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3,508 results for “reprogramming”

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zenodo32/100

Rewiring of endogenous signaling pathways to genomic targets for therapeutic cell reprogramming

<p>Data underlying the figures in the publication &ldquo;Rewiring of endogenous signaling pathways to genomic targets for therapeutic cell reprogramming&rdquo;, published in <em>Nat Commun</em>, <strong>2020</strong>, 11, 608. <a href="https://www.nature.com/articles/s41467-020-14397-8">https://www.nature.com/articles/s41467-020-14397-8</a></p> <p>Table of contents:</p> <p><strong>1. Source Data</strong>; Excel file with the data for <em>Figures 2, 3b, 3d, 3c, 4a, 4b, 4c, 5</em> as well as <em>S2, S3, S4, S5, S6, S7a, S7b, S8, S9, S10, S11, S12, S13a</em> and <em>S13b</em>.</p> <p><strong>Data 1 &ndash; Transgene expression by SEAP</strong></p> <p>Data for <em>Figures 2, S2, S4, S5, S7a, S8, S9, S12</em> and <em>S13b</em>.</p> <p>SEAP (human placental secreted alkaline phosphatase) levels were profiled in cell culture supernatants using a colorimetric assay. 100&thinsp;&micro;L 2x SEAP assay buffer (20&thinsp;mM homoarginine, 1&thinsp;mM MgCl2, 21% diethanolamine, pH 9.8) was mixed with 80&thinsp;&micro;L heat-inactivated (30&thinsp;min at 65&thinsp;&deg;C) cell culture supernatant. After the addition of 20&thinsp;&micro;L substrate solution (120&thinsp;mM p-nitrophenyl phosphate; cat. no. AC128860100, Thermo Fisher Scientific, Waltham, MA, USA), the absorbance time course was recorded at 405&thinsp;nm and 37&thinsp;&deg;C using a Tecan Genios PRO plate reader (cat. no. P97084; Tecan Group AG, Maennedorf, Switzerland) and the SEAP levels were determined as follows: first, absorbance change over time (slope) was calculated. According to the Beer&ndash;Lambert&rsquo;s law, absorbance is proportional to the concentration of a colored compound and depends on the light path length (d) and extinction coefficient (&epsilon;) (&epsilon; for p-nitrophenyl (&epsilon;pNP)&thinsp;=&thinsp;18.600&thinsp;M&minus;1&thinsp;cm&minus;1). Enzymatic activity EA [U/L] was calculated from the equation: EA&thinsp;=&thinsp;slope&thinsp;&times;&thinsp;dilution factor&thinsp;&times;&thinsp;&epsilon;pNP&minus;1&thinsp;&times;&thinsp;d&minus;1</p> <p>Values in the file present determined SEAP levels.</p> <p><strong>Data 2 &ndash; Endogenous gene expression by qPCR</strong></p> <p>Data for <em>Figures 3b, 3d, 4a, 4b, 5, S3, S6, S10, S11</em> and <em>S13a</em>.</p> <p>Total RNA of HEK293T cells was isolated using the Quick-RNA kit (Zymo Research, Irvine, CA, USA). Reverse transcription was performed using a High-Capacity cDNA Reverse Transcription Kit (cat. no. 4368814, Thermo Fisher Scientific, Waltham, MA, USA). Quantitative PCR was performed with the SsoAdvanced Universal SYBR&reg; Green Supermix (cat. no. 1725270, Bio-Rad, Hercules, CA, USA). The Eppendorf Realplex Mastercycler (Eppendorf GmbH) was set to the following amplification parameters: 30&thinsp;s at 95&thinsp;&deg;C and 40 cycles of 15&thinsp;s at 95&thinsp;&deg;C followed by 30&thinsp;s at X&thinsp;&deg;C (X&thinsp;=&thinsp;59 for insulin, 64 for IL-12, 59 or 64 for GAPDH). The relative threshold cycle (Ct) was determined and normalized to the endogenous glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript. The fold change for each transcript relative to the control was calculated using the comparative Ct method.</p> <p>Values in the file present determined mRNA levels relative to GAPDH.</p> <p><strong>Data 3 &ndash; Secreted protein level by ELISA</strong></p> <p>Data for <em>Figures 3c</em> and <em>4c</em>.</p> <p>Human Insulin was quantified with the Mercodia Insulin ELISA (cat. no. 10-1113-01, Mercodia, Uppsala, Sweden). IL-12 was quantified with the human IL-12 (p40) ELISA Kit (cat. no. KAC1561, Thermo Fisher Scientific, Waltham, MA, USA).</p> <p>Values in the file present protein levels as determined by ELISA kit.</p> <p><strong>Data 4 &ndash; Nanoluc luciferase</strong></p> <p>Data for <em>Figure S7b</em>.</p> <p>NanoLuc&reg; luciferase was quantified in cell culture supernatants using the Nano-Glo&reg; Luciferase Assay System (cat. no. N1110; Promega, Duebendorf, Switzerland). In brief, 7.5&thinsp;&micro;L of cell culture supernatant was added per well of a black 384-well plate and mixed with 7.5&thinsp;&micro;L substrate-containing assay buffer. Total luminescence was quantified using a Tecan Genios PRO plate reader (Tecan Group AG).</p> <p>Values in the file present luminescence as measured.</p>

