviral activity and induction of protective immunity of fusion-inhibitory lipopeptides derived from the C-terminal heptad-repeat domain of SARS-CoV-2 spike glycoprotein in transgenic mice expressing human ACE2 (K18-hACE2). The lipopeptides block SARS-CoV-2 infection in cell lines and lung-derived organotypic cultures. Intranasal administration in mice allows the maintenance of homeostatic transcriptomic immune profile in lungs, prevents body-weight loss, decreases viral load and shedding, and protects mice from death caused by SARS-CoV-2 variants.
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February 2025
Department of Cell Biology, Yale University School of Medicine, New Haven, CT, USA.
Mutations that increase LRRK2 kinase activity have been linked to Parkinson's disease and Crohn's disease. LRRK2 is also activated by lysosome damage. However, the endogenous cellular mechanisms that control LRRK2 kinase activity are not well understood.
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January 2025
Division of Neurology, Cincinnati Children's Hospital, 3333 Burnet Ave, Cincinnati, OH 45229, United States.
Myotonic Dystrophy type 2 (DM2) is a multisystem disease affecting many tissues, including skeletal muscle, heart, and brain. DM2 is caused by unstable expansion of CCTG repeats in an intron 1 of a gene coding for cellular nuclear binding protein (CNBP). The expanded CCTG repeats cause DM2 pathology due to the accumulation of RNA CCUG repeats, which affect RNA processing in patients' cells.
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