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Results: 596
ER-associated RNA silencing promotes ER quality control.
Sotirios Efstathiou, Franziska Ottens, Lena-Sophie Schütter, Sonia Ravanelli, Nikolaos Charmpilas, Aljona Gutschmidt, Jérémie Le Pen, Niels H Gehring, Eric A Miska, Jorge Bouças, Thorsten Hoppe
Jan 05, 2023
The endoplasmic reticulum (ER) coordinates mRNA translation and processing of secreted and endomembrane proteins. ER-associated degradation (ERAD) prevents the accumulation of misfolded proteins in the ER, but the physiological...
Does exposure to the food environment differ by socioeconomic position? Comparing area-based and person-centred metrics in the Fenland Study, UK
p53 and translation attenuation regulate distinct cell cycle checkpoints during endoplasmic reticulum (ER) stress.
Sally E Thomas, Elke Malzer, Adriana Ordóñez, Lucy E Dalton, Emily FA van T Wout, Elizabeth Liniker, Damian C Crowther, David A Lomas, Stefan J Marciniak
Feb 12, 2019
Cell cycle checkpoints ensure that proliferation occurs only under permissive conditions, but their role in linking nutrient availability to cell division is incompletely understood. Protein folding within the endoplasmic...
Animals Cell Cycle Cell Line Cell Line Tumor Cell Proliferation Cell Separation Drosophila melanogaster Endoplasmic Reticulum Flow Cytometry Gene Expression Regulation Genes p53 HEK293 Cells HeLa Cells Humans Plasmids Protein Biosynthesis Protein Phosphatase 1 RNA Interference Tumor Suppressor Protein p53
Plasma from pre-pubertal obese children impairs insulin stimulated Nitric Oxide (NO) bioavailability in endothelial cells
Natalia Di Pietro, M Loredana Marcovecchio, Sara Di Silvestre, Tommaso de Giorgis, Vincenzo Giuseppe Pio Cordone, Paola Lanuti, Francesco Chiarelli, Giuseppina Bologna, Angelika Mohn, Assunta Pandolfi
Aug 01, 2018
Childhood obesity is commonly associated with early signs of endothelial dysfunction, characterized by impairment of insulin signaling and vascular Nitric Oxide (NO) availability. However, the underlying mechanisms remain to be...
ER stress Endothelial dysfunction Insulin Resistance Nitric oxide obesity Activating Transcription Factor 6 Biological Availability Biomarkers Cell Nucleus Child Cyclic GMP Endoplasmic Reticulum Chaperone BiP Endoplasmic reticulum stress Human Umbilical Vein Endothelial Cells Humans Insulin Models Biological NF-kappa B Nitric oxide Nitric Oxide Synthase Type III obesity Phosphorylation Protein Transport Proto-Oncogene Proteins c-akt Puberty
Reliable measurement of free Ca2+ concentrations in the ER lumen using Mag-Fluo-4.
Synthetic Ca2+ indicators are widely used to report changes in free [Ca2+], usually in the cytosol but also within organelles. Mag-Fluo-4, loaded into the endoplasmic reticulum (ER) by incubating cells with Mag-Fluo-4 AM, has...
Lifetime imaging of a fluorescent protein sensor reveals surprising stability of ER thiol redox.
Edward Avezov, Benedict CS Cross, Gabriele S Kaminski Schierle, Mikael Winters, Heather P Harding, Eduardo Pinho Melo, Clemens F Kaminski, David Ron
Feb 12, 2020
Interfering with disulfide bond formation impedes protein folding and promotes endoplasmic reticulum (ER) stress. Due to limitations in measurement techniques, the relationships of altered thiol redox and ER stress have been...
iRhom pseudoproteases regulate ER stress-induced cell death through IP3 receptors and BCL-2.