opencc-by-4.0Jul 2021View details →
ClinicalTrials.gov32/100

Epigenetic Reprogramming in Relapse AML

ClinicalTrials.gov study NCT02412475. IPD Sharing: Not stated. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

Reprogramming to Prevent Progressive Pacemaker-induced Remodelling

ClinicalTrials.gov study NCT03627585. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

Intestinal Metabolic Reprogramming as a Key Mechanism of Gastric Bypass in Humans

ClinicalTrials.gov study NCT02710370. IPD Sharing: UNDECIDED. Countries: 1. Publications: 9.

restrictedIPD-UNDECIDEDFeb 2026View details →
ClinicalTrials.gov32/100

The Prognosis of Lipid Reprogramming With Rosuvastatin, in Castrated Egyptian Prostate Cancer Patients

ClinicalTrials.gov study NCT04776889. IPD Sharing: YES. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →
ClinicalTrials.gov32/100

Signatures of Immune Reprogramming in Anti-CD52 Therapy of MS: Markers for Risk Stratification and Treatment Response

ClinicalTrials.gov study NCT04082260. IPD Sharing: NO. Countries: 1. Publications: 1.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov32/100

Reprogramming Insoles In Regulating Blood Pressure In Hypertensive Subjects

ClinicalTrials.gov study NCT02401516. IPD Sharing: NO. Countries: 1. Publications: 15.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov32/100

The Role of Microbiome Reprogramming on Liver Fat Accumulation

ClinicalTrials.gov study NCT03914495. IPD Sharing: Not stated. Countries: 1. Publications: 20.

restrictedIPD-UNDECIDEDFeb 2026View details →
dryad32/100

Data from: Integrated network analysis identifies fight-club nodes as a class of hubs encompassing key putative switch genes that induce major transcriptome reprogramming during grapevine development

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publicNov 2015View details →
dryad32/100

Data from: Early life exposure to low levels of AHR agonist PCB126 (3,3’,4,4’,5-pentachlorobiphenyl) reprograms gene expression in adult brain

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publicSep 2017View details →
dryad32/100

Data from: Reprograming of epigenetic mechanisms controlling host insect immunity and development in response to egg-laying by a parasitoid wasp

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publicJun 2020View details →
dryad32/100

Data from: Nanotransfection-based vasculogenic cell reprogramming drives functional recovery in a mouse model of ischemic stroke

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publicJan 2021View details →
dryad32/100

Intracellular sodium elevation reprograms cardiac metabolism: Metabolomics data

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publicJul 2020View details →
zenodo28/100

Transcriptome and Metabolome Reprogramming in Tomato Plants by Trichoderma Harzianum strain T22 Primes and Enhances Defense Responses Against Aphids

<p><strong>Figure 1</strong></p> <p>Effect of&nbsp;<em>T. harzianum</em>&nbsp;T22 on aphid survival over time. Survival curves (percentage) of&nbsp;<em>M. euphorbiae</em>&nbsp;reared on the untreated water control and the&nbsp;<em>T. harzianum</em>&nbsp;T22 treated tomato plants are significantly different,&nbsp;<em>p</em>&nbsp;&lt; 0.05 (LogRank test).</p> <p>For the aphid longevity assay, 10 plants for each CTRL or T22 treatment were infested with 5 newly born first instar nymphs of&nbsp;<em>M. euphorbiae</em>. The presence of aphids and of shed exuviae, as an indicator of molting occurrence, was daily monitored. Survival curves were compared by LogRank analysis.</p>

opencc-by-4.0Apr 2020View details →
dryad28/100

Data from: Microglia responses to pro-inflammatory stimuli (LPS, IFNγ+TNFα) and reprogramming by resolving cytokines (IL-4, IL-10)

