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321 results for “AKT”

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zenodo40/100

Raw data for Kierdorf et al, "Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila"

<p>This upload contains the raw data corresponding to the publication&nbsp;&quot;Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila&quot; by Katrin Kierdorf et al., eLife 2020.</p>

opencc-by-4.0Jan 2020View details →
zenodo40/100

Dataset: Akoustis Technologies, Inc. (AKTS) Stock Performance

This dataset provides historical stock market performance data for specific companies. It enables users to analyze and understand the past trends and fluctuations in stock prices over time. This information can be utilized for various purposes such as investment analysis, financial research, and market trend forecasting.

opencc-zeroJun 2024View details →
zenodo40/100

Dataset: Akoustis Technologies, Inc. (AKTS) Stock Performance

This dataset provides historical stock market performance data for specific companies. It enables users to analyze and understand the past trends and fluctuations in stock prices over time. This information can be utilized for various purposes such as investment analysis, financial research, and market trend forecasting.

opencc-zeroJun 2024View details →
dryad36/100

The structural determinants of PH domain-mediated regulation of Akt revealed by segmental labeling

<p>Akt is a critical protein kinase that governs cancer cell growth and metabolism. Akt appears to be autoinhibited by an intramolecular interaction between its N-terminal pleckstrin homology (PH) domain and kinase domain, which is relieved by C-tail phosphorylation, but the precise molecular mechanisms remain elusive. Here we use a combination of protein semisynthesis, NMR, and enzymological analysis to characterize structural features of the PH domain in its autoinhibited and activated states. We find that Akt autoinhibition depends on the length/tension of the PH-kinase linker. We identify a role for a dynamic short segment in the PH domain that appears to regulate autoinhibition and PDK1-catalyzed phosphorylation of Thr308 in the activation loop. We determine that Akt allosteric inhibitor MK2206 drives distinct PH domain structural changes compared to baseline autoinhibited Akt. These results highlight how the conformational plasticity of Akt governs the delicate control of its catalytic properties.</p>

opencc-zeroAug 2020View details →
zenodo36/100

Single cell imaging of ERK and Akt activation dynamics and heterogeneity induced by G protein-coupled receptors - Scripts & Source data

<p>Source data and scripts to reproduce the figures that are part of the publication &quot;Single cell imaging of ERK and Akt activation dynamics and heterogeneity induced by G protein-coupled receptors&quot;.</p> <p>Journal of Cell Science (2022) 135, jcs259685, DOI: 10.1242/jcs.259685</p> <p>&nbsp;</p> <p>An earlier version of this work is published as a preprint: &quot;Heterogeneity and dynamics of ERK and Akt activation by G protein-coupled receptors depend on the activated heterotrimeric G proteins&quot;, DOI: <a href="https://doi.org/10.1101/2021.07.27.453948">10.1101/2021.07.27.453948</a></p>

opencc-by-4.0Jan 2022View details →
zenodo36/100

The role of Cornulin (CRNN) in the progression of cutaneous squamous cell carcinoma involving AKT activation in SCL-1

<p>Cutaneous squamous cell carcinoma (cSCC) is a prevalent type of skin cancer that has been on the rise in recent times, particularly among older individuals. Cornulin (CRNN) is increasingly recognized as an oncogene involved in developing various types of tumors. However, the precise contribution to cSCC remains unclear. Our study observed a significant increase in CRNN expression in cSCC samples compared to healthy skin. CRNN expression in the SCL-1 cell line derived from cSCC was reduced, leading to a halt in cell growth during the transition from the G1 phase to the S phase. This reduction inhibits cell division, promotes cell death, and decreases cell invasion and migration. CRNN overexpression has been found to enhance cell growth and prevent cells from undergoing natural cell death, and the cancer-promoting effects of CRNN are linked to AKT activation. Using a mouse xenograft model, we demonstrated that the inhibition of CRNN led to a decline in cSCC tumor growth in a living organism, providing evidence of CRNN&rsquo;s involvement in cSCC occurrence and development. This study establishes a foundation for evaluating the effectiveness of CRNN in treating cSCC, enabling further investigation in this area</p>

opencc-by-4.0May 2024View details →
zenodo36/100

Gm364 Coordinates MIB2/DLL3/Notch2 to Regulate Female Fertility through AKT Activation

<p><strong>Supplementary dataset 1. </strong>Related to fertility assays in Figure 1I and 1J. WT mating male mice were monthly rotated between cages according to this random allocation table. Dates are presumptive.</p> <p><strong>Supplementary </strong><strong>dataset</strong>&nbsp;<strong>2</strong><strong>.</strong>&nbsp;Related to figure 7A-C. This excel file contains FPKM values of three WT or Gm364-KO repeats, &nbsp;Log2-Ave value, and Log2(Ave-Gm364-KO/ave-WT) for each genes. &nbsp;To avoid the illegal calculation&nbsp;of value &ldquo;0&rdquo;, we added a minimal value &ldquo;0.001&rdquo;&nbsp;to all original values (we&nbsp;have verified that this did not&nbsp;alter any differential trends). The data were arranged to the ascending order&nbsp;of Log 2(Ave-Gm364-KO/ave-WT) values.</p> <p><strong>Supplementary </strong><strong>dataset</strong>&nbsp;<strong>3</strong><strong>.</strong>&nbsp;Related to figure 7D and 7E. This excel file contains six sheets. &quot;CPG-all info&quot;, &quot;CHG-all info&quot;, and &quot;CHH-all info&quot; contain all original information for CPG, CHG, or CHH promoter regions of each genes; &quot;CpG methyl value&quot;, &quot;CHG methyl value&quot;, and &quot;CHH&nbsp;methyl value&quot; contain methylation values, Ave methylation values of three WT or Gm364-KO repeats, &nbsp;Log2-Ave value, and Log2(Ave-Gm364-KO/ave-WT) for CPG, CHG, or CHH promoter regions of each genes. To avoid the illegal calculation&nbsp;of value &ldquo;0&rdquo;, we added a minimal value &ldquo;0.001&rdquo;&nbsp;to all original values (we&nbsp;have verified that this did not&nbsp;alter any differential trends). The data were arranged to the ascending order&nbsp;of Log 2(Ave-Gm364-KO/ave-WT) values.</p> <p><strong>Supplementary dataset 4. </strong>Related to figure 8A and 8G. This excel file contains two sheets. &quot;RNA seq up &amp; down top 20&quot; contains top 20 up-regulated &amp; down-regulated DEGs; &quot;RRBS up &amp; down top 20&quot; contains top 20 up-regulated &amp; down-regulated DMRs.</p> <p>&nbsp;</p>