Iqbal Dulloo, Peace Atakpa-Adaji, Yi-Chun Yeh, Clémence Levet, Sonia Muliyil, Fangfang Lu, Colin W Taylor, Matthew Freeman
Apr 11, 2022
The folding capacity of membrane and secretory proteins in the endoplasmic reticulum (ER) can be challenged by physiological and pathological perturbations, causing ER stress. If unresolved, this leads to cell death. We report a...
Identification of a Novel Regulator of ER Stress-Induced Apoptosis
Genevieve S Joseph
Jan 01, 0001
The survival and development of a multicellular organism is reliant upon proper cell and organelle function, and the tight regulation of cell number. The endoplasmic reticulum (ER) is the cellular compartment where membrane and...
Published by: Rockefeller University
The oral selective oestrogen receptor degrader (SERD) AZD9496 is comparable to fulvestrant in antagonising ER and circumventing endocrine resistance.
Agostina Nardone, Hazel Weir, Oona Delpuech, Henry Brown, Carmine De Angelis, Maria Letizia Cataldo, Xiaoyong Fu, Martin J Shea, Tamika Mitchell, Jamunarani Veeraraghavan, Chandandeep Nagi, Mark Pilling, Mothaffar F Rimawi, Meghana Trivedi, Susan G Hilsenbeck, Gary C Chamness, Rinath Jeselsohn, C Kent Osborne, Rachel Schiff
Jan 02, 2020
BACKGROUND: The oestrogen receptor (ER) is an important therapeutic target in ER-positive (ER+) breast cancer. The selective ER degrader (SERD), fulvestrant, is effective in patients with metastatic breast cancer, but its...
Ca2+ signals initiate at immobile IP3 receptors adjacent to ER-plasma membrane junctions.
Nagendra Babu Thillaiappan, Alap P Chavda, Stephen C Tovey, David L Prole, Colin W Taylor
Jun 12, 2018
IP3 receptors (IP3Rs) release Ca2+ from the ER when they bind IP3 and Ca2+. The spatial organization of IP3Rs determines both the propagation of Ca2+ signals between IP3Rs and the selective regulation of cellular responses. Here...
OPA1 Modulates Mitochondrial Ca2+ Uptake Through ER-Mitochondria Coupling.
Benjamín Cartes-Saavedra, Josefa Macuada, Daniel Lagos, Duxan Arancibia, María E Andrés, Patrick Yu-Wai-Man, György Hajnóczky, Verónica Eisner
Jan 28, 2022
Autosomal Dominant Optic Atrophy (ADOA), a disease that causes blindness and other neurological disorders, is linked to OPA1 mutations. OPA1, dependent on its GTPase and GED domains, governs inner mitochondrial membrane (IMM)...
IP3 Receptors Preferentially Associate with ER-Lysosome Contact Sites and Selectively Deliver Ca2+ to Lysosomes.
Peace Atakpa, Nagendra Babu Thillaiappan, Stefania Mataragka, David L Prole, Colin W Taylor
Dec 21, 2018
Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) allow extracellular stimuli to redistribute Ca2+ from the ER to cytosol or other organelles. We show, using small interfering RNA (siRNA) and vacuolar H+-ATPase (V-ATPase)...
Ca(2+) IP(3) receptor concanamycin A Endoplasmic Reticulum genetically encoded Ca(2+) sensor lysosome membrane contact site proximity ligation assay store-operated Ca(2+) entry Calcium Calcium Signaling Cytosol Endoplasmic Reticulum HEK293 Cells HeLa Cells Humans Hydrogen-Ion Concentration Inositol 1 4 5-Trisphosphate Receptors Lysosomes
Marketing messages accompanying online selling of low/er and regular strength wine and beer products in the UK
Background: Increased availability of low/er strength alcohol products has the potential to reduce alcohol consumption if they are marketed as substitutes for higher strength products rather than as additional products. The...
Mitofusin-mediated ER stress triggers neurodegeneration in pink1/parkin models of Parkinson's disease.
