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The conserved K3 residue in the N-terminal region of Rab10 small GTPase is required for tubular endosome formation: N-terminal tagging causes Rab10 dysfunction.
J Cell Sci
January 2025
Laboratory of Membrane Trafficking Mechanisms, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Aobayama, Aoba-ku, Sendai, Miyagi 980-8578, Japan.
Various N-terminal tags have often been used to identify the functions and localization of Rab small GTPases, but their impact on Rab proteins themselves has been poorly investigated. Here, we used a knockout (KO)-rescue approach to systematically evaluate the effect of N-terminal tagging of two Rabs, Rab10 and Rab27A, on Rab10-KO HeLa cells and Rab27A-deficient melanocytes (melan-ash cells), respectively. The results showed that all of the N-terminal-tagged Rab27A proteins mediated actin-based melanosome transport in the melan-ash cells, but none of the N-terminal-tagged Rab10 proteins fully rescued the defect in tubular endosome formation in the Rab10-KO cells.
View Article and Find Full Text PDFBackground: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).
View Article and Find Full Text PDFUbiquitin-specific protease 25 ameliorates ulcerative colitis by regulating the degradation of phosphor-STAT3.
Cell Death Dis
January 2025
Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Ubiquitin-specific protease 25 (USP25), a member of the deubiquitination family, plays an important role in protein ubiquitination, degradation, inflammation, and immune regulation. However, the role and mechanism of USP25 in ulcerative colitis (UC) remain unclear. To study the role and mechanism of USP25 in UC, bioinformatics analysis and research are conducted on clinical patients with UC, Usp25 knockout (Usp25) mice, intestinal epithelial cell-specific knockout signal transducer and activator of transcription 3 (Stat3) (Villin-Cre Stat3) mice, and human colonic epithelial cells.
View Article and Find Full Text PDFChemogenetic Inhibition of Prefrontal Cortex Ameliorates Autism-Like Social Deficits and Absence-Like Seizures in a Gene-Trap Haploinsufficiency Mouse Model.
Genes (Basel)
December 2024
Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.
Background: (absent, small, or homeotic-like 1), a histone methyltransferase, has been identified as a high-risk gene for autism spectrum disorder (ASD). We previously showed that postnatal severe deficiency in the prefrontal cortex (PFC) of male and female mice caused seizures. However, the synaptic mechanisms underlying autism-like social deficits and seizures need to be elucidated.
View Article and Find Full Text PDFLysyl Oxidase Mediates Proliferation and Differentiation in the Esophageal Epithelium.
Biomolecules
December 2024
Division of Gastroenterology, Hepatology, and Nutrition, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
In homeostatic conditions, the basal progenitor cells of the esophagus differentiate into a stratified squamous epithelium. However, in the setting of acid exposure or inflammation, there is a marked failure of basal cell differentiation, leading to basal cell hyperplasia. We have previously shown that lysyl oxidase (LOX), a collagen crosslinking enzyme, is upregulated in the setting of allergic inflammation of the esophagus; however, its role beyond collagen crosslinking is unknown.
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