Neurofibromin controls many cell processes, such as growth, learning, and memory. If neurofibromin is not working properly, it can lead to health problems, including issues with the nervous, skeletal, and cardiovascular systems and cancer. This review examines neurofibromin's binding partners, signaling pathways and potential therapeutic targets. In addition, it summarizes the different post-translational modifications that can affect neurofibromin's interactions with other molecules. It is essential to investigate the molecular mechanisms that underlie neurofibromin variants in order to provide with functional connections between neurofibromin and its associated proteins for possible therapeutic targets based on its biological function.
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http://dx.doi.org/10.1038/s42003-023-04815-0 | DOI Listing |
This study evaluates the oncolytic potential of the Moscow strain of reovirus against human metastatic melanoma and glioblastoma cells. The Moscow strain effectively infects and replicates within human melanoma cell lines and primary glioblastoma cells, while sparing non-malignant human cells. Infection leads to the selective destruction of neoplastic cells, mediated by functional viral replication.
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December 2024
Departments of Surgery & Molecular Microbiology and Immunology, University of Missouri, Columbia, MO 65212, USA.
Pathogenic viruses trigger or disrupt multiple signaling networks to establish an environment optimized for their own replication and productive infection [...
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December 2024
Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, MH, India.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's lymphoma, Kaposi's sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis.
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December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
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December 2024
Department of Dermatology, School of Medicine, University of California Davis, Sacramento, CA 95817, USA.
Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA gamma herpesvirus. Like other herpesviruses, KSHV establishes a latent infection with limited gene expression, while KSHV occasionally undergoes the lytic replication phase, which produces KSHV progenies and infects neighboring cells. KSHV genome encodes 80+ open reading frames.
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