I Celardo, AC Costa, S Lehmann, C Jones, N Wood, NE Mencacci, GR Mallucci, SHY Loh, LM Martins
Nov 10, 2017
Mutations in PINK1 and PARKIN cause early-onset Parkinson's disease (PD), thought to be due to mitochondrial toxicity. Here, we show that in Drosophila pink1 and parkin mutants, defective mitochondria also give rise to...
Animals Disease Models Animal Drosophila Proteins Drosophila melanogaster Endoplasmic Reticulum Endoplasmic reticulum stress Humans Membrane Proteins Mitochondria Mutation Nerve Degeneration Neuroprotection Parkinson Disease Phosphorylation Protein Serine-Threonine Kinases Signal Transduction Ubiquitin-Protein Ligases Unfolded Protein Response eIF-2 Kinase
Cellular mechanisms of endoplasmic reticulum stress signaling in health and disease. 2. Protein misfolding and ER stress.
The endoplasmic reticulum (ER) is a major site of protein synthesis, most strikingly in the specialized secretory cells of metazoans, which can produce their own weight in proteins daily. Cells possess a diverse machinery to...
GPN does not release lysosomal Ca2+ but evokes Ca2+ release from the ER by increasing the cytosolic pH independently of cathepsin C.
Peace Atakpa, Laura M van Marrewijk, Michael Apta-Smith, Sumita Chakraborty, Colin W Taylor
Jan 30, 2019
The dipeptide glycyl-l-phenylalanine 2-naphthylamide (GPN) is widely used to perturb lysosomes because its cleavage by the lysosomal enzyme cathepsin C is proposed to rupture lysosomal membranes. We show that GPN evokes a...
Ca2+ signals Cathepsin C Cytosolic pH Endoplasmic Reticulum GPN lysosome Biological Transport CRISPR-Cas Systems Calcium Calcium Channels Calcium Signaling Cathepsin C Cell Line Tumor Cytosol Dipeptides Endoplasmic Reticulum Gene Editing Gene Expression Gene Knockdown Techniques HEK293 Cells HeLa Cells Humans Hydrogen-Ion Concentration Inositol 1 4 5-Trisphosphate Receptors Leukocytes Lysosome-Associated Membrane Glycoproteins Lysosomes Ploidies Ryanodine Receptor Calcium Release Channel
A consensus prognostic gene expression classifier for ER positive breast cancer.
Andrew E Teschendorff, Ali Naderi, Nuno L Barbosa-Morais, Sarah E Pinder, Ian O Ellis, Sam Aparicio, James D Brenton, Carlos Caldas
Jan 03, 2018
BACKGROUND: A consensus prognostic gene expression classifier is still elusive in heterogeneous diseases such as breast cancer. RESULTS: Here we perform a combined analysis of three major breast cancer microarray data sets to...
MFN2 mutations in Charcot-Marie-Tooth disease alter mitochondria-associated ER membrane function but do not impair bioenergetics.
Delfina Larrea, Marta Pera, Adriano Gonnelli, Rubén Quintana-Cabrera, H Orhan Akman, Cristina Guardia-Laguarta, Kevin R Velasco, Estela Area-Gomez, Federica Dal Bello, Diego De Stefani, Rita Horvath, Michael E Shy, Eric A Schon, Marta Giacomello
Jun 28, 2019
Charcot-Marie-Tooth disease (CMT) type 2A is a form of peripheral neuropathy, due almost exclusively to dominant mutations in the nuclear gene encoding the mitochondrial protein mitofusin-2 (MFN2). However, there is no...
The pathogenic mechanism of the Mycobacterium ulcerans virulence factor, mycolactone, depends on blockade of protein translocation into the ER.
Belinda S Hall, Kirsti Hill, Michael McKenna, Joy Ogbechi, Stephen High, Anne E Willis, Rachel E Simmonds
Mar 01, 2021
Infection with Mycobacterium ulcerans is characterised by tissue necrosis and immunosuppression due to mycolactone, the necessary and sufficient virulence factor for Buruli ulcer disease pathology. Many of its effects are known...
