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1,988 results for “proliferation”
Data: DEAE-Dextran enhances the lentiviral transduction of primary human mesenchymal stromal cells from all major tissue sources without affecting their proliferation and phenotype
<p>This data set includes all the raw data collected for the following article: "DEAE-Dextran enhances the lentiviral transduction of primary human mesenchymal stromal cells from all major tissue sources without affecting their proliferation and phenotype"</p>
Underlying data for: "Capturing the mechanosensitivity of cell proliferation in models of epithelium"
<p>For our publication "Capturing the mechanosensitivity of cell proliferation in models of epithelium" (available as a preprint at <a title="BioRXiv Link" href="https://doi.org/10.1101/2023.01.31.526438" target="_blank" rel="noopener">DOI: 10.1101/2023.01.31.526438 )</a> we here provide the raw data for the included plots and the code used to generate the Delayed Fisher Kolmogorov (DFK) data referenced in the main publication</p> <p>The archive '<em>underlying_data.zip</em>' contains raw data underlying the plots in the publication. <br>The archive '<em>puls_proliferation_rate-1.0.zip</em>' contains the code for generating DFK trajectories referenced in the publication and its SI. <br>The archive '<em>ddesolver-1.0.zip</em>' contains the python code for solving delayed differential equations used by the puls_proliferation_rate project. It is included to ensure completeness and reproducibility of the simulations. </p>
Transcriptome analysis of the effect of over-expressing H2A.J mutants in proliferating WI38 fibroblasts for the paper entitled: The H2A.J histone variant contributes to Interferon-Stimulated Gene expression in senescence by its weak interaction with H1 and the derepression of repeated DNA sequences
<p>Abstract for overall study:</p> <p>The histone variant H2A.J was previously shown to accumulate in senescent human fibroblasts with persistent DNA damage to promote inflammatory gene expression, but its mechanism of action was unknown. We show that H2A.J accumulation contributes to weakening the association of histone H1 to chromatin and increasing its turnover. Decreased H1 in senescence is correlated with increased expression of some repeated DNA sequences, increased expression of STAT/IRF transcription factors, and transcriptional activation of Interferon-Stimulated Genes (ISGs). The H2A.J-specific Val-11 moderates the transcriptional activity of H2A.J, and H2A.J-specific Ser-123 can be phosphorylated in response to DNA damage with potentiation of its transcriptional activity by the phospho-mimetic S123E mutation. Our work demonstrates the functional importance of H2A.J-specific residues and potential mechanisms for its function in promoting inflammatory gene expression in senescence.</p> <p>Specific description for this dataset:</p> <p>H2A.J differs from canonical H2A only by a valine at position 11 instead of alanine, and the 7 C-terminal amino acids containing a potential minimal phosphorylation site SQ for DNA-damage response kinases. To test the functional importance of these H2A.J-specific sequences, we mutated Val-11 to Ala as is found in all canonical H2A sequences, and we mutated Ser-123 to either Glu to mimic a phospho-serine residue or to Ala to prevent phosphorylation. We also substituted the C-terminus of H2A.J with the C-terminus of H2A. These mutants, WT-H2A.J and canonical H2A-type1 were ectopically expressed in proliferating fibroblasts, and their microarray transcriptomes were compared to that of proliferating and senescent fibroblasts without ectopic histone expression. Genome-wide transcriptome analysis indicated that senescent fibroblasts clustered distinctly from proliferating fibroblasts, and proliferating fibroblasts expressing the H2A.J-V11A and H2A.J-S123E mutants clustered distinctly from fibroblasts expressing the other H2A.J mutants, WT-H2A.J, and H2A. Hallmark gene set enrichment analysis of the transcriptomes of fibroblasts expressing H2A.J-V11A or H2A.J-S123E versus control proliferating fibroblasts indicated that they showed the same highly significant enrichment for the Epithelial-Mesenchyme Transition, TNF-Alpha Signaling Via NF-kB, and Inflammatory Response gene sets. Notable inflammatory genes including IL1A, IL1B, IL6, CXCL8, and CCL2 are contained in these gene sets and are often induced in senescence as part of the senescence-associated secretory phenotype. Heat maps showed that the H2A.J-V11A and H2A.J-S123E mutants were particularly apt at activating the expression of these inflammatory genes in proliferating fibroblasts</p>
Code and data from "Mother cells control daughter cell proliferation in intestinal organoids to minimize proliferation fluctuations"
<p>Includes the microscopy images, cell tracking data and scripts used in the publication Huelsz-Prince, Guizela, et al. "Mother cells control daughter cell proliferation in intestinal organoids to minimize proliferation fluctuations." <em>eLife </em> 11:e80682 (2022). <a href="https://doi.org/10.7554/eLife.80682"> https://doi.org/10.7554/eLife.80682</a> .</p>
