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1,242 results for “Cell proliferation”
Fig. 10 in Effects of Roscovitine on Schedule of Divisional Morphogenesis, Basal Bodies Proliferation and Cell Divisions in Tetrahymena thermophila
Fig. 10. Western blot of T. thermophila fractions with monoclonal antibody anti-cdc14A. H – homogenate, S – supernatant, C – cortical fraction (pellet).
Data sets for de Oliveira et al.: "Leishmania major telomerase RNA knockout: from altered cell proliferation to decreased parasite infectivity"
<p><strong><span>This file contains relevant data about the article: "</span></strong><em><span>Leishmania major</span></em><strong><span> telomerase RNA knockout: from altered cell proliferation to decreased parasite infectivity"</span></strong></p>
Processed data for "Characterising the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER"
<p>This dataset contains the processed data for the figures and analyses performed in the publication "Characterising the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER" from Lucas O., Ward S., Zaidi R., Bunkum A., ..., Zaccaria S. Nature genetics, in press, 2024.</p> <p>The processed data are separated into three respective folders:</p> <ul> <li>GT contains all the data related to the analysis of the generated ground truth datasets;</li> <li>NSCLC contains all the data related to the analysis of the NSCLC dataset;</li> <li>TNBC_HGSC contains all the data related to the analysis of the TNBC and HGSC datasets. </li> </ul>
Hydroxyurea inhibits proliferation and stimulates apoptosis through inducible nitric oxide synthase in erythroid cells.
<p><a name="_Hlk164856369"></a><span>Hydroxyurea (HU) arrests cells in S-phase through the inhibition of ribonucleotide reductase and DNA synthesis, which is contributed significantly by the release of nitric oxide (NO). </span><span><span>W</span></span><span><span>e investigated the mediation of inducible NO synthase (NOS2) in HU c</span></span><span><span>ytostatic effects</span></span><span><span>, <a name="_Hlk165036602"></a>using <em>in vitro</em> shRNA-induced knock-down of NOS2 or </span></span><span><span><span>specific</span></span></span><span><span><span> </span></span></span><span><span><span>NOS2 inhibitor (1400W), and supported by Nos2 knockout mice (Nos2<sup>-/-</sup>) to observe <em>ex vivo</em> murine erythroid progenitors (mERP).</span></span><a name="_Hlk165036694"></a></span><span><span><span>As a long-term effect, HU increased NOS2 expression in human erythroleukemic HEL92.1.7 cells (via NFκB signaling) and mERP. As a short-term result, HU increased the activity of purified and HEL92.1.7 cell-derived NOS2</span></span></span><span><span>, as confirmed by NO / citrulline production and <em>in silico</em> molecular docking via hydrogen bonds.</span> </span><span><span>Molecular dynamic simulation showed a slight decrease in NOS2 receptor rigidity upon HU binding, confirming the stability of HU at the active site of the NOS2 receptor. Both 1400W and shRNA prevented the <em>in vitro</em> reduction of proliferation and induction of apoptosis of HEL92.1.7 cells by HU. Thus, shRNA blocked preferentially early apoptosis and only shRNA overcame HU-induced S-phase arrest of HEL92.1.7 cells. Both 1400W and Nos2 knockout prevented the <em>in vivo</em> decrease in proliferation and induction of apoptosis of mERP by HU from wild-type and Nos2-/- mice, respectively. Therefore, HU increased NOS2 activity and expression via NFκB signaling. This study demonstrated the NOS2 dependance in the HU inhibition of</span></span><span><span> </span></span><span><span>proliferation and stimulation of</span></span><span><span> apoptosis of erythroid cells. </span></span></p>
Raw data for the article: Human Amnion Epithelial Cells Impair T Cell Proliferation: The Role of HLA-G and HLA-E Molecules
<p>The immunoprivilege status characteristic of human amnion epithelial cells (hAECs) has been recently highlighted in the context of xenogenic transplantation. However, the mechanism(s) involved in such regulatory functions have been so far only partially been clarified. Here, we have analyzed the expression of HLA-Ib molecules in isolated hAEC obtained from full term placentae. Moreover, we asked whether these molecules are involved in the immunoregulatory functions of hAEC. Human amnion-derived cells expressed surface HLA-G and HLA-F at high levels, whereas the commonly expressed HLA-E molecule has been measured at a very low level or null on freshly isolated cells. HLA-Ib molecules can be expressed as membrane-bound and soluble forms, and in all hAEC batches analyzed we measured high levels of sHLA-G and sHLA-E when hAEC were maintained in culture, and such a release was time-dependent. Moreover, HLA-G was present in extracellular vesicles (EVs) released by hAEC. hAEC suppressed T cell proliferation in vitro at different hAEC:T cell ratios, as previously reported. Moreover, inhibition of T cell proliferation was partially reverted by pretreating hAEC with anti-HLA-G, anti-HLA-E and anti-β2 microglobulin, thus suggesting that HLA-G and -E molecules are involved in hAEC-mediated suppression of T cell proliferation. Finally, either large-size EV (lsEV) or small-size EV (ssEV) derived from hAEC significantly modulated T-cell proliferation. In conclusion, we have here characterized one of the mechanism(s) underlying immunomodulatory functions of hAEC, related to the expression and release of HLA-Ib molecules.</p>
