Find research datasets worth reusing

opennotspecifiedNov 2019View details →

F I G U R E 6 in Characterisation of stem and proliferating cells on the retina and lens of loach Misgurnus anguillicaudatus

F I G U R E 6 The immunohistochemistry of (a), (b) peroxisome proliferator-activated receptor (PPAR)α and (c), (d) PPARγ in the eye () of Misgurnus anguillicaudatus. The main sites for PPARα expression were ganglion cell layer, inner plexiform, outer plexiform and visual layers. R, Retina; C, cornea; L, lens (L); GCL, ganglion cell layer; IP, inner plexiform IN, inner nuclear; OP, outer plexiform; ON, outer nuclear; vl, photoreceptor layer; PE, pigment epithelium layer (PE). The total number of fish used was n = 5

opencc-by-4.0Dec 2021View details →

tRNA-derived fragment tRF-Glu49 inhibits cell proliferation, migration and invasion in cervical cancer by targeting FGL1

A transfer RNA (tRNA)-derived fragment was found to be a new possible biological marker and target in carcinoma therapy. However, the effect exerted by tRFs on cervical carcinoma is still unclear. We identify the potential tumor suppressor gene tRF-Glu49 in cervical carcinoma through tRF and ti-RNA microarray investigation. We then demonstrated that tRF-Glu49 showed downregulation within the cervical carcinoma tissue and was associated with less aggressive clinical features and a better prognosis. Phenotypic studies revealed that tRF-Glu49 inhibited cervical cell proliferation, migration, and invasion processes. Mechanistic investigation revealed that tRF-Glu49 directly regulated the oncogene, fibrinogen-like protein-1 (FGL1). In general, according to the result achieved in this study, tRF-Glu49 can modulate cervical cell proliferation, migration, and invasion processes through the target process for FGL1, and tRF-Glu49 is likely to be a possible prognostic biological marker in patients with cervical carcinoma.

opencc-by-4.0Jan 2022View details →

Oncogenic BRAF V600E induces glial proliferation through ERK and neuronal death through JNK

Raw Data Files for the manuscript entitled "Oncogenic BRAF V600E induces glial proliferation through ERK and neuronal death through JNK".

opencc-zeroMar 2022View details →

Cyclin F drives proliferation through SCF-dependent degradation of the retinoblastoma-like tumor suppressor p130/RBL2

Cell cycle gene expression programs fuel proliferation and are universally dysregulated in cancer. The retinoblastoma (RB)-family of proteins, RB1, RBL1/p107, and RBL2/p130, coordinately represses cell cycle gene expression, inhibiting proliferation, and suppressing tumorigenesis. Phosphorylation of RB-family proteins by cyclin-dependent kinases is firmly established. Like phosphorylation, ubiquitination is essential to cell cycle control, and numerous proliferative regulators, tumor suppressors, and oncoproteins are ubiquitinated. However, little is known about the role of ubiquitin signaling in controlling RB-family proteins. A systems genetics analysis of CRISPR/Cas9 screens suggested the potential regulation of the RB-network by cyclin F, a substrate recognition receptor for the SCF family of E3 ligases. We demonstrate that RBL2/p130 is a direct substrate of SCFcyclin F. We map a cyclin F regulatory site to a flexible linker in the p130 pocket domain, and show that this site mediates binding, stability, and ubiquitination. Expression of a mutant version of p130, which cannot be ubiquitinated, severely impaired proliferative capacity and cell cycle progression. Consistently, we observed reduced expression of cell cycle gene transcripts, as well a reduced abundance of cell cycle proteins, analyzed by quantitative, iterative immunofluorescent imaging. These data suggest a key role for SCFcyclin F in the CDK-RB network and raise the possibility that aberrant p130 degradation could dysregulate the cell cycle in human cancers.

opencc-by-4.0Mar 2022View details →

Dataset for Ligand-independent oligomerization of TACI is controlled by the transmembrane domain and regulates proliferation of activated B cells.

