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Comparison of localization and release of multivesicular bodies and secretory granules in islet cells: Dysregulation during type-2 diabetes.
J Extracell Biol
November 2024
Cell Metabolism Lab (GA-08), Department of Developmental Biology and Genetics (DBG) Indian Institute of Science (IISc) Bengaluru India.
Multivesicular bodies (MVBs) are vesicles of endosomal origin containing intraluminal vesicles, which upon fusion with plasma membrane, secrete exosomes. They play a significant role in the physiology and pathology of type-2 diabetes (T2D) due to disrupted intercellular communication. The role of MVBs and their influence on insulin secretory granules (ISGs) of β-cells or their characterization is yet to be uncovered.
View Article and Find Full Text PDFDysregulation of protein degradation and alteration of secretome in α-synuclein-exposed astrocytes: implications for dopaminergic neuronal dysfunction.
Cell Commun Signal
December 2024
Department of Biophysics, National Institute of Mental Health and Neurosciences, Institute of National Importance, Bengaluru, Karnataka, 560029, India.
Background: A key factor in the propagation of α-synuclein pathology is the compromised protein quality control system. Variations in membrane association and astrocytic uptake between different α-synuclein forms suggest differences in exocytosis or membrane cleavage, potentially impacting the secretome's influence on dopaminergic neurons. We aimed to understand differences in protein degradation mechanisms of astrocytes for both wild-type (WT) and mutant forms of α-synuclein, specifically during periods of reduced degradation efficiency.
View Article and Find Full Text PDFHyperglucagonemia and glucagon hypersecretion in early type 2 diabetes result from multifaceted dysregulation of pancreatic mouse α-cells.
Pflugers Arch
November 2024
Instituto de Investigación, Desarrollo E Innovación en Biotecnología Sanitaria de Elche (IDiBE), Universidad Miguel Hernández de Elche, Avenida de La Universidad S/N, 03202, Elche, Spain.
Hyperglucagonemia has been implicated in the pathogenesis of type 2 diabetes (T2D). In contrast to β-cells, studies on the function of the pancreatic α-cell in T2D are scarce. Consequently, the processes underlying hyperglucagonemia and α-cell dysfunction are largely unknown, limiting the appropriate design of specific pharmacological and therapeutic strategies.
View Article and Find Full Text PDFUnveiling mitochondria as central components driving cognitive decline in alzheimer's disease through cross-transcriptomic analysis of hippocampus and entorhinal cortex microarray datasets.
Heliyon
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Biological Engineering Program, Faculty of Engineering, King Mongkut's University of Technology Thonburi, Bangkok, Thailand.
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by symptoms such as memory loss and impaired learning. This study conducted a cross-transcriptomic analysis of AD using existing microarray datasets from the hippocampus (HC) and entorhinal cortex (EC), comparing them with age-matched non-AD controls. Both of these brain regions are critical for learning and memory processing and are vulnerable areas that exhibit abnormalities in early AD.
View Article and Find Full Text PDFKinase function of TgTKL1 is essential for its role in propagation and pathogenesis.
mSphere
November 2024
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Blacksburg, Virginia, USA.
Article Synopsis
- The Tyrosine Kinase-Like (TKL) family includes eight kinases, with six believed to be vital for the growth of the Toxoplasma parasite.
- Research on TgTKL1 has highlighted its crucial role as a nuclear kinase in the parasite's lifecycle and its impact on virulence in animal models.
- Experiments using CRISPR-Cas9 to create a TgTKL1 mutant revealed that loss of its kinase function hampers parasite growth, alters gene expression, specifically downregulating invasion-related genes, and renders the mutant completely non-virulent in mice.
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