Live Cell Microscope UK: EVOS M5000 Roundup W30
A curated batch of independent peer-reviewed papers mentioning the EVOS M5000 Imaging System. Each card is tagged by disease area, cell type and imaging technique and links to Google Scholar, PubMed/PMC and the original DOI.
TOPORS, a tumor suppressor protein, contributes to the maintenance of higher-order chromatin architecture.
— Cancer
In the nucleus, chromosomes are hierarchically folded into active (A) and inactive (B) compartments composed of topologically associating domains (TADs). Genomic regions interact with nuclear lamina, termed lamina-associated domains (LADs). However, the molecular mechanisms under...
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Frequently asked questions about this study
What role does TOPORS play in the nucleus? TOPORS, a tumour suppressor protein, helps maintain higher-order chromatin architecture, including the organization of topologically associating domains and lamina-associated domains.
How did the EVOS M5000 support the chromatin architecture findings? The EVOS M5000 provided fluorescence images of nuclear organization, helping the authors link TOPORS function to the spatial arrangement of chromatin compartments.
The Killing of Human Neuroblastoma Cells by the Small Molecule JQ1 Occurs in a p53-Dependent Manner.
— Cancer
BACKGROUND: MYCN amplification is a prognostic biomarker associated with poor prognosis of neuroblastoma in children. The overall survival of children with MYCN-amplified neuroblastoma has only marginally improved within the last 20 years. The Bromodomain and Extra-Terminal motif...
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Frequently asked questions about this study
How does JQ1 kill MYCN-amplified neuroblastoma cells? JQ1 kills human neuroblastoma cells in a p53-dependent manner, offering a mechanistic explanation for its selective toxicity in MYCN-driven childhood neuroblastoma.
How did the EVOS M5000 track JQ1-induced neuroblastoma cell death? The EVOS M5000 supplied fluorescence imaging and quantitative readouts of cell viability and death, letting the authors connect JQ1 treatment to p53-dependent killing.
STAT3-induced long noncoding RNA LINC00668 promotes migration and invasion of non-small cell lung cancer via the miR-193a/KLF7 axis.
— Cancer
Long noncoding RNAs (lncRNAs) have been demonstrated to play significant roles in non-small cell lung cancer (NSCLC) progression. Recently, a newly identified lncRNA, LncRNA LINC00668 (LINC00668), was reported to be involved in the regulation of progression of several tumors. How...
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Frequently asked questions about this study
What oncogenic axis does this study describe in non-small cell lung cancer? STAT3-induced lncRNA LINC00668 promotes migration and invasion of non-small cell lung cancer by regulating the miR-193a/KLF7 axis, revealing a new pathway driving NSCLC progression.
How did the EVOS M5000 support the migration and invasion findings? The EVOS M5000 captured fluorescence images and quantitative readouts from migration and invasion assays, allowing the team to measure how LINC00668 manipulation altered NSCLC cell behaviour.
Engineering Intracellular Protein Sensors in Mammalian Cells.
— Cell Biology & Signaling
Proteins can function as biomarkers of pathological conditions, such as neurodegenerative diseases, infections or metabolic syndromes. Engineering cells to sense and respond to these biomarkers may help the understanding of molecular mechanisms underlying pathologies, as well as ...
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Frequently asked questions about this study
What synthetic biology tool did the authors engineer? They engineered mammalian cells to build intracellular protein sensors that can detect disease-relevant biomarkers, providing a platform for studying pathological mechanisms and potentially guiding diagnostics.
How did the EVOS M5000 confirm the sensor function? Fluorescence imaging on the EVOS M5000 allowed the researchers to observe the engineered sensors responding to target proteins inside living cells, validating that the designed constructs worked as intended.
R-spondins engage heparan sulfate proteoglycans to potentiate WNT signaling.
— Cell Biology & Signaling
R-spondins (RSPOs) amplify WNT signaling during development and regenerative responses. We previously demonstrated that RSPOs 2 and 3 potentiate WNT/β-catenin signaling in cells lacking leucine-rich repeat-containing G-protein coupled receptors (LGRs) 4, 5 and 6 (Lebensohn and Ro...