Data_Figure 2_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 2 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 (10.1007_s00018-019-03227-w_CMLS_Fig2). Corresponding raw data obtained from a) Migration potential as four files in CSV format (31003A-179400_ date_examiner_17BHSD12_16_1_1-4. b) mRNA content analyzed by RT-PCR provided as ten files in CSV format (31003A-179400_date_examiner_17BHSD12_1_1-2_1-6) and proliferation investigation on xCELLigence provided as six files in CSV format (31003A-179400_date_examiner_17BHSD12_9_2_1-6). All further experiment related information and subsequent data analysis provided as four meta-data-files (31003A-179400_ date_examiner_17BHSD12_16/1/9_dataset_M_1) as TXT format.</p>
Data_Figure 6_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 6 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. 6). Corresponding raw data obtained from a1/2) cellomics HTC array scan analysis provided as six files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_6_1-6), b1/2) oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) provided as 10 files in CSV format (31003A-179400_20190521_MT_17BHSD12_10_3-4_1-5); c 1/2 ), cellomics HTC array scan analysis provided as 12 files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_7-8_1-8). d) Western blot and densitometry provided as eight files in CSV format (31003A-179400_Date_examiner_17BHSD12_2_3-4_1-5). All further experiment related information protocols and subsequent data analysis provided as meta-data-files (31003A-179400_date_examiner_17BHSD12_8/10/2_dataset_M_1) as TXT format and (31003A-179400_date_examiner_17BHSD12_2_dataset_M_2-3) as PNG format.</p>
Data_Figure 7_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 7 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. 7). Corresponding raw data obtained from a1/2) Western blot and densitometry provided as eight files in CSV format (31003A-179400_date_examiner_17BHSD12_2_5-6_1-6); b) mRNA content analyzed by RT-PCR provided as four files in CSV format (31003A-179400_date_examiner_17BHSD12_1_6_1-4); c 1/2) cellomics HTC array scan analysis provided as 11 files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_9-10_1-6); d1/2); Western blot and densitometry provided as eight files in CSV format (31003A-179400_date_examiner_17BHSD12_2_7-8_1-6). All further experiment related information protocols and subsequent data analysis provided as meta-data-files (31003A-179400_date_examiner_17BHSD12_2/1/8_dataset_M_1) as TXT format and (31003A-179400_date_examiner_17BHSD12_2_dataset_M_2-3) as PNG format.</p>
Data_Figure 5_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 5 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. 5). Corresponding raw data obtained from oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) provided as 10 files in CSV format (31003A-179400_20190521_MT_17BHSD12_10_1-2_1-5). All further experiment related information and subsequent data analysis provided as two meta-data-file: (31003A-179400_20190521_MT_17BHSD12_10_1-2_1) as TXT format.</p>
Data_Figure 4_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 4 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. 4). Corresponding raw data obtained from: a1/2) Migration potential as five files in CSV format (31003A-179400_date_examiner_17BHSD12_16_3_1-5); b 1/2) Migration potential as four files in CSV format (31003A-179400_date_examiner_17BHSD12_16_4_1-4); c1/2/3) mRNA content analyzed by RT-PCR provided as four files in CSV format (31003A-179400_date_examiner_17BHSD12_1_4_1-4); cellomics HTC array scan analysis provided as three files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_3-4_1-4); d) Migration potential as five files in CSV format (31003A-179400_ date_examiner_17BHSD12_16_5_1-5); e) mRNA content analyzed by RT-PCR provided as six files in CSV format (31003A-179400_date_examiner_17BHSD12_1_5_1-6); f) Migration potential as four files in CSV format (31003A-179400_date_examiner_17BHSD12_16_6_1-4), cellomics HTC array scan analysis provided as three files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_5_1-5); g) ELISA measurement provided as four files in CSV format (31003A-179400_date_examiner_17BHSD12_20_1_1-4). All further experiment related information protocols and subsequent data analysis provided as 10 meta-data-files (31003A-179400_date_examiner_17BHSD12_8/16/1/20_dataset_M_1) as TXT format.</p>
Data_supplemental figure 2_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 supplemental figure 2 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. S2). Corresponding raw data obtained from cellomics HTC array scan analysis provided as seven files in CSV format (31003A-179400_Date_examiner_17BHSD12_8_11-12_1-4) All further experiment related information protocols as meta-data-files (31003A-179400_date_examiner_17BHSD12_8_11-12_M_1) as TXT format.</p>
Taxonomy of barriers that hinders Local Flexibility Market proliferation
<p>This dataset contains the results of the state of the art survey to retrieve the barriers that that hinders Local Flexibility Market proliferation. Scientific literature, interviews with different stakeholders, technical reports from the main energy agencies and the European and national legislation have been consulted to build the taxonomy. Three files are provided:</p> <ul> <li>a spreadsheet with the list of barriers and the document were it is found and</li> <li>a diagram with the end taxonomy of barriers</li> <li>a document with an explanation of the barriers included in each category of the taxonomy</li> </ul>
