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http://dx.doi.org/10.1113/JP288563 | DOI Listing |
Zhejiang Da Xue Xue Bao Yi Xue Ban
September 2025
Department of Plastic Surgery, the Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou 310009, China.
Skin wound repair is critically regulated by peripheral nerves, whose injury or dysfunction represents a key factor impairing the healing of pathological wounds such as diabetic ulcers and deep burns. The mechanisms through which peripheral nerves participate in cutaneous wound healing primarily involve the modulation of immune responses, the regulation of stem cell niches, and the promotion of angiogenesis. Sensory neurons initiate and mediate essential local immune responses, contribute to the epidermal stem cell microenvironment, and support regenerative potential.
View Article and Find Full Text PDFFam Cancer
August 2025
Institute of Medical Genetics, School of Medicine, Cardiff University, Cardiff, CF14 4XN, UK.
SMARCB1 is a core unit of the BAF chromatin remodelling complex and its functional impairment interferes with the self-renewal and pluripotency of stem cells, lineage commitment, cellular identity and differentiation. SMARCB1 is also an important tumour suppressor gene and somatic SMARCB1 pathogenic variants (PVs) have been detected in ~ 5% of all human cancers. Additionally, germline SMARCB1 PVs have been identified in patients with conditions as clinically diverse as Rhabdoid Tumour Predisposition Syndrome type 1 (RTPS1), schwannomatosis and neurodevelopmental disorders such as Coffin-Siris syndrome (CSS).
View Article and Find Full Text PDFNat Commun
August 2025
Department of Pathology and Laboratory Medicine, Rutgers University-Robert Wood Johnson Medical School, Piscataway, NJ, USA.
Netrin-4 is a tumor suppressor that interferes with formation of the laminin lattice. We employed cryo-electron microscopy to determine a structure of the protein complex consisting of the N-terminal fragments from netrin-4 and laminin γ1. The structure reveals that netrin-4 binds laminin γ1 at the molecular interface where laminin β1 would have bound, thus inhibiting the assembly of the heterotrimeric laminin polymer nodes consisting of α1, β1, and γ1 subunits, and their polymerization into the extracellular lattice.
View Article and Find Full Text PDFActa Neuropathol Commun
July 2025
Department of Pediatrics, School of Medicine, Washington University in St. Louis, 660 S Euclid Ave, St. Louis, MO, 63110, USA.
CLN3 disease is a neuronopathic lysosomal storage disorder that severely impacts the central nervous system (CNS) while also inducing notable peripheral neuromuscular symptoms. Although considerable attention has been directed towards the neurodegenerative consequences within the CNS, the involvement of peripheral tissues, including skeletal muscles and their innervation, has been largely neglected. We hypothesized that, CLN3 deficiency could directly influence peripheral nerves and investigated the neuromuscular system in Cln3 mice.
View Article and Find Full Text PDFMol Neurobiol
July 2025
Department of Biology and Biotechnology, University of Pavia, 27100, Pavia, Italy.
Osteogenesis imperfecta (OI), also known as brittle bone disease, is a rare congenital connective tissue disorder linked to collagen I defects, commonly known for its skeletal implications. However, collagen fibers play several key roles also in the central nervous system (CNS) starting from CNS development, regulating axonal growth, synaptogenesis, and terminal differentiation of Schwann cells. Collagen I plays an active role in defining brain architecture and in the developing peripheral.
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