Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Endogenous retrovirsuses (ERVs) have long been known to influence gene expression in plants in important ways, but what of their roles in mammals? Our relatively sparse knowledge in that area was recently increased with the finding that ERVs can influence the expression of mammalian resident genes by disrupting transcriptional termination. For many mammalian biologists, retrotransposition is considered unimportant except when it disrupts the reading frame of a gene, but this view continues to be challenged. It has been known for some time that integration into an intron can create novel transcripts and integration upstream of a gene can alter the expression of the transcript, in many cases producing phenotypic consequences and disease. The new findings on transcriptional termination extend the opportunities for retrotransposons to play a role in human disease.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/bies.201200056 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Oropouche virus NSs protein suppresses host transcription by targeting the RNA polymerase II RPB1 protein.
J Virol
September 2025
Department of Pathology, The University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Unlabelled: Oropouche fever is a debilitating disease caused by Oropouche virus (OROV), an arthropod-borne member of the Peribunyaviridae family. Despite its public health significance, the molecular mechanisms driving OROV pathogenesis remain poorly understood. In other bunyaviruses, the nonstructural NSs protein encoded by the small (S) genome segment acts as a major virulence factor.
View Article and Find Full Text PDFTranscriptional condensates enrich phosphorylated PRMT2 to stimulate H3R8me2a deposition and hypoxic response in glioblastoma.
Sci China Life Sci
September 2025
State Key Laboratory of Experimental Hematology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University Cancer Institute and Hospital, Tianjin Key Labora
Histone arginine methylation by protein arginine methyltransferases (PRMTs) is crucial for transcriptional regulation and is implicated in cancers. Despite their therapeutic potential, some PRMTs present challenges as drug targets due to their context-dependent activities. Here, we demonstrate that hypoxia triggers the rapid condensation of PRMT2, which is essential for its histone H3R8 asymmetric dimethylation (H3R8me2a) activity.
View Article and Find Full Text PDFMicrovascular preservation & cardiomyocyte hyperplasia underlie adaptive right ventricle development in congenital heart disease-pulmonary arterial hypertension.
Am J Physiol Heart Circ Physiol
September 2025
Division of Pediatric Critical Care, Department of Pediatrics, University of California, San Francisco, USA.
Right ventricular (RV) failure is the primary cause of death among patients with pulmonary arterial hypertension (PAH). Patients with congenital heart disease-associated PAH (CHD-PAH) demonstrate improved outcomes compared to patients with other forms of PAH, which is related to the maintenance of an adaptively hypertrophied RV. In an ovine model of CHD-PAH, we aimed to elucidate the cellular, microvascular, and transcriptional adaptations to congenital pressure overload that support RV function.
View Article and Find Full Text PDFTFIIH-p52∆C defines a ninth xeroderma pigmentosum complementation-group XP-J and restores TFIIH stability to p8-defective trichothiodystrophy.
J Clin Invest
September 2025
Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
Few drugs are available for rare diseases due to economic disincentives. However, tailored medications for extremely-rare disorders (N-of-1) offer a ray of hope. Artificial antisense oligonucleotides (ASOs) are now best known for their use in spinal muscular atrophy (SMA).
View Article and Find Full Text PDFIntrinsically disordered region of Clr4/Suv39 regulates its enzymatic activity and ensures heterochromatin spreading.
Nucleic Acids Res
September 2025
Division of Chromatin Regulation, National Institute for Basic Biology, Okazaki 444-8585, Japan.
Methylation of histone H3 at lysine 9 (H3K9me), a hallmark of heterochromatin, is catalyzed by Clr4/Suv39. Clr4/Suv39 contains two conserved domains-an N-terminal chromodomain and a C-terminal catalytic domain-connected by an intrinsically disordered region (IDR). Several mechanisms have been proposed to regulate Clr4/Suv39 activity, but how it is regulated under physiological conditions remains largely unknown.
View Article and Find Full Text PDF