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Frequently asked questions about this study
What mechanistic insight does the study add to WNT signaling? R-spondins potentiate WNT/β-catenin signalling by engaging heparan sulfate proteoglycans, even in cells lacking LGR receptors, revealing an alternative receptor-independent mechanism.
How did the EVOS M5000 help demonstrate RSPO potentiation of WNT signalling? The EVOS M5000 provided fluorescence-based imaging of WNT reporter activity and cell morphology, enabling the authors to quantify how R-spondins enhanced signalling across different receptor backgrounds.
SON and SRRM2 are essential for nuclear speckle formation.
— Cell Biology & Signaling
Nuclear speckles (NS) are among the most prominent biomolecular condensates. Despite their prevalence, research on the function of NS is virtually restricted to colocalization analyses, since an organizing core, without which NS cannot form, remains unidentified. The monoclonal a...
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Frequently asked questions about this study
What did the study identify as the core organizers of nuclear speckles? SON and SRRM2 were found to be essential for nuclear speckle formation, acting as an organizing core without which these prominent nuclear condensates cannot assemble.
How did the EVOS M5000 reveal the role of SON and SRRM2? Using fluorescence imaging on the EVOS M5000, the researchers tracked nuclear speckle assembly and disruption after manipulating SON and SRRM2, directly visualizing the proteins' essential roles.
Negative Regulation of TLR Signaling by BCAP Requires Dimerization of Its DBB Domain.
— Infectious Disease & Immunology
The B cell adaptor protein (BCAP) is a multimodular regulator of inflammatory signaling in diverse immune system cells. BCAP couples TLR signaling to phosphoinositide metabolism and inhibits MyD88-directed signal transduction. BCAP is recruited to the TLR signalosome forming mult...
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Frequently asked questions about this study
What structural requirement does BCAP need to regulate TLR signalling? Negative regulation of TLR signalling by BCAP requires dimerization of its DBB domain, explaining how this adaptor protein assembles at the signalosome to dampen inflammatory signalling.
How did the EVOS M5000 support the BCAP dimerization study? The EVOS M5000 captured fluorescence images of immune cells expressing BCAP variants, helping the authors correlate DBB-domain dimerization with reduced TLR-driven inflammatory responses.
Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19.
— Infectious Disease & Immunology
Viral pandemics, such as the one caused by SARS-CoV-2, pose an imminent threat to humanity. Because of its recent emergence, there is a paucity of information regarding viral behavior and host response following SARS-CoV-2 infection. Here we offer an in-depth analysis of the tran...
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Frequently asked questions about this study
What does the study say about the host response to SARS-CoV-2? An imbalanced host response to SARS-CoV-2 drives the development of COVID-19, highlighting dysregulated innate immunity and viral behaviour as key factors behind severe disease.
How did the EVOS M5000 help analyse the SARS-CoV-2 host response? The EVOS M5000 provided fluorescence imaging of infected cells and tissue samples, supporting the visual and quantitative assessment of viral replication and host-cell damage.
Pathogenesis of SARS-CoV-2 in Transgenic Mice Expressing Human Angiotensin-Converting Enzyme 2.
— Infectious Disease & Immunology
COVID-19 has spread worldwide since 2019 and is now a severe threat to public health. We previously identified the causative agent as a novel SARS-related coronavirus (SARS-CoV-2) that uses human angiotensin-converting enzyme 2 (hACE2) as the entry receptor. Here, we successfully...
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Frequently asked questions about this study
What did the transgenic mouse model reveal about SARS-CoV-2 pathogenesis? Mice expressing human ACE2 developed COVID-19-like disease after SARS-CoV-2 infection, recapitulating key features of human pathogenesis and confirming hACE2 as the critical entry receptor.
How did the EVOS M5000 contribute to the mouse pathogenesis study? The EVOS M5000 was used to image tissue sections and cellular samples from infected transgenic mice, helping the authors document viral distribution, tissue damage, and disease progression.