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SLC26A3 (DRA, the Congenital Chloride Diarrhea Gene): A Novel Therapeutic Target for Diarrheal Diseases.
Cell Mol Gastroenterol Hepatol
December 2024
- Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, USA; - Jesse Brown VA Medical Center, Chicago, IL, USA. Electronic address:
Diarrhea associated with enteric infections, gut inflammation, and genetic defects poses a major health burden and results in significant morbidity and mortality. Impaired fluid and electrolyte absorption and/or secretion in the intestine are the hallmark of diarrhea. Electroneutral NaCl absorption in the mammalian GI tract involves the coupling of Na/H and Cl/HCO exchangers.
View Article and Find Full Text PDFIs LPAR5 agonist a new treatment for microvilli inclusion disease?
Am J Physiol Gastrointest Liver Physiol
January 2025
Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States.
Syntaxin 3B: A SNARE Protein Required for Vision.
Int J Mol Sci
October 2024
Department of Neurobiology and Anatomy, McGovern Medical School at the University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Article Synopsis
- Syntaxin 3 is part of a protein family crucial for the fusion of vesicles with membranes, impacting various cellular processes.
- Mutations in the syntaxin 3A splice form are linked to a serious gut disorder, while additional mutations involving syntaxin 3B can lead to early-onset retinal diseases.
- The review focuses on new research highlighting the functions of syntaxin 3B in membrane fusion and neurotransmitter release specifically in the vertebrate retina.
Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.
Am J Physiol Gastrointest Liver Physiol
December 2024
Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee, United States.
Functional loss of the motor protein myosin Vb (MYO5B) induces various defects in intestinal epithelial function and causes a congenital diarrheal disorder, namely, microvillus inclusion disease (MVID). Utilizing the MVID model mice (MYO5BΔIEC) and [MYO5B(G519R)], we previously reported that functional MYO5B loss disrupts progenitor cell differentiation and enterocyte maturation that result in villus blunting and deadly malabsorption symptoms. In this study, we determined that both absence and a point mutation of MYO5B impair lipid metabolism and alter mitochondrial structure, which may underlie the progenitor cell malfunction observed in the MVID intestine.
View Article and Find Full Text PDFArticle Synopsis
- - Functional loss of the motor protein MYO5B leads to serious intestinal issues, including microvillus inclusion disease (MVID), characterized by progenitor cell dysfunction and malabsorption symptoms.
- - Research using MVID model mice showed that both the absence and mutation of MYO5B disrupt lipid metabolism and mitochondrial structure, resulting in reduced fatty acid oxidation and altered energy metabolism.
- - Treatment with Compound-1, which targets LPAR5, was found to improve intestinal function and weight loss in mice with MYO5B mutations, suggesting a potential therapeutic approach for treating MVID.
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