FGFR1 amplification or overexpression and hormonal resistance in luminal breast cancer
Silvana Mouron, Luis Manso, Eduardo Caleiras, Jose L. Rodriguez-Peralto, Oscar M. Rueda, Carlos Caldas, Ramon Colomer, Miguel Quintela-Fandino, Maria J. Bueno
Feb 13, 2021
Abstract: Background: FGFR1 amplification, but not overexpression, has been related to adverse prognosis in hormone-positive breast cancer (HRPBC). Whether FGFR1 overexpression and amplification are correlated, what is their...
A novel CISD2 mutation associated with a classical Wolfram syndrome phenotype alters Ca2+ homeostasis and ER-mitochondria interactions.
Cécile Rouzier, David Moore, Cécile Delorme, Sandra Lacas-Gervais, Samira Ait-El-Mkadem, Konstantina Fragaki, Florence Burté, Valérie Serre, Sylvie Bannwarth, Annabelle Chaussenot, Martin Catala, Patrick Yu-Wai-Man, Véronique Paquis-Flucklinger
Jun 28, 2018
Wolfram syndrome (WS) is a progressive neurodegenerative disease characterized by early-onset optic atrophy and diabetes mellitus, which can be associated with more extensive central nervous system and endocrine complications....
Impaired Mitochondrial ATP Production Downregulates Wnt Signaling via ER Stress Induction.
Roberto Costa, Roberta Peruzzo, Magdalena Bachmann, Giulia Dalla Montà, Mattia Vicario, Giulia Santinon, Andrea Mattarei, Enrico Moro, Rubén Quintana-Cabrera, Luca Scorrano, Massimo Zeviani, Francesca Vallese, Mario Zoratti, Cristina Paradisi, Francesco Argenton, Marisa Brini, Tito Calì, Sirio Dupont, Ildikò Szabò, Luigi Leanza
Sep 13, 2019
Wnt signaling affects fundamental development pathways and, if aberrantly activated, promotes the development of cancers. Wnt signaling is modulated by different factors, but whether the mitochondrial energetic state affects Wnt...
Decreasing pdzd8-mediated mito-ER contacts improves organismal fitness and mitigates Aβ42 toxicity.
Victoria L Hewitt, Leonor Miller-Fleming, Madeleine J Twyning, Simonetta Andreazza, Francesca Mattedi, Julien Prudent, Franck Polleux, Alessio Vagnoni, Alexander J Whitworth
Aug 14, 2022
Mitochondria-ER contact sites (MERCs) orchestrate many important cellular functions including regulating mitochondrial quality control through mitophagy and mediating mitochondrial calcium uptake. Here, we identify and...
FGFR1 amplification or overexpression and hormonal resistance in luminal breast cancer
Silvana Mouron, Luis Manso, Eduardo Caleiras, Jose L Rodriguez-Peralto, Oscar M Rueda, Carlos Caldas, Ramon Colomer, Miguel Quintela-Fandino, Maria J Bueno
Apr 09, 2021
BACKGROUND: FGFR1 amplification, but not overexpression, has been related to adverse prognosis in hormone-positive breast cancer (HRPBC). Whether FGFR1 overexpression and amplification are correlated, what is their distribution...
FGFR1 amplification FGFR1 overexpression Luminal breast cancer palbociclib Rogaratinib Adult Aged Aged 80 and over Antineoplastic Agents Biomarkers Tumor Breast Neoplasms Cell Line Tumor Cyclin-Dependent Kinase 4 Cyclin-Dependent Kinase 6 Disease Management Disease Susceptibility Drug Resistance Multiple Drug Resistance Neoplasm Female Gene Amplification Gene Expression Humans In Situ Hybridization Fluorescence Middle Aged Molecular Targeted Therapy Neoplasm Staging Prognosis RNA Messenger Receptor Fibroblast Growth Factor Type 1 Receptors Estrogen Treatment Outcome Young Adult
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