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Equine Infectious Anemia Virus Cellular Partners Along the Viral Cycle.
Viruses
December 2024
ANSES Animal Health Laboratory, PhEED Unit, 14430 Goustranville, France.
Equine infectious anemia virus (EIAV) is the simplest described within the family, related to the human immunodeficiency viruses (HIV-1 and HIV-2). There is an important interplay between host cells and viruses. Viruses need to hijack cellular proteins for their viral cycle completion and some cellular proteins are antiviral agents interfering with viral replication.
View Article and Find Full Text PDFApoptosis in Cancer Biology and Therapy.
Annu Rev Pathol
January 2025
Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA; email:
Since its inception, the study of apoptosis has been intricately linked to the field of cancer. The term apoptosis was coined more than five decades ago following its identification in both healthy tissues and malignant neoplasms. The subsequent elucidation of its molecular mechanisms has significantly enhanced our understanding of how cancer cells hijack physiological processes to evade cell death.
View Article and Find Full Text PDFMechanisms of enhancer-driven oncogene activation.
Int J Cancer
January 2025
Department of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
An aggressive subtype of acute myeloid leukemia (AML) is caused by enhancer hijacking resulting in MECOM overexpression. Several chromosomal rearrangements can lead to this: the most common (inv(3)/t(3;3)) results in a hijacked GATA2 enhancer, and there are several atypical MECOM rearrangements involving enhancers from other hematopoietic genes. The set of enhancers which can be hijacked by MECOM can also be hijacked by BCL11B.
View Article and Find Full Text PDFHost factor DIAPH1 regulates pseudorabivirus replication by modulating the dynamics of cytoskeleton.
Int J Biol Macromol
January 2025
College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China. Electronic address:
As obligate parasites, viruses exploit host cell organelles and molecular components to complete their life cycle. Among which, viruses firstly hijack the cytoskeleton of host cells to ensure their efficiently cell entry and replication. Although formin family members play a key role in both microfilament and microtubule cytoskeletal remodeling, few studies addressed the detailed function and mechanism of formins in the process of viral infection.
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