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1,988 results for “proliferation”
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
Open the record for dataset details and reuse information.
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>
Characterization of intrauterine growth, proliferation and biomechanical properties of the murine larynx
<p>Raw data for all variables in study</p>
Germline proliferation trades off with lipid metabolism in Drosophila
<p>Little is known about the metabolic basis of life-history trade-offs but lipid stores seem to play a pivotal role. During reproduction, an energetically highly costly process, animals mobilize fat reserves. Conversely, reduced or curtailed reproduction promotes lipid storage in many animals. Systemic signals from the gonad seem to be involved: <em>C. elegans</em> lacking germline stem cells display endocrine changes, have increased fat stores and are long-lived. Similarly, germline-ablated <em>D. melanogaster </em>exhibit major somatic physiological changes, but whether and how germline loss affects lipid metabolism remains largely unclear. Here we show that germline-ablated flies have profoundly altered energy metabolism at the transcriptional level and store excess fat as compared to fertile flies. Germline activity thus constrains or represses fat accumulation, and this effect is conserved between flies and worms. More broadly, our findings confirm that lipids represent a major energetic currency in which costs of reproduction are paid.</p>
Raw Data for the article: miRNA expression analysis in the human heart: Undifferentiated progenitors vs. bioptic tissues-Implications for proliferation and ageing
<p>In developed countries, cardiovascular diseases are currently the first cause of death. Cardiospheres (CSs) and cardiosphere-derived cells (CDCs) have been found to have the ability to regenerate the myocardium after myocardial infarction (MI). In recent years, much effort has been made to gain insight into the human heart repair mechanisms, in which miRNAs have been shown to play an important role. In this regard, to elucidate the involvement of miRNAs, we evaluated the miRNA expression profile across human heart biopsy, CSs and CDCs using microarray and next-generation sequencing (NGS) technologies. We identified several miRNAs more represented in the progenitors, where some of them can be responsible for the proliferation or the maintenance of an undifferentiated state, while others have been found to be downregulated in the undifferentiated progenitors compared with the biopsies. Moreover, we also found a correlation between downregulated miRNAs in CSs/CDCs and patient age (eg miR-490) and an inverse correlation among miRNAs upregulated in CSs/CDCs (eg miR-31).</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>
Long-term proliferation of large annual thistles in dry Mediterranean rangelands
<p><strong>Data set 1</strong>: 2005-2018, climate, treatments, total plot biomass, <em>Carthamus</em> <em>glaucus </em>cover & biomas, <em>Scolymus maculatus </em>cover & biomass</p> <p><strong>Data set 2</strong>: 2019, treatments, <em>Carthamus glaucus </em>biomas, <em>Scolymus maculatus </em>biomass</p>
An in vivo stable isotope labeling method to investigate individual matrix protein synthesis, ribosomal biogenesis, and chondrocyte proliferation in murine articular cartilage
<p>These experiments have used a stable-isotope method using <em>in vivo</em> deuterium oxide labeling and mass spectrometry to measure protein concentration, protein half-life, cell proliferation, and ribosomal biogenesis in a single sample of murine articular cartilage. We hypothesized that a 60-day labeling period would capture age-related declines in cartilage matrix protein content, protein synthesis rates, and chondrocyte proliferation. Knee cartilage was isolated from 25- and 90-week-old female C57BL/6J mice treated with deuterium oxide for 15, 30, 45 and 60 days. We measured protein abundance and half-lives using high resolution accurate mass spectrometry (HRAM) and d2ome data processing software. </p>
Supplementary code and data for: Symbiotic bacteria and fungi proliferate during diapause and may enhance overwintering survival in a solitary bee
<div> <div> <div> <p>Host-microbe interactions underlie the development and fitness of many macroorganisms, including bees. Whereas many social bees benefit from vertically transmitted gut bacteria, current data suggests that solitary bees, which comprise the vast majority of species diversity within bees, lack a specialized gut microbiome. Here we examine the composition and abundance of bacteria and fungi throughout the complete life cycle of the ground-nesting solitary bee Anthophora bomboides standfordiana. In contrast to expectations, immature bee stages maintain a distinct core microbiome consisting of Actinobacterial genera (Streptomyces, Nocardiodes) and the fungus Moniliella spathulata. Dormant (diapausing) larval bees hosted the most abundant and distinctive bacteria and fungi, attaining 33 and 52 times their initial copy number, respectively. We tested two adaptive hypotheses regarding microbial functions for diapausing