Prioritization of barriers that hinders Local Flexibility Market proliferation
<p>This dataset contains the prioritization provided by a panel of 15 experts to a set of 28 barriers categories for 8 different roles of the future energy system. A Delphi method was followed and the scores provided in the three rounds carried out are included. The dataset also contains the scripts used to assess the results and the output of this assessment. </p> <p>A list of the information contained in this file is:</p> <ul> <li> <p><strong>data folder</strong>: this folders includes the scores given by the 15 experts in the 3 rounds. Every round is in an individual folder. There is a file per expert that has the scores between -5 (not relevant at all) to 5 (completely relevant) per barrier (rows) and actor (columns). There is also a file with the description of the experts in terms of their position in the company, the type of company and the country.</p> </li> <li> <p><strong>fig folder</strong>: this folder includes the figures created to assess the information provided by the experts. For each round, the following figures are created (in each respective folder):</p> <ul> <li> <p>Boxplot with the distribution of scores per barriers and roles. </p> </li> <li> <p>Heatmap with the mean scores per barriers and roles.</p> </li> <li> <p>Boxplots with the comparison of the different distributions provided by the experts of each group (depending on the keywords) per barrier and role.</p> </li> <li> <p>Heatmap with the mean score per barrier weighted depeding on the importance of the role in each use case and the final prioritization.</p> </li> </ul> </li> </ul> <p>Finally, bar plots with the mean scores differences between rounds and boxplot with comparisons of the scores distributions are also provided.</p> <ul> <li> <p><strong>stat folder</strong>: this folder includes the files with the results of the different statistical assessment carried out. For each round, the following figures are created (in each respective folder):</p> <ul> <li> <p>The statistics used to assess the scores (Intraclass correlation coefficient, Inter-rater agreement, Inter-rater agreement p-value, Homogeneity of Variances, Average interquartile range, Standard Deviation of interquartile ranges, Friedman test p-value Average power post hoc) per barrier and per role.</p> </li> <li> <p>The results of the post hoc of the Friedman Test per berries and per roles.</p> </li> <li> <p>The average score per barrier and per role.</p> </li> <li> <p>The mean value of the scores provided by the experts grouped by the keywords per barrier and role. P-value of the comparison of these two values.</p> </li> <li> <p>The end prioritization of the barrier for the use case (averaging the scores or fuzzy merging of the critical sets)</p> </li> </ul> </li> </ul> <p>Finally, the differences between the mean and standard deviations of the scores between two consecutive rounds are provided.</p>
Data from: Predation drives the evolution of brain cell proliferation and brain allometry in male Trinidadian killifish, Rivulus hartii
<p>The external environment influences brain cell proliferation, and this might contribute to brain plasticity underlying adaptive behavioural changes. Additionally, internal genetic factors influence brain cell proliferation rate. However, to date, researchers have not examined the importance of environmental vs. genetic factors in causing natural variation in brain cell proliferation. Here, we examine brain cell proliferation and brain growth trajectories in free-living populations of Trinidadian killifish, Rivulus hartii, exposed to contrasting predation environments. Compared to populations without predators, populations in high predation environments exhibited higher rates of brain cell proliferation and a steeper brain growth trajectory (relative to body size). To test whether these differences in the wild persist in a common garden environment, we reared first generation fish originating from both predation environments in uniform laboratory conditions. Just as in the wild, brain cell proliferation and brain growth in the common garden were greater in high predation populations than in no predation populations. The similar results in field and common garden studies indicate that population differences in these brain features are intrinsic, probably genetic, differences arising from natural selection acting on overall brain growth and life history rather than differences arising through phenotypic plasticity.</p>
Gene expression data and proliferation rates for NCI-60
<p>Data set dimensions: 57 rows x 54357 columns</p> <p> </p> <p>This is a data set contains RMA normalized log expression values for 54356 genes identified with their ENSEMBL ID (columns 1-54356) for 57 cancer cell lines and their respective proliferation rates (column 54357).</p> <p>Gene expression was obtained from the GSE29682 GEO HuEx 1.0 ST microarray data.</p>
Figure 4 in Investigation the effects of vitreous humor on proliferation and dedifferentiation of differentiated NTERA2 cells
Figure 4. Western blot analysis show that the NT2 cells are known as perfectly positive cells for OCT4 protein expression.
