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2,678 results for “cell signalling”
White Blood Cell Signaling and Defense Mechanisms in Patients With Diabetes Mellitus Type 2 and Periodontitis
ClinicalTrials.gov study NCT01848379. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Cell Signaling and Resistance to Oxidative Stress: Effects of Aging and Exercise
ClinicalTrials.gov study NCT03419988. IPD Sharing: NO. Countries: 1. Publications: 1.
How Secreted-embryo-derived Trypsin Initiates, Maintains and Terminates Ca2+ Signals in Uterine Epithelial Cells
ClinicalTrials.gov study NCT04865367. IPD Sharing: NO. Countries: 1. Publications: 15.
Evaluating the Efficacy of Neratinib on Live Cell HER2 Signaling Transduction Analysis Positive Triple Negative Breast
ClinicalTrials.gov study NCT03812393. IPD Sharing: NO. Countries: 1. Publications: 2.
A Study of Intracellular Signaling in Muscle and Fat Cells During Ketosis
ClinicalTrials.gov study NCT02157155. IPD Sharing: Not stated. Countries: 1. Publications: 14.
ENABLE-1 (Engaging Toll-like Receptor Signalling for B-cell Lymphoma Chimeric Antigen Receptor Therapy)
ClinicalTrials.gov study NCT04049513. IPD Sharing: YES. Countries: 1. Publications: 4.
Autogenous Mesenchymal Stem Cell Culture-Derived Signalling Molecules as Enhancers of Bone Formation in Bone Grafting
ClinicalTrials.gov study NCT04998058. IPD Sharing: NO. Countries: 1. Publications: 2.
miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells
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Mechanical manipulation of cancer cell tumorigenicity via heat shock protein signaling
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Endocannabinoid signalling in stem cells and cerebral organoids drives differentiation to deep layer projection neurons via CB1 receptors
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Data from: Early mechanistic events induced by low molecular weight polycyclic aromatic hydrocarbons in mouse lung epithelial cells: a role for eicosanoid signaling
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Confocal images from: Cell density, alignment, and orientation correlate with C-signal-dependent gene expression during Myxococcus xanthus development
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Data from: A RhoG-mediated signaling pathway that modulates invadopodia dynamics in breast cancer cells
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Neuronal octopamine signaling regulates mating-induced germline stem cell increase in female Drosophila melanogaster
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UBE3A Wnt signaling Cell Assay
<p>Describes the development of a Wnt signaling cell-based reporter assay for UBE3A.</p>
Data from: Loss of mTORC2 signaling in oligodendrocyte precursor cells delays myelination
Myelin abnormalities are increasingly being recognized as an important component of a number of neurologic developmental disorders. The integration of many signaling pathways and cell types are critical for correct myelinogenesis. The PI3-K and mechanistic target of rapamycin (mTOR) pathways have been found to play key roles. mTOR is found within two distinct complexes, mTORC1 and mTORC2. mTORC1 activity has been shown to play a major role during myelination, while the role of mTORC2 is not yet well understood. To determine the role of mTORC2 signaling in myelinogenesis, we generated a mouse lacking the critical mTORC2 component Rictor in oligodendrocyte precursors (OPCs). Targeted deletion of Rictor in these cells decreases and delays the expression of myelin related proteins and reduces the size of cerebral white matter tracts. This is developmentally manifest as a transient reduction in myelinated axon density and g-ratio. OPC cell number is reduced at birth without detectable change in proliferation with proportional reductions in mature oligodendrocyte number at P15. The total number of oligodendrocytes as well as extent of myelination, does improve over time. Adult conditional knock-out (CKO) animals do not demonstrate a behavioral phenotype likely due in part to preserved axonal conduction velocities. These data support and extend prior studies demonstrating an important but transient contribution of mTORC2 signaling to myelin development.
Data from: Systematic study of the surface plasmon resonance signals generated by cells for sensors with different characteristic lengths
The objectives of this study were to establish an in-depth understanding of the signals induced by mammalian cells in surface plasmon resonance (SPR) sensing. To this end, two plasmonic structures with different propagation and penetration distances were used: conventional surface plasmon resonance and long-range surface plasmon resonance. Long-range SPR showed a lesser sensitivity to the absolute number of round cells but a greater resolution due to its very narrow spectral dip. The effect of cell spreading was also investigated and the resonance angle of long-range SPR was mostly insensitive unlike in the conventional SPR counterpart. Experimental data was compared with suitable models used in the SPR literature. Although these simple averaging models could be used to describe some of the experimental data, important deviations were observed which could be related to the fact that they do not take into consideration critical parameters such as plasmon scattering losses, which is particularly crucial in the case of long-range SPR structures. The comparison between conventional and long-range SPR for cellular schemes revealed important fundamental differences in their responses to the presence of cells, opening new horizons for SPR-based cell assays. From this study, long-range SPR is expected to be more sensitive towards both the detection of intracellular events resulting from biological stimulation and the detection of microorganisms captured from complex biological samples.
Data from: Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation
The mammalian diffuse stellate cell system comprises retinoid-storing cells capable of remarkable transformations from a quiescent to an activated myofibroblast-like phenotype. Activated pancreatic stellate cells (PSCs) attract attention owing to the pivotal role they play in development of tissue fibrosis in chronic pancreatitis and pancreatic cancer. However, little is known about the actual role of PSCs in the normal pancreas. These enigmatic cells have recently been shown to respond to physiological stimuli in a manner that is markedly different from their neighbouring pancreatic acinar cells (PACs). Here, we demonstrate the capacity of PSCs to generate nitric oxide (NO), a free radical messenger mediating, for example, inflammation and vasodilatation. We show that production of cytosolic NO in PSCs is unambiguously related to cytosolic Ca2+ signals. Only stimuli that evoke Ca2+ signals in the PSCs elicit consequent NO generation. We provide fresh evidence for the striking difference between signalling pathways in PSCs and adjacent PACs, because PSCs, in contrast to PACs, generate substantial Ca2+-mediated and NOS-dependent NO signals. We also show that inhibition of NO generation protects both PSCs and PACs from necrosis. Our results highlight the interplay between Ca2+ and NO signalling pathways in cell–cell communication, and also identify a potential therapeutic target for anti-inflammatory therapies.
Pulses of RhoA Signaling Stimulate Actin Polymerization and Flow in Protrusions to Drive Collective Cell Migration
<p>In animals, cells often move as collectives to shape organs, close wounds, or—in the case of disease—metastasize. To accomplish this, cells need to generate force to propel themselves forward. The motility of singly migrating cells is driven largely by an interplay between Rho GTPase signaling and the actin network. Whether cells migrating as collectives use the same machinery for motility is unclear. Using the zebrafish posterior lateral line primordium as a model for collective cell migration, we find that active RhoA and myosin II cluster on the basal sides of the primordium cells and are required for primordium motility. Positive and negative feedbacks cause RhoA and myosin II activities to pulse. These pulses of RhoA signaling stimulate actin polymerization at the tip of the protrusions and myosin II-dependent actin flow and protrusion retraction at the base of the protrusions, and deform the basement membrane underneath the migrating primordium. This suggests that RhoA-induced actin flow on the basal sides of the cells constitutes the motor that pulls the primordium forward, a scenario that likely underlies collective migration in other—but not all—contexts.</p>
Glioblastoma cells increase expression of notch signaling and synaptic genes within infiltrated brain tissue
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.