opencc-by-4.0Oct 2020View details →
ClinicalTrials.gov36/100

AKT Inhibitor MK-2206 in Treating Patients With Relapsed or Refractory Acute Myeloid Leukemia

ClinicalTrials.gov study NCT01253447. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

AKT Inhibitor, Ipatasertib, With Endocrine and CDK 4/6 Inhibitor for Patients With Metastatic Breast Cancer (TAKTIC)

ClinicalTrials.gov study NCT03959891. IPD Sharing: YES. Countries: 1. Publications: 0.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov36/100

Akt Inhibitor MK2206 in Treating Patients With Advanced Gastric or Gastroesophageal Junction Cancer

ClinicalTrials.gov study NCT01260701. IPD Sharing: Not stated. Countries: 2. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Akt Inhibitor MK2206 in Treating Patients With Progressive, Recurrent, or Metastatic Adenoid Cyst Carcinoma

ClinicalTrials.gov study NCT01604772. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Bicalutamide With or Without Akt Inhibitor MK2206 in Treating Patients With Previously Treated Prostate Cancer

ClinicalTrials.gov study NCT01251861. IPD Sharing: Not stated. Countries: 2. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Akt Inhibitor MK2206 in Treating Patients With Advanced Breast Cancer

ClinicalTrials.gov study NCT01277757. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Vevorisertib (ARQ 751) as a Single Agent or in Combination With Other Anti-Cancer Agents, in Solid Tumors With PIK3CA / AKT / PTEN Mutations (MK-4440-001)

ClinicalTrials.gov study NCT02761694. IPD Sharing: YES. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov36/100

Study of Akt Inhibitor MK2206 in Patients With Relapsed Lymphoma

ClinicalTrials.gov study NCT01258998. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Selumetinib and Akt Inhibitor MK2206 or mFOLFOX Therapy Comprising Oxaliplatin and Fluorouracil in Treating Patients With Metastatic Pancreatic Cancer Previously Treated With Chemotherapy

ClinicalTrials.gov study NCT01658943. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Testing AZD5363 as a Potential Targeted Treatment in Cancers With AKT Genetic Changes (MATCH-Subprotocol Y)

ClinicalTrials.gov study NCT04439123. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov36/100

Akt Inhibitor MK2206 in Treating Patients With Recurrent or Advanced Endometrial Cancer

ClinicalTrials.gov study NCT01307631. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
dryad36/100

The structural determinants of PH domain-mediated regulation of Akt revealed by segmental labeling

Open the record for dataset details and reuse information.

publicAug 2020View details →
zenodo32/100

Akt inhibitor and Tacrolimus arrange apoptotic gene expression levels in MCF7 cells

<p>Apoptosis balances the cells produced as a result of cell division and controls the differentiation in general tissue homeostatic mechanisms. It is known that apoptosis is a gene-oriented program and has effects on cell proliferation and differentiation by regulating several pro-apoptotic and anti-apoptotic gene families<span>.</span>&nbsp;In this study we investigated gene expression levels of tumor suppressor gene <em>p53</em>, survival protein and growth factor receptor <em>PDGFR</em>&beta;, anti-apoptotic protein <em>NF&kappa;</em>&beta;, pro-apoptotic proteins <em>Bax</em> and <em>Caspase 9</em>. According to our gene expression results, we showed that levels of p53, Bax and Caspase 9 in MCF7 cells were increased with Akt inhibitor application. Previous studies have reported that Akt inhibitor induces apoptosis by expressing these genes. Also our NF&kappa;B gene expression results support these findings. This effect of the Akt inhibitor shows that the PI3K/Akt/mTOR signaling pathway is one of the primary effective routes on apoptosis in MCF7 cells. It was observed that FK506 administration with Akt inhibitor contributed positively in favor of apoptosis in all parameters, although alone treatment FK506 showed no&nbsp;increase as Akt inhibitor in p53, Bax and Caspase 9 expression. This effect of FK506 showed that the Calcineurin/NFAT pathway is a secondary effective route on apoptosis. However, this positive effect of the co-administration of FK506 with Akt inhibitor on breast cancer gives us important clues for our subsequent studies. When we evaluated our findings of apoptosis and gene expression, it was observed that the combined treatment of the FK506 and Akt inhibitor, which did not show much effect alone, was highly effective and promising in reducing cancer proliferation and regulating apoptotic genes. These results indicate that the intracellular pathways which are used by the cancer act together and support each other.</p>

opencc-by-4.0Apr 2022View details →

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Last verified 2026-04-29Open record