Data_Figure4_Loss of Claudin-3 Impairs Hepatic Metabolism, Biliary Barrier Function, and Cell Proliferation in the Murine Liver
<p>Data of Figure 4 from “Loss of Claudin-3 Impairs Hepatic Metabolism, Biliary Barrier Function, and Cell Proliferation in the Murine Liver”</p> <p>Dataset (doi: 10.1016/j.jcmgh.2021.04.003) contains the original publication as PDF-format (10.1038_s41598-020-59701-0). Corresponding raw data obtained from LC-MS/MS analysis provided as two files in CSV format (31003A-179400_10.1016j.jcmgh.2021.04.003_CGC_4-1.csv, 31003A-179400_10.1016j.jcmgh.2021.04.003_CGC_4-2.csv). All further experiment related information provided as two meta-data-files (31003A-179400_10.1016j.jcmgh.2021.04.003_CGC _4_1-2_M_1.PDF, 31003A-179400_10.1016j.jcmgh.2021.04.003_CGC _4_1-2_M_2.PDF) as PDF format.</p>
Figure 3 in The study of exposure times and dose-escalation of tick saliva on mouse embryonic stem cell proliferation
Figure 3. Effect of D. marginatus SGE (0-160 µg/ml) on mouse embryonic stem cell proliferation and viability. Values represent relative fold change of cell viability normalized to untreated negative control. The Geisser–Greenhouse correction and Dunnett´s test on multiple comparison were used. All experiments have the P value <0.05, on three different time laps. The results are mean ± standard deviation (SD) from a representative experiment carried out in triplicate and were seeded in equal amount in 3 different 96-well cultured plates.
Figure 2 in The study of exposure times and dose-escalation of tick saliva on mouse embryonic stem cell proliferation
Figure 2. Effect of R. bursa SGE (0-160 µg/ml) on mouse embryonic stem cell proliferation and viability. Values represent relative fold change of cell viability normalized to untreated negative control. The Geisser–Greenhouse correction and Dunnett´s test on multiple comparison were used. The results are mean ± standard deviation (SD) from a representative experiment carried out in triplicate and were seeded in equal amount in 3 different 96-well cultured plates.
Data from: Predation drives the evolution of brain cell proliferation and brain allometry in male Trinidadian killifish, Rivulus hartii
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Data from: Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells
<p>CSV files of whole-Genome Knockout Screens for Proliferation and Tumorigenic Growth. The data is retrieved from:</p> <p>Title: "Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells"</p> <p>DOI: https://doi.org/10.1016/j.celrep.2020.03.029</p> <p>The excel sheet with data shown in figure 1B is converted to CSV files.</p>
Light counteracts microgravity alterations in plant proliferating cells
<p><b>Premise:</b> Light and gravity are fundamental cues for plant development. In space, without gravity, understanding the role of a light stimulus is key for enabling plant acclimation to extraterrestrial environment. Here we tested the hypothesis that the alterations caused by the absence of gravity in root meristematic cells can be counteracted by light.</p> <p><b>Methods: </b>Seedlings of <i>Arabidopsis thaliana</i> wild type and two mutants of the essential nucleolar protein nucleolin <i>(nuc1, nuc2)</i> were grown in simulated microgravity, either under a white light photoperiod, or under continuous darkness. Key parameters of cell proliferation (cell cycle regulation) and cell growth (ribosome biogenesis), as well as of auxin transport, were measured in the root meristem using in situ cellular markers and transcriptomic methods, compared with a 1<i>g</i> control.</p> <p><b>Results:</b> The incorporation of a photoperiod regime has been sufficient to attenuate or suppress the effects caused by gravitational stress at the cellular level in the root meristem. In all cases, parameters recorded from samples receiving light stimuli in simulated microgravity were closer to 1<i>g </i>values than those obtained from samples grown in darkness. Differential results were obtained in the two nucleolin mutants.</p> <p><b>Conclusions: </b>Light signals may totally or partially replace gravity signals, significantly improving plant growth and development in microgravity. Despite that, molecular alterations are still compatible with the expected acclimation mechanisms that should be better understood. The differential sensitivity of <i>nuc1</i> and <i>nuc2</i> mutants to gravitational stress points to new strategies to produce more resilient plants to travel with humans in new extraterrestrial endeavors.</p>
Efficient improvement of the proliferation, differentiation, and anti-arthritic capacity of mesenchymal stem cells by simply culturing on the immobilized FGF2 derived peptide, 44-ERGVVSIKGV-53
