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The integral role of in brain function: from neurogenesis to synaptic plasticity and social behavior.

Acta Neurobiol Exp (Wars)

January 2025

Laboratory of Animal Models, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.

The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity.

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Organoids are multicellular structures formed from populations of individual cells allowing modeling of structural and functional aspects of organs and tissues in normal and diseased states. They offer unique opportunities to model and treat disease. Using a mouse embryonic stem cell line, we have cultured organoids that express markers of spinal cord motor neurons as well as motor neurons found within the peripheral nervous system.

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Beta-catenin is essential for diverse biological processes, such as body axis determination and cell differentiation, during metazoan embryonic development. Beta-catenin is thought to exert such functions through complexes formed with various proteins. Although β-catenin complex proteins have been identified in several bilaterians, little is known about the structural and functional properties of β-catenin complexes in early metazoan evolution.

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Background: Collagen XI is a fibril-forming collagen typically associated with type II collagen tissues but is also expressed in type I collagen-rich tendons, especially during development. We previously showed that tendon-targeted (Scx-Cre) Col11a1 knockout mice have smaller tendons in adulthood with aberrant fibril structure and impaired mechanical properties. However, the manifestation of this phenotype is not clearly understood.

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Retinopathy in Parkinson's disease: A potential biomarker for early diagnosis and clinical assessment.

Neuroscience

January 2025

Eye School of Chengdu University of TCM, Chengdu, China; Key Laboratory of Sichuan Province Ophthalmopathy Prevention & Cure and Visual Function Protection with TCM Laboratory, Chengdu, China; Ineye Hospital of Chengdu University of TCM, Chengdu, China; Retinal Image Technology and Chronic Vascular Disease Prevention&Control and Collaborative Innovation Center, Chengdu, China. Electronic address:

Parkinson's disease (PD) is a prevalent neurodegenerative disorder caused by degeneration of dopaminergic neurons, originating from the substantia nigra pars compacta, and characterized by motor symptoms such as bradykinesia, muscle rigidity, resting tremor, and postural instability, as well as non-motor symptoms such as anxiety, depression, reduced sense of smell, cognitive impairment, and visual dysfunction. Emerging evidence highlights the retina as a promising site for non-invasive exploration of PD pathology, due to its shared embryonic origin with the central nervous system. In recent years, with the development of ophthalmic technology, the acquisition of retinal-related function and structure has gradually become mature.

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