The use of Cre-loxP technology for the purpose of cell type-specific gene ablation has revolutionized developmental biology and biomedicine. Several transgenic mouse lines have been developed for the analysis of gene function in the gastrointestinal tract, but in all of these the expression of Cre is limited to the epithelial cell layer. No Cre- expressing transgenic mouse lines ("Cre lines") exist for the deletion of loxP-flanked genes specifically in gut mesoderm. To address this deficiency, we have derived a bacterial artificial chromosome based transgenic mouse line in which the Cre gene is controlled by the Foxl1 promoter and enhancer elements. X-Gal staining of Foxl1-Cre; Rosa26R bi-transgenic lines confirm that Foxl1-Cre results in recombination specifically in the gastrointestinal mesenchyme. The Foxl1-Cre line will facilitate the dissection of mesenchymal to epithelial signaling that is known to play a major role in the patterning and function of the gastrointestinal tract.
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http://dx.doi.org/10.1002/dvg.20315 | DOI Listing |
J Inherit Metab Dis
January 2025
Department of Internal Medicine, Division of Endocrinology and Metabolic Disease, Maastricht University Medical Center+, Maastricht, The Netherlands.
Hereditary fructose intolerance (HFI) is characterized by liver damage and a secondary defect in N-linked glycosylation due to impairment of mannose phosphate isomerase (MPI). Mannose treatment has been shown to be an effective treatment in a primary defect in MPI (i.e.
View Article and Find Full Text PDFMol Autism
December 2024
Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Background: Angelman syndrome (AS), a severe neurodevelopmental disorder resulting from the loss of the maternal UBE3A gene, is marked by changes in the brain's white matter (WM). The extent of WM abnormalities seems to correlate with the severity of clinical symptoms, but these deficits are still poorly characterized or understood. This study provides the first large-scale measurement of WM volume reduction in children with AS.
View Article and Find Full Text PDFJ Neuroinflammation
December 2024
Department of Medicine, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada.
Central nervous system (CNS) resident memory CD8 T cells (T) that express IFN-γ contribute to neurodegenerative processes, including synapse loss, leading to memory impairment. Here, we show that CCR2 signaling in CD8 T that persist within the hippocampus after recovery from CNS infection with West Nile virus (WNV) significantly prevents the development of memory impairments. Using CCR2-deficient mice, we determined that CCR2 expression is not essential for CNS T cell recruitment or virologic control during acute WNV infection.
View Article and Find Full Text PDFMol Med
December 2024
Department of Otolaryngology-Head and Neck Surgery, Chonnam National University Medical School and Chonnam National University Hospital, 42 Jaebong-Ro, Dong-Gu, Gwangju, 61469, Republic of Korea.
Background: Recent studies have identified hearing loss (HL) as a primary risk factor for Alzheimer's disease (AD) onset. However, the mechanisms linking HL to AD are not fully understood. This study explored the effects of drug-induced hearing loss (DIHL) on the expression of proteins associated with AD progression in mouse models.
View Article and Find Full Text PDFCell Mol Life Sci
December 2024
National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.
Idiopathic pulmonary fibrosis (IPF) is a prevalent interstitial lung disease with high mortality. CD38 is a main enzyme for intracellular nicotinamide adenine dinucleotide (NAD) degradation in mammals. It has been reported that CD38 participated in pulmonary fibrosis through promoting alveolar epithelial cells senescence.
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