Membrane trafficking specificity between distinct compartments ensures that cargo proteins and lipids are delivered to their target organelle. However, accurate recognition of cargo carriers by tethering factors on target membranes is poorly understood. TBC1D23 is now identified as an adaptor that links endosome-derived vesicles with golgins at the trans-Golgi.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/ncb3649 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The etiology and prevention of early-stage tau pathology in higher cortical circuits: Insights from aging rhesus macaques.
Alzheimers Dement
January 2025
Department of Neuroscience, Yale Medical School, New Haven, Connecticut, USA.
Aging rhesus macaques provide a unique model for learning how age and inflammation drive early-stage pathology in sporadic Alzheimer's disease, and for testing potential therapeutics. Unlike mice, aging macaques have extensive association cortices and inflammatory signaling similar to humans, are apolipoprotein E ε4 homozygotes, and naturally develop tau and amyloid pathology with marked cognitive deficits. Importantly, monkeys provide the unique opportunity to study early-stage, soluble hyperphosphorylated tau (p-tau), including p-tau217.
View Article and Find Full Text PDFATG9A facilitates the closure of mammalian autophagosomes.
J Cell Biol
February 2025
Autophagy, Inflammation and Metabolism Center of Biomedical Research Excellence, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Canonical autophagy captures within specialized double-membrane organelles, termed autophagosomes, an array of cytoplasmic components destined for lysosomal degradation. An autophagosome is completed when the growing phagophore undergoes ESCRT-dependent membrane closure, a prerequisite for its subsequent fusion with endolysosomal organelles and degradation of the sequestered cargo. ATG9A, a key integral membrane protein of the autophagy pathway, is best known for its role in the formation and expansion of phagophores.
View Article and Find Full Text PDFHIV-1 exploits LBPA-dependent intraepithelial trafficking for productive infection of human intestinal mucosa.
PLoS Pathog
December 2024
Amsterdam UMC, location University of Amsterdam, Experimental Immunology, Amsterdam, The Netherlands.
The gastrointestinal tract is a prominent portal of entry for HIV-1 during sexual or perinatal transmission, as well as a major site of HIV-1 persistence and replication. Elucidation of underlying mechanisms of intestinal HIV-1 infection are thus needed for the advancement of HIV-1 curative therapies. Here, we present a human 2D intestinal immuno-organoid system to model HIV-1 disease that recapitulates tissue compartmentalization and epithelial-immune cellular interactions.
View Article and Find Full Text PDFImmunoisolation of Plant Endosomal Vesicles to Explore Uptake of Pathogen Effector Proteins During Infection of Nicotiana benthamiana.
Methods Mol Biol
December 2024
Division of Plant Sciences, School of Life Sciences, James Hutton Institute, University of Dundee, Dundee, UK.
Endocytosis is an essential cellular process that uptakes substances into cells at the plasma membrane from the extracellular space and plays a major role in plant development and responses to environmental stimuli. Research has shown that plant membrane-resident proteins are endocytosed and transported into plant endosomes in response to pathogen-secreted elicitors. However, there is no conclusive experimental evidence demonstrating how secreted cytoplasmic effectors from oomycetes and fungi enter host cells during infection.
View Article and Find Full Text PDFEndosomal pH is an evolutionarily conserved driver of phenotypic plasticity in colorectal cancer.
NPJ Syst Biol Appl
December 2024
Department of Developmental Biology and Genetics, Indian Institute of Science, Bengaluru, 560012, India.
Dysregulated pH is now recognised as a hallmark of cancer. Recent evidence has revealed that the endosomal pH regulator Na/H exchanger NHE9 is upregulated in colorectal cancer to impose a pseudo-starvation state associated with invasion, highlighting an underexplored mechanistic link between adaptive endosomal reprogramming and malignant transformation. In this study, we use a model that quantitatively captures the dynamics of the core regulatory network governing epithelial mesenchymal plasticity.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!