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.
22
datasets available to search
ShareScore release 0.9.0
Dataset results
22 results for “NSD3”
Constructing Lentiviral NSD3-Short-3xFLAG Constructs to Transduce AML Cell Lines
<p>SGC Open Lab Notebook Project - Understanding the Role of NSD3 in Cancer </p> <p>Funding Acknowledgment: The SGC is a registered charity (number 1097737) that receives funds from AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Canada Foundation for Innovation, Eshelman Institute for Innovation, Genome Canada through Ontario Genomics Institute [OGI-055], Innovative Medicines Initiative (EU/EFPIA) [ULTRA-DD grant no. 115766], Janssen, Merck KGaA, Darmstadt, Germany, MSD, Novartis Pharma AG, Ontario Ministry of Research, Innovation and Science (MRIS), Pfizer, São Paulo Research Foundation-FAPESP, Takeda, and Wellcome.</p>
Western Blotting NSD3 in AML Cell Lines
<p>SGC Open Lab Notebook Project - Understanding the Role of NSD3 in Cancer </p> <p>Experiment 011 - Western blot of MOLM-13, UCSD-AML1, and HL-60 AML cell lines probing for NSD3. </p>
Exploring NSD3 Driven Gene Expression Profiles in Lung Squamous Cell Carcinoma
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp026 Objective:</strong> NSD3 is frequently amplified as part of the 8p11-12 focal amplification in several types of cancer. Here we set out to explore the gene expression profiles of NSD3 amplified versus non-amplified lung squamous cancer samples from the TCGA. However, because this event takes place in the context of a focal amplification we will also compare samples with high versus low NSD3 expression. The goal of this experiment is to identify putative oncogenic signalling pathways NSD3 may regulate, as well as inform on the biological role of this protein in the context of gene expression. </p>
Mutagenesis of RRL-NSD3-Short-3xFLAG Lentiviral Vector
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp013 Objective: </strong>The NSD3’s PWWP1 domain is present in both long and short isoforms. It has been shown to bind H3K36me2 (Sankaran et al.(2016) - PMID:26912663) and be required for the maintenance of AML (Chen et al.(2015 - PMID: 26912663). However, it is still unclear how this domain contributes to NSD3’s function at enhancers. To study this aspect of NSD3’s biology, I will mutate W284 to alanine in the RRLNSD3-3xFLAG-IRES-Puro plasmids I described earlier (exp010) by site-directed mutagenesis. This is the second tryptophan within the PWWP1 motif and is critical for substrate recognition (Qin, S & Min, J(2014) - PMID:25277115). This construct will be useful for understanding how NSD3 recognition of methylated histones influences its putative activity in cancer.</p>
Mutagenesis to Replace IRES with T2A in NSD3-Short-3xFLAG Lentiviral Expression Vector
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp016 Objective: </strong>Bicistronic elements are common features in lentiviral expression systems that allow expression of two protein products from a single promoter. The two most common bicistronic elements are the internal ribosome entry site (IRES), which allows cap-independent translation of a second open reading frame within an mRNA, and the 2A system, which introduces a self-cleaving peptide between two desired protein products. There are several advantages to the the 2A system over an IRES, which include matched expression levels of your two protein products of interest as well as having a smaller footprint (~1/10 size in kb), which may improve viral titre. Therefore, I will use site-directed mutagenesis to alter the NSD3short lentiviral expression plasmid to replace the IRES sequence with a T2A sequence.</p>
Transfection of NSD3-tareting siRNA in H1299 Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp019 Objective: </strong> I have identified a putative phenotype in H1299 cells upon overexpression of the NSD3 short<br> isoform. I am also interested in any phenotype resulting from decreased amounts of NSD3 in cells. To<br> do so, I am first testing conditions for RNAi-mediated knockdown of NSD3 in H1299 cells by treating cells<br> with several concentrations of siRNA and evaluating knockdown by western blotting</p>
Characterizing NSD3 Amplification in Lung Cancer
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp020 Objective: </strong>NSD3 (WHSC1L1) is amplified in ~5% of Non-Small Cell Lung Cancer patients( cBioPortal : Cerami et<br> al. Cancer Discov. 2012 and Gao et al. Sci. Signal. 2013). However, the implications of this event on the<br> formation and progression of the disease are unclear. While NSD3 may be a driver of lung cancer, it is also<br> plausible that this locus is simply amplified at a higher frequency in the context of cancer-associated genomic<br> instability. To dive deeper into this question I will use The Cancer Genome Atlas (TCGA) lung cancer<br> data-sets to look for associations between NSD3 amplification and mutational status as well as gene expression<br> profiles. This data has been generated by the TCGA Research Network: http://cancergenome.nih.gov/. I<br> hypothesize that if NSD3 amplification is a driving force in a subset of lung tumors, these samples will share<br> similar gene expression profiles and exhibit higher expression levels of NSD3. Here, I am using FirebrowserR<br> (Deng M., et al. Database. 2017 - PMID:28062517), an R client for Broad Institute’s Firehose Web API,<br> which allows TCGA data processed by the Firehose Pipeline to be directly imported into R for analysis.</p>