Microglia respond to CNS injuries and diseases with complex reactions, often called "activation." A pro-inflammatory phenotype (also called classical or M1 activation) lies at one extreme of the reactivity spectrum. There were several motivations for this study. First, bacterial endotoxin (lipopolysaccharide, LPS) is the most commonly used pro-inflammatory stimulus for microglia, both in vitro and in vivo; however, pro-inflammatory cytokines (e.g., IFNγ, TNFα) rather than LPS will be encountered with sterile CNS damage and disease. We lack direct comparisons of responses between LPS and such cytokines. Second, while transcriptional profiling is providing substantial data on microglial responses to LPS, these studies mainly use mouse cells and models, and there is increasing evidence that responses of rat microglia can differ. Third, the cytokine milieu is dynamic after acute CNS damage, and an important question in microglial biology is: How malleable are their responses? There are very few studies of effects of resolving cytokines, particularly for rat microglia, and much of the work has focused on pro-inflammatory outcomes. Here, we first exposed primary rat microglia to LPS or to IFNγ+TNFα (I+T) and compared hallmark functional (nitric oxide production, migration) and molecular responses (almost 100 genes), including surface receptors that can be considered part of the sensome. Protein changes for exemplary molecules were also quantified: ARG1, CD206/MRC1, COX-2, iNOS, and PYK2. Despite some similarities, there were notable differences in responses to LPS and I+T. For instance, LPS often evoked higher pro-inflammatory gene expression and also increased several anti-inflammatory genes. Second, we compared the ability of two anti-inflammatory, resolving cytokines (IL-4, IL-10), to counteract responses to LPS and I+T. IL-4 was more effective after I+T than after LPS, and IL-10 was surprisingly ineffective after either stimulus. These results should prove useful in modeling microglial reactivity in vitro; and comparing transcriptional responses to sterile CNS inflammation in vivo.

opencc-zeroDec 2017View details →
zenodo28/100

Deep learning reveals the metabolic dependency of hypoxic tumor cells and the critical function of FLAD1 mediated mitochondrial metabolic reprogramming

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opencc-by-4.0Apr 2024View details →
zenodo28/100

Dataset for "Reprogramming macrophages with R848-loaded artificial protocells to modulate skin and skeletal wound healing"

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opencc-by-4.0Jun 2024View details →
dryad28/100

Data from: Reprogramming the antigen specificity of B cells using genome-editing technologies

We have developed a method to introduce novel paratopes into the human antibody repertoire by modifying the immunoglobulin (Ig) genes of mature B cells directly using genome editing technologies. We used CRISPR-Cas9 in a homology directed repair strategy, to replace the heavy chain (HC) variable region in B cell lines with that from an HIV broadly neutralizing antibody, PG9. Our strategy is designed to function in cells that have undergone VDJ recombination using any combination of variable (V), diversity (D) and joining (J) genes. The modified locus expresses PG9 HC which pairs with native light chains resulting in the cell surface expression of HIV specific B cell receptors (BCRs). Endogenous activation-induced cytidine deaminase (AID) in engineered cells allowed for Ig class switching and generated BCR variants with improved anti-HIV neutralizing activity. Thus, BCRs engineered in this way retain the genetic flexibility normally required for affinity maturation during adaptive immune responses. Peripheral blood derived primary B cells from three different donors were edited using this strategy. Engineered cells could bind the PG9 epitope by FACS and sequenced mRNA from these cells showed PG9 HC expressed as several different isotypes after culture with CD40 ligand and IL-4.

opencc-zeroDec 2018View details →
ClinicalTrials.gov28/100

Adapting Body Reprogramming for Severe Asthma: a Feasibility Study

ClinicalTrials.gov study NCT04980755. IPD Sharing: NO. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →
ClinicalTrials.gov28/100

Epigenetic Reprogramming in Relapse/Refractory AML

ClinicalTrials.gov study NCT03263936. IPD Sharing: UNDECIDED. Countries: 3. Publications: 0.

restrictedIPD-UNDECIDEDFeb 2026View details →

ScienceDex guides

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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.

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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.

allen-brain-atlas
neuroscienceopenDocumentation, web resources, and API references are available online.
Last verified 2026-04-30Open record

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.

abode-home-cage
behavioral-neuroscienceopenThe DataShare record exposes download links for annotations, documentation, license text, and the zipped per-snippet data directory.
Last verified 2026-04-30Open record

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.

dandi-nwb
electrophysiologyopenPublished Dandiset metadata and archive endpoints are available through the production DANDI API.
Last verified 2026-04-30Open record

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.

ibl
behavioral-neuroscienceopenPublic sessions can be searched and loaded from the IBL public data server through ONE.
Last verified 2026-04-29Open record

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.

openneuro
neuroscienceopenPublished datasets are available on demand over the internet.
Last verified 2026-04-29Open record

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