bees. First, using isolated bacteria and fungi, we found that Streptomyces from brood cells inhibited the growth of multiple pathogenic filamentous fungi, suggesting a role in pathogen protection during overwintering, when bees face high pathogen pressure. Second, sugar alcohol composition changed in tandem with major changes in fungal abundance, suggesting links with bee cold tolerance or overwintering biology. We find that Anthophora bomboides hosts a conserved core microbiome that may provide key fitness advantages through larval development and diapause, which raises the question of how this microbiome is maintained and faithfully transmitted between generations. Our results suggest that focus on microbiomes of mature or active insect developmental stages may overlook stage-specific symbionts and microbial fitness contributions during host dormancy.</p> </div> </div> </div>
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>
Membrane rigidity regulates E. coli proliferation rates
<p>Combining single cell experiments, population dynamics and theoretical methods of membrane mechanics, we put forward that the rate of cell proliferation in E. coli colonies can be regulated by modifiers of the mechanical properties of the bacterial membrane. Bacterial proliferation was modelled as mediated by cell division through a membrane constriction divisome based on FtsZ, a mechanically competent protein at elastic interaction against membrane rigidity. Using membrane fluctuation spectroscopy in the single cells, we revealed either membrane stiffening when considering hydrophobic long chain fatty substances, or membrane softening if short-chained hydrophilic molecules are used. Membrane stiffeners caused hindered growth under normal division in the microbial cultures, as expected for membrane rigidification. Membrane softeners, however, altered regular cell division causing persistent microbes that abnormally grow as long filamentous cells proliferating apparently faster. We invoke the concept of effective growth rate under the assumption of a heterogeneous population structure composed by distinguishable individuals with different FtsZ-content leading the possible forms of cell proliferation, from regular division in two normal daughters to continuous growing filamentation and budding. The results settle altogether into a master plot that captures a universal scaling between membrane rigidity and the divisional instability mediated by FtsZ at the onset of membrane constriction.</p> <p><br> </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>
Infection with 'Candidatus Liberibacter asiaticus' improves the fecundity of Diaphorina citri aiding its proliferation: a win-win strategy
<p>The coevolution between insect vectors and pathogens has long been of interest in molecular ecology and evolutionary biology, and <em>Diaphorina citri</em> is the main insect vector of the bacterium, ‘<em>Candidatus</em> Liberibacter asiaticus’ (<em>C</em>Las), the putative cause of the severe Asian form of huanglongbing. <em>C</em>Las-positive <em>D. citri</em> are more fecund than their <em>C</em>Las-negative counterparts; however, the molecular mechanism underlying of increased fecundity remains unclear. Here, we found that <em>C</em>Las promoted ovarian development and increased the expression of the <em>vitellogenin</em> <em>receptor</em> (<em>Dc</em><em>VgR</em>) in ovaries. <em>Dc</em><em>VgR</em> RNAi significantly decreased fecundity and <em>C</em>Las titer in ovaries, extended the preoviposition period, shortened the oviposition period, and blocked ovarian development. Combined <em>in vivo</em> and <em>in vitro</em> experiments showed that miR-275 suppressed <em>Dc</em><em>VgR</em> expression by binding to its 3’ untranslated region. Overexpression of miR-275 resulted in a decline of <em>Dc</em><em>VgR</em> expression and <em>C</em>Las titer in ovaries and caused reproductive defects that mimicked <em>Dc</em><em>VgR</em> knockdown phenotypes. After infection with <em>C</em>Las, the juvenile hormone (JH) signaling pathway was upregulated thereby increasing <em>Dc</em><em>VgR</em> expression via the JH receptor, <em>methoprene-tolerant</em> (Met), and downstream key transcription factor <em>Krüppel homolog 1</em>. As a result, <em>C</em>Las hijacks the JH signaling pathway and host miR-275 that targets <em>Dc</em><em>VgR</em> to improve <em>D. citri</em> fecundity, while simultaneously increasing the replication of <em>C</em>Las itself, suggesting a mutualistic interaction in <em>D. citri </em>ovaries with <em>C</em>Las.</p>
Supplemental data to "Acute and persistent effects of oral glutamine supplementation on growth, cellular proliferation, and tight junction protein transcript abundance in jejunal tissue of low and normal birthweight pre-weaning piglets"
<p>Supplementary data to "Acute and persistent effects of oral glutamine supplementation on growth, cellular proliferation, and tight junction protein transcript abundance in jejunal tissue of low and normal birthweight pre-weaning piglets"</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)
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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.