NSD3-Short Promotes Migration of A549 Lung Cancer Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp025 Objective:</strong> In a previous experiment (exp024), we observed an increase in E-cadherin expression in response to knockdown of the short isoform of NSD3. To determine if this change is functionally relevant, we performed wound healing assays to measure any corresponding alteration in the migratory potential of A549 lung epithelial cancer cells.</p>
NSD3-Short Represses E-cadherin Expression in A549 Lung Epithelial Cancer Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp024 Objective: </strong>In a previous experiment (exp023), we show that siRNA-mediated knockdown of NSD3 increases expression of E-cadherin, a marker of epithelial cell identity. To determine which isoform of NSD3 is involved in promoting epithelial to mesenchymal transition, I have designed siRNA that targets either the long or short isoform and again use E-cadherin expression as a marker. Additionally, I have started using A549 lung epithelial cancer cells (https://www.atcc.org/Products/All/CCL-185) as my primary model. This cell line proliferates faster and is more amenable to <em>in vitro</em> experimentation than the H1299 cell line I was using previously.</p>
Quantification of E-cadherin Expression in H1299 NSD3 Knockdown Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp023 Objective: </strong>Having observed downregulation of E-cadherin protein levels in response to NSD3 overexpression in H1299 cells (exp021), I was next interested in testing the consequences of NSD3 knockdown. To do so, I transfected H1299 cells with siRNA targeting NSD3, both short and long isoforms, and assayed E-cadherin expression by western blotting. </p>
Analysis of NSD3 Isoform Expression from TCGA-LUSC Data
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp028 Objective: </strong>There are two major NSD3 isoforms expressed, long (aa 1-1437) and short (aa 1-645, differing in sequence from 620-645). Importantly, the short isoform was shown to be required for the maintenance of acute myeloid leukemia (AML) [1]. This isoform lacks a SET domain and thus methyltransferase activity. It is not clear if the two isoforms are co-expressed or independently regulated. As a first attempt to study differential regulation of the two isoforms, I have used the TCGA-LUSC dataset to analyze relative expression levels in the context of squamous cell lung cancer (LUSC) [2]. </p> <p><strong>References:</strong> </p> <p>1. Shen C, Ipsaro JJ, Shi J, et al. NSD3-short is an adaptor protein that couples BRD4 to the CHD8 chromatin remodeler. Molecular cell. 2015;60(6):847-859. doi:10.1016/j.molcel.2015.10.033. <br> 2. Weinstein JN, Collisson EA, Mills GB, et al. The Cancer Genome Atlas Pan-Cancer Analysis Project. Nature genetics. 2013;45(10):1113-1120. doi:10.1038/ng.2764.</p>
Elevated NSD3 Histone Methylation Activity Drives Squamous Cell Lung Cancer
GEO Series GSE149272. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
NSD3-short is an adaptor protein that couples BRD4 to the CHD8 chromatin remodeler (RNA-Seq)
GEO Series GSE71185. Mus musculus. 13 samples. Type: Expression profiling by high throughput sequencing.
Bio NSD3 PWWP1 Expression and Purification Protocol
<p>Bio NSD3 PWWP1 Expression and Purification Protocol</p>
Effect of NSD3 on MDA-MB-231 breast cancer cells (RNA-seq)
GEO Series GSE152546. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
NSD3-short is an adaptor protein that couples BRD4 to the CHD8 chromatin remodeler (ChIP-Seq)
GEO Series GSE71183. Mus musculus. 9 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
NSD3-short is an adaptor protein that couples BRD4 to the CHD8 chromatin remodeler
GEO Series GSE71186. Mus musculus. 22 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Profiling NSD3-dependent neural crest gene expression reveals known and novel candidate regulatory factors
GEO Series GSE161565. Gallus gallus. 10 samples. Type: Expression profiling by high throughput sequencing.
Systematic perturbations of SETD2, NSD1, NSD2, NSD3 and ASH1L reveal their distinct contributions to H3K36 methylation
GEO Series GSE243566. Mus musculus. 125 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
An NSD3-targeting PROTAC (Proteolysis Targeting Chimeric) suppresses the NSD3 and cMyc oncogenic nodes in cancer cells
GEO Series GSE158296. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
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.