ArticleMolecular biology of the cell1998
Selective perturbation of apical membrane traffic by expression of influenza M2, an acid-activated ion channel, in polarized madin-darby canine kidney cells.
Article in Molecular biology of the cell, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 64 citations in OpenAlex.
- The M2 proteins of bat influenza A viruses reveal atypical features compared to conventional M2 proteins.Journal of virology · 2023Article
- The emerging roles of retromer and sorting nexins in the life cycle of viruses.Virologica Sinica · 2022Review
- Vacuolar-type proton ATPase is required for maintenance of apicobasal polarity of embryonic visceral endoderm.Scientific reports · 2021Article
- Site-directed M2 proton channel inhibitors enable synergistic combination therapy for rimantadine-resistant pandemic influenza.PLoS pathogens · 2020Article
- Dysregulation of M segment gene expression contributes to influenza A virus host restriction.PLoS pathogens · 2019Article
- Influenza M2 protein regulates MAVS-mediated signaling pathway through interacting with MAVS and increasing ROS production.Autophagy · 2019Article
- Influenza A Virus M2 Protein: Roles from Ingress to Egress.International journal of molecular sciences · 2017Review
- Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- The ORF61 Protein Encoded by Simian Varicella Virus and Varicella-Zoster Virus Inhibits NF-κB Signaling by Interfering with IκBα Degradation.Journal of virology · 2015Article
- Influenza virus M2 targets cystic fibrosis transmembrane conductance regulator for lysosomal degradation during viral infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Spatiotemporal dynamics of triglyceride storage in unilocular adipocytes.Molecular biology of the cell · 2014Article
- TBC1D9B functions as a GTPase-activating protein for Rab11a in polarized MDCK cells.Molecular biology of the cell · 2014Article
- A phosphotyrosine switch for cargo sequestration at clathrin-coated buds.The Journal of biological chemistry · 2014Article
- Altered dynamics of a lipid raft associated protein in a kidney model of Fabry disease.Molecular genetics and metabolism · 2014Article
- VAMP7 modulates ciliary biogenesis in kidney cells.PloS one · 2014Article
- Multiple motifs regulate apical sorting of p75 via a mechanism that involves dimerization and higher-order oligomerization.Molecular biology of the cell · 2013Article
- Influenza matrix protein 2 alters CFTR expression and function through its ion channel activity.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- PIP5KIβ selectively modulates apical endocytosis in polarized renal epithelial cells.PloS one · 2013Article
- Sialylation of N-linked glycans mediates apical delivery of endolyn in MDCK cells via a galectin-9-dependent mechanism.Molecular biology of the cell · 2012Article
- Multiple biosynthetic trafficking routes for apically secreted proteins in MDCK cells.Traffic (Copenhagen, Denmark) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The function of acidification along the endocytic pathway is not well understood, in part because the perturbants used to modify compartmental pH have global effects and in some cases alter cytoplasmic pH. We have used a new approach to study the effect of pH perturbation on postendocytic traffic in polarized Madin-Darby canine kidney (MDCK) cells. Influenza M2 is a small membrane protein that functions as an acid-activated ion channel and can elevate the pH of the trans-Golgi network and endosomes. We used recombinant adenoviruses to express the M2 protein of influenza virus in polarized MDCK cells stably transfected with the polymeric immunoglobulin (Ig) receptor. Using indirect immunofluorescence and immunoelectron microscopy, M2 was found to be concentrated at the apical plasma membrane and in subapical vesicles; intracellular M2 colocalized partly with internalized IgA in apical recycling endosomes as well as with the trans-Golgi network marker TGN-38. Expression of M2 slowed the rate of IgA transcytosis across polarized MDCK monolayers. The delay in transport occurred after IgA reached the apical recycling endosome, consistent with the localization of intracellular M2. Apical recycling of IgA was also slowed in the presence of M2, whereas basolateral recycling of transferrin and degradation of IgA were unaffected. By contrast, ammonium chloride affected both apical IgA and basolateral transferrin release. Together, our data suggest that M2 expression selectively perturbs acidification in compartments involved in apical delivery without disrupting other postendocytic transport steps.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.