This data set provides: a) Details about plasmids used in this study. It is a pdf file, describing expressed sequences and other features of plasmids listed in Supplementary Table 2. b) An Excel file with data used to make graphs of the publication

opencc-by-4.0Mar 2022View details →

Dataser from paper "Proliferation of osteoblast precursor cells on the surface of TiO2 nanowires anodically grown on a -type biomedical titanium alloy"

Dataser from paper "Proliferation of osteoblast precursor cells on the surface of TiO2 nanowires anodically grown on a -type biomedical titanium alloy": - Contact Angle: Images and measurements. - Fluorescence Microscopy Images: Images. - MTT and pixel counting: Measurements.

opencc-zeroMar 2022View details →

Data from: Host sex modulates the energetics of pathogen proliferation and its dependence on environmental resources

Sex differences in immunity are predicted to underlie much of the frequently observed sex differences in the prevalence or severity of infection. We propose the additional hypothesis that differences in the ability of males and females to acquire and use resources will also affect how readily a pathogen can convert host energy into transmission stages, thereby contributing to sex differences in infection dynamics. To test this we manipulated the resource environment of male and female Daphnia magna by altering the availability of food and then exposed hosts to a bacterial pathogen. We measured the production of transmission spores and virulence via the reduction in life span, together with feeding rates and changes in mass-independent metabolic rate, as a measure of the intake and expenditure of energy during infection. When raised in the presence of high resource levels, females more readily allowed for resources in the environment to be translated to pathogen exploitation, as represented by increased spore production, greater virulence, and higher energy use. In contrast, the traits of infected males were robust to changes in resource availability. High food availability thus exaggerated the degree of sexual dimorphism observed between the sexes. It also modified the relationship between host energy use, virulence, and pathogen spore production for each sex. These results suggest that a host's resource environment can affect how a male or female is exploited by a pathogen and may thus be an additional factor driving sex-specific patterns of disease susceptibility or severity.

opencc-by-4.0May 2024View details →

Effect of gedunin on cell proliferation and apoptosis impact in skin melanoma cells A431 via PI3K/JNK signaling pathway

Open the record for dataset details and reuse information.

opennotspecifiedAug 2016View details →

FIGURE 1. Saprolegnia milanezii. A. Empty fusiform zoosporangium. B. Zoosporangium with internal proliferation and primary zoospore discharge. C in Saprolegnia milanezii sp. nov., a new species of Saprolegniales (Oomycota, Straminipila) from Brazil

FIGURE 1. Saprolegnia milanezii. A. Empty fusiform zoosporangium. B. Zoosporangium with internal proliferation and primary zoospore discharge. C. Basipetal renewal of the zoosporangium. D. Gemma functioning as zoosporangium. E. Proliferous gemmae. F. Gemma with several tubes for zoospore discharge. Scale bar = 10 μm.

opencc-zeroDec 2015View details →

Data from: Cell proliferation and migration during early development of a symbiotic scleractinian coral

In scleractinian reef-building corals, patterns of cell self-renewal, migration and death remain virtually unknown, limiting our understanding of cellular mechanisms underlying initiation of calcification, and ontogenesis of the endosymbiotic dinoflagellate relationship. In this study we pulse-labeled the coral Stylophora pistillata for 24 h with BrdU at four life stages (planula, early metamorphosis, primary polyp, and adult colony) to investigate coral and endosymbiont cell proliferation during development, while simultaneously recording TUNEL-positive, i.e. apoptotic, nuclei. In the primary polyp, the fate of BrdU-labeled cells was tracked during a 3 days chase. The pharynx and gastrodermis were identified as the most proliferative tissues in the developing polyp, and BrdU-labeled cells accumulated in the surface pseudostratified epithelium and the skeletogenic calicodermis during the chase, revealing cell migration to these epithelia. Surprisingly, the lowest cell turnover was recorded in the calicodermis at all stages, despite active, ongoing skeletal deposition. In dinoflagellate symbionts, DNA synthesis was systematically higher than in coral host gastrodermis, especially in planula and early metamorphosis. The symbiont to host cell ratio remained however constant, indicating successive post-mitotic control mechanisms by the host of its dinoflagellate density in early life stages, increasingly shifting to apoptosis in the growing primary polyp.