<p>All data needed to evaluate the results presented in the paper: Soo Bin Lee, Ahmed Abdal Dayem, Sebastian Kmiecik, Kyung Min Lim, Dong Sik Seo, Hyeong-Taek Kim, Polash Kumar Biswas, Minjae Do, Deok-Ho Kim, Ssang-Goo Cho, Efficient improvement of the proliferation, differentiation, and anti-arthritic capacity of mesenchymal stem cells by simply culturing on the immobilized FGF2 derived peptide, 44-ERGVVSIKGV-53,<br>Journal of Advanced Research, Volume 62,<br>2024,<br>Pages 119-141,<br>ISSN 2090-1232,<br>https://doi.org/10.1016/j.jare.2023.09.041.</p>
Extraordinarily rapid proliferation of cultured muscle satellite cells from migratory birds
<p>Migratory birds experience bouts of muscle growth and depletion as they prepare for, and undertake prolonged flight. Our studies of migratory bird muscle physiology <i>in vitro</i> led to the discovery that sanderling (<i>Calidris alba</i>) muscle satellite cells proliferate more rapidly than other normal cell lines. Here we determined the proliferation rate of muscle satellite cells isolated from five migratory species (sanderling; ruff, <i>Calidris pugnax</i>; western sandpiper, <i>Calidris mauri</i>; yellow-rumped warbler, <i>Setophaga coronata</i>; Swainson's thrush, <i>Catharus ustulatus</i>) from two families (shorebirds and songbirds) and with different migratory strategies. Ruff and sanderling satellite cells exhibited rapid proliferation, with population doubling times of 9.3±1.3 and 11.4±2.0 hrs whereas the remaining species' cell doubling times were ≥24 hrs. The results indicate that the rapid proliferation of satellite cells is not associated with total migration distance but may be related to flight bout duration and interact with lifespan.</p>
Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
<p class="MsoNormal"><span>Endogenous </span><span>humoral factors </span><span>that</span><span> link systemic and/or local insulin demand to pancreatic β-cells have not been identified. Here</span><span>,</span><span> we demonstrated that T-cadherin, a unique glycosylphosphatidylinositol-anchored cadherin primarily expressed in vascular endothelial cells and cardiac and skeletal muscle cells, but not in pancreatic β-cells, was secreted as soluble forms and was important for β-cell proliferation. <em>Cdh13</em> (T-cadherin) knockout mice exhibited impaired glucose handling due to attenuated β-cell proliferation under high-fat diet conditions. The gene expression analyses indicated the impairment in cell cycle and Notch signaling in the islets of T-cadherin knockout mice under high-fat diet conditions. In streptozotocin-induced diabetes, the replacement of soluble T-cadherin improved β-cell mass and blood glucose </span><span>levels</span><span> in T-cadherin knockout mice. </span><span>R</span><span>ecombinant soluble T-cadherin upregulated Notch signaling in cultured murine islets. We concluded that soluble T-cadherin could work as an endogenous humoral factor whose signaling pathways including Notch signaling regulate β-cell proliferation under diabetic conditions in mice.</span></p>
Light counteracts microgravity alterations in plant proliferating cells
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Data from: NEK4 suppresses cell proliferation in BT20 triple-negative breast cancer cells by diminishing expression of cell cycle genes, while its depletion mitigates proliferation in other cell lines
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Extraordinarily rapid proliferation of cultured muscle satellite cells from migratory birds
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Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
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Sphingosine-1-phosphate signaling regulates the ability of Müller glia to become neurogenic, proliferating progenitor-like cells
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Data_Figure 3_Impact of 17β‑HSD12, the 3‑ketoacyl‑CoA reductase of long‑chain fatty acid synthesis, on breast cancer cell proliferation and migration
<p>Data of figure 3 from Impact of 17β‑HSD12, the 3‑ketoacyl‑CoA reductase of long‑chain fatty acid synthesis, on breast cancer cell proliferation and migration</p> <p>Dataset (doi: 10.1007/s00018-019-03227-w) contains the original figure as TIF-format (10.1194_jlr.M092908_Fig. 3). Corresponding raw data obtained from a) cellomics HTC array scan analysis provided as three files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_2_1-3). Migration potential as three files in CSV format (31003A-179400_ date_examiner_17BHSD12_16_2_1-3); b) mRNA content analyzed by RT-PCR provided as six files in CSV format (31003A-179400_date_examiner_17BHSD12_1_3_1-6); c) western blot and densitometry provided as eight files in CSV format 31003A-179400_date_examiner_2_1-2_1-8). All further experiment related information protocols and subsequent data analysis provided as meta-data-files (31003A-179400_date_examiner_17BHSD12_8/16/1_dataset_M_1) as TXT format and (31003A-179400_date_examiner_17BHSD12_2_dataset_M_2-3) as PNG format.</p>
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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.