Pathogenic bacteria that colonize the human intestinal tract have evolved strategies to overcome acidic conditions when they pass through the gastrointestinal tract. Amino acid-mediated acid resistance systems are effective survival strategies in a stomach that is full of amino acid substrate. The amino acid antiporter, amino acid decarboxylase, and ClC chloride antiporter are all engaged in these systems, and each one plays a role in protecting against or adapting to the acidic environment. The ClC chloride antiporter, a member of the ClC channel family, eliminates negatively charged intracellular chloride ions to avoid inner membrane hyperpolarization as an electrical shunt of the acid resistance system. In this review, we will discuss the structure and function of the prokaryotic ClC chloride antiporter of amino acid-mediated acid resistance system.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10394335 | PMC |
http://dx.doi.org/10.4014/jmb.2303.03009 | DOI Listing |
Zhonghua Yi Xue Yi Chuan Xue Za Zhi
January 2025
Department of Neurology, the Affiliated Children's Hospital of Xiangya School of Medicine, Central South University (Hunan Children's Hospital), Changsha, Hunan 410007, China.
Objective: To explore the clinical manifestations and genetic characteristics of a child with Leukoencephalopathy with ataxia (LKPAT) caused by a CLCN2 gene variant.
Methods: A retrospective analysis was conducted on the clinical data of a child admitted to Hunan Children's Hospital in June 2024 due to "intermittent convulsions for 13 days". Peripheral blood samples were collected from the child and his parents for whole exome sequencing, followed by Sanger sequencing validation and pathogenicity analysis of candidate variants.
Adv Mater
January 2025
School of Chemical Engineering, The University of Adelaide, Adelaide, SA, 5005, Australia.
Life Sci
February 2025
Department of Pharmacology, Cardiac & Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China. Electronic address:
Aims: Impairment of nitric oxide (NO) production is a major cause of endothelial dysfunction and hypertension. ClC-5 Cl channel is abundantly expressed in the vascular endothelium. However, it remains unclear how it regulates endothelial function.
View Article and Find Full Text PDFFront Genet
December 2024
Dino Ferrari Center, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Myotonia congenita, both in a dominant (Thomsen disease) and recessive form (Becker disease), is caused by molecular defects in that encodes the major skeletal muscle chloride channel, ClC-1. This channel is important for the normal repolarization of muscle action potentials and consequent relaxation of the muscle, and its dysfunction leads to impaired muscle relaxation after voluntary or evoked contraction and muscle stiffness. More than 300 pathogenic variants have been found in association with congenital myotonia, inherited as recessive or dominant traits (with complete or incomplete penetrance).
View Article and Find Full Text PDFAnn Clin Transl Neurol
December 2024
NextGen Precision Health, University of Missouri, Columbia, Missouri, USA.
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