opencc-zeroAug 2021View details →

Data from: Poor endometrial proliferation after clomiphene is associated with altered estrogen action

Context: Suboptimal endometrial thickening is associated with lower pregnancy rates and occurs in some infertile women treated with clomiphene. Objective: To examine cellular and molecular differences in the endometrium of women with suboptimal versus optimal endometrial thickening following clomiphene. Design: Translational prospective cohort study from 2018-2020. Setting: University-affiliated clinic. Patients or Participants: Reproductive age women with unexplained infertility treated with 100mg of clomiphene cycle days 3-7 who developed optimal (≥8mm; n=6, controls) or suboptimal (<6mm; n=7, subjects) endometrial thickness. Interventions: Pre-ovulatory blood and endometrial sampling. Main outcome measures: Endometrial tissue architecture, abundance and location of specific proteins, RNA expression, ERa binding. Results: The endometrium of suboptimal subjects compared to optimal controls was characterized by a reduced volume of glandular epithelium (16% vs 24%, P=0.01), decreased immunostaining of markers of proliferation (PCNA, ki67) and angiogenesis (PECAM-1), increased immunostaining of pan-leukocyte marker CD45 and ERb, but decreased ERa immunostaining (all P<0.05). RNASeq identified 398 differentially expressed genes between groups. Pathway analysis of differentially expressed genes indicated reduced proliferation (Z-score= -2.2, P<0.01), decreased angiogenesis (Z-score = -2.87, P<0.001), increased inflammation (Z-score= +2.2, P<0.01), and ERb activation (Z-score= +1.6, P<0.001) in suboptimal subjects. ChIP-seq identified 6 genes bound by ERα that were differentially expressed between groups (P<0.01), some of which may play a role in implantation. Conclusions: Women with suboptimal endometrial thickness after clomiphene exhibit aberrant estrogen receptor expression patterns, architectural changes and altered gene and protein expression, suggesting reduced proliferation and angiogenesis in the setting of increased inflammation.

opencc-by-4.0Aug 2021View details →

Figure S2. Autophagy inhibitor bafilomycin A1 blocks proliferation of MEC-1 cells

MEC-1 cells (3 ×105 cells/mL) were labeled with CFSE and treated with vehicle control (0.1% DMSO; CTRL DMSO) or 10 nM and 100 nM bafilomycin A1 or for 72 h. Retention of CFSE was determined using flow cytometry. Data are means ±SEM of 2 independent experiments.

opencc-by-4.0Dec 2022View details →

Supplementary files for the article entitled: PIEZO2 promotes cell proliferation and metastasis in colon carcinoma through the SLIT2/ROBO1/VEGFC pathway

All results were analyzed using the Statistical Package for the Social Sciences version 20.0 (IBM Corporation, Armonk, NY, USA). The results of Schoenfeld residuals method were analyzed using the R 4.2.2 software and survminer package.

Fig. 5 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway

Fig. 5. Nerolidol suppressed the protein and mRNA expression of ATM in rat leiomyoma cells. (A, B) ELT3 cells were treated with nerolidol for 48 h and were then harvested for the western blot analysis of phosphorylated ATM and total ATM (A) and for determining ATM mRNA expression using quantitative RT-PCR (B). GAPDH was used as the loading control. The inserted numbers in (A) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (C, D, E, F) ELT3 cells were treated with the indicated concentrations of KU-55933, an ATM inhibitor, for 48 h, following which the cells were harvested for further analysis. (C) The expression levels of p-ATMser1981, total ATM, p-Aktser473, total Akt, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) represent the relative expression level compared to that of the vehicle control (indicated as 0 μM). (D, E) Cell cycle analysis was performed after propidium iodide staining and FACS, and the results were analyzed using the FlowJo software (D). The percentages of cells in each cell cycle phase are plotted in (E). (F) Cell proliferation was determined using the MTT assay. DMSO (0.1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the control group.

