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Correction to: PFP@PLGA/CuSbS‑mediated PTT ablates hepatocellular carcinoma by inhibiting the RAS/MAPK/MT‑CO1 signaling pathway.
Nano Converg
September 2024
Department of Abdominal Ultrasound, The First Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Mutation-induced LZTR1 polymerization provokes cardiac pathology in recessive Noonan syndrome.
Cell Rep
July 2024
Stem Cell Unit, Clinic for Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany; DZHK (German Center for Cardiovascular Research), Göttingen, Germany; Cluster of Excellence "Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells" (MBExC), University of Göttingen, Göttingen, Germany; Translational Neuroinflammation and Automated Microscopy, Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Göttingen, Germany. Electronic address:
Noonan syndrome patients harboring causative variants in LZTR1 are particularly at risk to develop severe and early-onset hypertrophic cardiomyopathy. In this study, we investigate the mechanistic consequences of a homozygous variant LZTR1 by using patient-specific and CRISPR-Cas9-corrected induced pluripotent stem cell (iPSC) cardiomyocytes. Molecular, cellular, and functional phenotyping in combination with in silico prediction identify an LZTR1-specific disease mechanism provoking cardiac hypertrophy.
View Article and Find Full Text PDFAuthor Correction: Direct and selective pharmacological disruption of the YAP-TEAD interface by IAG933 inhibits Hippo-dependent and RAS-MAPK-altered cancers.
Nat Cancer
July 2024
Novartis BioMedical Research, Basel, Switzerland.
RASopathies - what they reveal about RAS/MAPK signaling in skeletal muscle development.
Dis Model Mech
June 2024
University of California Davis MIND Institute, Sacramento, CA 95817, USA.
RASopathies are rare developmental genetic syndromes caused by germline pathogenic variants in genes that encode components of the RAS/mitogen-activated protein kinase (MAPK) signal transduction pathway. Although the incidence of each RASopathy syndrome is rare, collectively, they represent one of the largest groups of multiple congenital anomaly syndromes and have severe developmental consequences. Here, we review our understanding of how RAS/MAPK dysregulation in RASopathies impacts skeletal muscle development and the importance of RAS/MAPK pathway regulation for embryonic myogenesis.
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