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Reprogramming Stars #19: Upgrading Cell Fate Conversions with Engineered Reprogramming Factors-An Interview with Dr. Ralf Jauch.
Cell Reprogram
December 2024
CNC-Centre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
In Vitro Gene Therapy Using Human iPS-Derived Mesoangioblast-Like Cells (HIDEMs) Combined with Microdystrophin () Expression as the New Strategy for Duchenne Muscular Dystrophy (DMD) Experimental Treatment.
Int J Mol Sci
November 2024
Institute of Human Genetics Polish Academy of Sciences, 60-479 Poznan, Poland.
Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by disruptions in the dystrophin gene. This study aims to investigate potential a therapeutic approach using genetically modified human iPS-derived mesoangioblast-like cells (HIDEMs) in mouse model. This study utilizes patient-specific myoblasts reprogrammed to human induced pluripotent stem cells (iPSCs) and then differentiated into HIDEMs.
View Article and Find Full Text PDFReprogramming Stars #18: Engineering Cell Fates and Preventing Disease by Repressing Unwanted Plasticity-An Interview with Dr. Moritz Mall.
Cell Reprogram
October 2024
CNC-Centre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Translation initiation or elongation inhibition triggers contrasting effects on survival during pathogen infection.
mBio
November 2024
Department of Biological Sciences, Indian Institute of Science Education and Research, Mohali, Punjab, India.
Article Synopsis
- Diverse microbial pathogens block host protein synthesis, prompting the host to increase immune gene transcripts in a defensive response that may not always aid survival.
- Research indicates that inhibiting translation initiation improves survival, while inhibiting translation elongation worsens it, revealing contrasting effects on host survival.
- The study highlights the complex roles of translation initiation and elongation in immune responses and host survival during pathogen infections, suggesting distinct mechanisms at play.
Redirecting Tumor Evolution with Nanocompiler Precision for Enhanced Therapeutic Outcomes.
Adv Healthc Mater
December 2024
Department of Ultrasound, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Precisely programming the highly plastic tumor expression profile to render it devoid of drug resistance and metastatic potential presents immense challenges. Here, a transformative nanocompiler designed to reprogram and stabilize the mutable state of tumor cells is introduced. This nanocompiler features a trio of components: 2-deoxy-d-glucose-modified lipid nanoparticles to inhibit glucose uptake, iron oxide nanoparticles to induce oxidative stress, and a deubiquitinase inhibitor to block adaptive protein profile changes in tumor cells.
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