Fig. 3 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway

Fig. 3. Nerolidol treatment led to the generation of intracellular ROS and impaired the mitochondrial membrane potential. (A) ELT3 cells were harvested after trypsin/EDTA treatment and then treated with 20 mM NAC, followed by DCFDA staining for 30 min. The cells were then treated with nerolidol for another additional 30 min, and DCF fluorescence was detected using flow cytometry. H2O2 was used as the positive control. The data were analyzed using the FlowJo software. (B, C) ELT3 cells were harvested and treated with nerolidol for 30 min. The cells were then stained with JC-1 dye for 15 min, followed by flow cytometry analysis. FCCP was used as the positive control. The data were analyzed using the FlowJo software. (B) The gated cells in the graphs indicate the cells with low mitochondrial membrane potential, and the quantitative results are plotted in (C). (D) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 5 mM NAC. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. (E) ELT3 cells were treated with the indicated concentration of nerolidol for 48 h with or without co-treatment with 20 μM ferrostatin-1. Cell proliferation was determined using the MTT assay. Ethanol (1 %) was used as the vehicle control. The data are presented as relative percentage compared to that of the vehicle control. The p-values were calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; ***, p <0.001 compared to the vehicle control group (C). ***, p <0.001 compared to the nerolidol single treatment group (D, E).

Fig. 4 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway

Fig. 4. Treatment with nerolidol triggered DNA damage in rat leiomyoma cells. (A, B) ELT3 cells were harvested and treated with 100 μM nerolidol for 30 min, followed by determination of DNA damage using the comet assay. H2O2 (200 μM) was used as the positive control. The tail moments are indicated by red arrows in (A), as quantified using a live video imaging system, and dot plots show the mean ± SD in (B). (C, D, E) ELT3 cells were treated with 100 μM nerolidol for 1 h, followed by incubation with anti-p-γH2AXser139 antibody and FITC-conjugated secondary antibody. Nuclei were visualized using DAPI (blue). (C) P-γH2AXser139 expression was quantified using an automated imaging system. The relative positive cell number and the nuclear p-γH2AXser139 intensities are plotted in (D) and (E), respectively. The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Fig. 2. Nerolidol induced G1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway

Fig. 2. Nerolidol induced G1 cell cycle arrest by downregulating Akt phosphorylation and cell cycle-related proteins. ELT3 cells were treated with the indicated concentrations of nerolidol for 48 h and were then harvested after trypsin/EDTA treatment. (A, B) For cell cycle analysis, the harvested cells were fixed with 70 % ethanol, followed by propidium iodide staining, and the DNA content was measured using flow cytometry. The results were analyzed using the FlowJo software (A). Blue, olive green, and green represent the G1, S, and G2/M phases, respectively. The percentage of each cell cycle phase was plotted in (B). The p-value was calculated using one-way ANOVA with Tukey's multiple post hoc test for each group.*, p <0.05; **, p <0.01, and ***, p <0.001 compared to the vehicle control group (1 % EtOH). (C) Total cellular protein content was measured, and the expression levels of phosphorylated Akt, total Akt, cyclin D1, CDK4, and CDK6 were determined using western blot analysis. β-Actin was used as the loading control. The inserted numbers in (C) indicate the relative expression level compared to that of the vehicle control (indicated as 0 μM). (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Fig. 1 in Nerolidol inhibits proliferation of leiomyoma cells via reactive oxygen species-induced DNA damage and downregulation of the ATM/ Akt pathway

Fig. 1. Nerolidol inhibited the proliferation of rat leiomyoma cells. ELT3 cells were seeded in 24-well plates and treated with the indicated concentrations of nerolidol for 48 h. (A) Images were captured under an inverted microscope at 100 × magnification. (B) The cells were trypsinized, and the number of viable (upper panel) or dead (lower panel) cells was counted after staining with trypan blue with a hemocytometer. (C) Cell proliferation was also determined using the MTT assay. Ethanol (1 %) was used as the vehicle control, which is indicated as 0 μM. The data are presented as relative percentage compared to the vehicle control. The p-value was calculated using one way ANOVA with Tukey's multiple post hoc test for each group. *, p <0.05 and ***, p <0.001 compared to the vehicle control group. The IC50 values were calculated using the IC50 Calculator (https://www.aatbio.com/tools/ic50-calculator).