Figure 2 in Investigation the effects of vitreous humor on proliferation and dedifferentiation of differentiated NTERA2 cells
Figure 2. Cell cycle analysis of NT2-RA cells after treatment with different amounts of VH at (A) 3 days and (B) 6 days post-treatment. After treatment with RA the number of cells at S phase decreased. These numbers were recovered after three and six days treatment with different amounts of VH.
Figure 5 in Optimizing in vitro factors for improvement of shoot proliferation of 'Flordaguard' peach rootstock
Figure 5. Shoots proliferation from node explant of 'Flordaguard' peach rootstock cultured in semi-solid MS-½N (without PGR). A. Mean number of shoots per explant; B. number of elongated shoots; C. and mean length of shoots obtained in half strength MS (½N) – double-phase under different concentrations of BAP (0.5–3.0 mg L-1) for 'Flordaguard' peach rootstock.
Figure 4 in Optimizing in vitro factors for improvement of shoot proliferation of 'Flordaguard' peach rootstock
Figure 4. Shoots proliferation from node explant of 'Flordaguard' peach rootstock cultured on full strength MS medium. A. Growth and development of isolated shoot with symptoms of hyperhydricity; B. Growth and development of multiple shoot with shoot-tip necrosis (STN).
Figure 3 in Optimizing in vitro factors for improvement of shoot proliferation of 'Flordaguard' peach rootstock
Figure 3. Shoot proliferation in 'Flordaguard' peach rootstock. A. Induction of multiple shoot in explants cultured in half strength MS (½N) containing 1.0 mg L-1 of GA and 1.0 g L-1 of activated charcoal (double-phase medium); B. Growth and development of isolated shoots after 20 3 days in double-phase medium.
◂Fig. 5 Gametogenesis in male and female Veneriserva pygoclava. A–D Semi-thin histological sections of female Veneriserva pygoclava, stained with toluidine blue. A Cross-section of a female Veneriserva. B Close-up of large mature oocytes without discernible nurse cells. C Developing oocytes attached to mesenteries (mes), and oogonia proliferating from the ventral side of the dorsal blood vessel (bv). D Details of vitellogenic oocytes and nurse cells. Arrowheads indicate brownstained yolk platelets and yolk bodies. E Live sperm cells captured in a light micrograph. F–G Cross-sections of male Veneriserva. Note the absence of a gut in the cross-sections. Abbreviations—ac acicula, acr acrosome, bv blood vessel, coe coelomic cavity, mes mesentery, nc nurse cell, nn nurse cell nucleus, nu sperm cell nucleus, Oo oocyte, on oocyte nucleus, sp spermatogonia, vnc ventral nerve cord in Hardly Venus's servant-morphological adaptations of Veneriserva to an endoparasitic lifestyle and its phylogenetic position within Dorvilleidae (Annelida)
◂Fig. 5 Gametogenesis in male and female Veneriserva pygoclava. A–D Semi-thin histological sections of female Veneriserva pygoclava, stained with toluidine blue. A Cross-section of a female Veneriserva. B Close-up of large mature oocytes without discernible nurse cells. C Developing oocytes attached to mesenteries (mes), and oogonia proliferating from the ventral side of the dorsal blood vessel (bv). D Details of vitellogenic oocytes and nurse cells. Arrowheads indicate brownstained yolk platelets and yolk bodies. E Live sperm cells captured in a light micrograph. F–G Cross-sections of male Veneriserva. Note the absence of a gut in the cross-sections. Abbreviations—ac acicula, acr acrosome, bv blood vessel, coe coelomic cavity, mes mesentery, nc nurse cell, nn nurse cell nucleus, nu sperm cell nucleus, Oo oocyte, on oocyte nucleus, sp spermatogonia, vnc ventral nerve cord
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