Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
321
datasets available to search
ShareScore release 0.9.0
Dataset results
321 results for “AKT”
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).
Dinaciclib and Akt Inhibitor MK2206 in Treating Patients With Pancreatic Cancer That Cannot Be Removed by Surgery
ClinicalTrials.gov study NCT01783171. IPD Sharing: Not stated. Countries: 2. Publications: 1.
mTORC1/2 Inhibitor AZD2014 or the Oral AKT Inhibitor AZD5363 for Recurrent Endometrial and Ovarian
ClinicalTrials.gov study NCT02208375. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study of the Safety and Activity of the MEK Inhibitor Given Together With the AKT Inhibitor to Patients With Multiple Myeloma or Solid Tumor Cancers
ClinicalTrials.gov study NCT01476137. IPD Sharing: Not stated. Countries: 1. Publications: 1.
AZD5363 in Patients With Advanced Solid Tumors Harboring AKT Mutations
ClinicalTrials.gov study NCT03310541. IPD Sharing: Not stated. Countries: 1. Publications: 1.
p-AKT Expression on Clinical Outcomes in Malignant Lymphoma
ClinicalTrials.gov study NCT01789060. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Phase I, Open-Label, First-Time-In-Human Study of the Oral AKT Inhibitor GSK2141795
ClinicalTrials.gov study NCT00920257. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Evexomostat Plus PI3K or AKT Inhibitor and Fulvestrant in Patients With a PI3K Alteration and HR+/Her2- Breast Cancer
ClinicalTrials.gov study NCT05455619. IPD Sharing: NO. Countries: 1. Publications: 2.
Continuation Study of the Oral AKT Inhibitor GSK2110183
ClinicalTrials.gov study NCT01531894. IPD Sharing: YES. Countries: 5. Publications: 0.
PTEN-AKT-FOXO3 Gene Expression Relation With Low-ovarian Reserve in Endometriomas
ClinicalTrials.gov study NCT04058912. IPD Sharing: NO. Countries: 1. Publications: 2.
Fulvestrant +/- Akt Inhibition in Advanced Aromatase Inhibitor Resistant Breast Cancer
ClinicalTrials.gov study NCT01992952. IPD Sharing: Not stated. Countries: 1. Publications: 2.
AKT NUTQIDA AUTENTIK MATNLAR YARATISHDA SOHAGA BO'LGAN LEKSIK BIRLIKLARDAN FOYDALANISH IMKONIYATLARI
Open the record for dataset details and reuse information.
Data from: Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation
Macrophage activation/polarization to distinct functional states is critically supported by metabolic shifts. How polarizing signals coordinate metabolic and functional reprogramming, and the potential implications for control of macrophage activation, remains poorly understood. Here we show that IL-4 signaling co-opts the Akt-mTORC1 pathway to regulate Acly, a key enzyme in Ac-CoA synthesis, leading to increased histone acetylation and M2 gene induction. Only a subset of M2 genes is controlled in this way, including those regulating cellular proliferation and chemokine production. Moreover, metabolic signals impinge on the Akt-mTORC1 axis for such control of M2 activation. We propose that Akt-mTORC1 signaling calibrates metabolic state to energetically demanding aspects of M2 activation, which may define a new role for metabolism in supporting macrophage activation.
Small NBL Dataset for Analysis of AKT Signaling
<p>ExpressionData.csv</p> <p>----------------------------</p> <p>A small subset of transcriptomics data (30 genes) curated for learning Gene Regulatory Networks (GRNs) pertaining to signaling by the ALK pathway. Genes were selected by referencing the "signaling by ALK" pathway from Reactome (https://reactome.org/content/detail/R-HSA-201556). This subset of data belongs the TARGET-NBL project (<a href="https://portal.gdc.cancer.gov/projects/TARGET-NBL">https://portal.gdc.cancer.gov/projects/TARGET-NBL</a>), hosted via the Genomic Data Commons Data Portal (https://portal.gdc.cancer.gov/). Please refer to GDCs data access policies (<a href="https://gdc.cancer.gov/about-gdc/gdc-policies">https://gdc.cancer.gov/about-gdc/gdc-policies</a>) if planning to use the data. </p> <p> </p> <p>refNetwork.csv</p> <p>----------------------</p> <p>Contains a reference network of known pairwise regulatory relationships among the genes of which we have transcriptomics data available in "ExpressionData.csv." These relationships were again determined by referencing the "signaling by ALK" pathway from Reactome (https://reactome.org/content/detail/R-HSA-201556).</p>
Akt Inhibitor MK2206 in Treating Patients With Relapsed or Refractory Diffuse Large B-Cell Lymphoma
ClinicalTrials.gov study NCT01481129. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Akt Inhibitor MK2206 in Treating Patients With Recurrent or Metastatic Head and Neck Cancer
ClinicalTrials.gov study NCT01349933. IPD Sharing: Not stated. Countries: 3. Publications: 0.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.