Project description:Control ChIP-seq on neural crest cell originated from neural crest cell For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:CTCF ChIP-seq on neural crest cell originated from neural crest cell For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:Control Mint-ChIP-seq of neural crest cell originated from neural crest cell For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
Project description:Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others Data sharing with others
Project description:We utilized quantitative analyses of the proteome, transcriptome, and ubiquitinome to study how ubiquitination and NEDD4 control neural crest cell survival and stem-cell-like properties. We report 276 novel NEDD4 targets in neural crest cells and show that loss of NEDD4 leads to a striking global reduction in specific ubiquitin lysine linkages.
Project description:To facilitate analysis and sharing of mass spectrometry (MS)-based proteomics data we created two tools called CURTAIN (https://curtain.proteo.info) and CURTAIN-PTM (https://curtainptm.proteo.info). They are designed to enable the non-MS expert to interactively pursue volcano plots, deconvolute primary experimental data so that replicates can be visualized in bar charts or violin plots allowing statistical analysis and export of plots in SVG format. They also permit assessment of experimental quality by correlation matrix and profile plot. Within CURTAIN, the user can analyze domain structure, AlphaFold predicted structure, reported interactors, relative expression and UniProt disease, pharmaceutical and mutagenesis information on all selected hits. CURTAIN-PTM permits comparison of all identified PTM sites on protein(s) of interest with selected databases. For phosphorylation site analysis CURTAIN-PTM links with the Kinase Library to predict upstream kinases that phosphorylate sites of interest. We provide examples of the utility of CURTAIN and CURTAIN-PTM in analyzing how targeted degradation of the PPM1H Rab phosphatase that counteracts the Parkinson’s LRRK2 kinase impacts cellular protein levels and phosphorylation sites. We re-analyzed a ubiquitinylation dataset, characterizing PINK1-Parkin pathway in primary neurons, revealing new data of interest not previously highlighted. CURTAIN and CURTAIN-PTM are free to use and open-source and will enable researchers to share their data and maximize the impact of proteomics data. We advocate that published proteomic data be submitted containing a shareable CURTAIN web-link, allowing readers to better explore the data.
Project description:The histone methyltransferase Polycomb repressive complex 2 (PRC2) is required for specification of the neural crest, and mis-regulation of neural crest development can cause severe congenital malformations. PRC2 is necessary for neural crest induction, but the embryonic, cellular, and molecular consequences of PRC2 activity after neural crest induction are incompletely understood. Here we show that Eed, a core subunit of PRC2, is required for craniofacial osteoblast differentiation and mesenchymal proliferation after induction of the neural crest. Integrating mouse genetics with single-cell RNA sequencing and epigenomic profiling, our results reveal that conditional knockout of Eed after neural crest cell induction causes severe craniofacial hypoplasia, impaired craniofacial osteogenesis, and attenuated craniofacial mesenchymal cell proliferation that is first evident in post-migratory neural crest cell populations. We show that Eed drives mesenchymal differentiation and proliferation in vivo and in primary craniofacial cell cultures by regulating diverse transcription factor programs that are required for specification of post-migratory neural crest cells. These data enhance understanding of epigenetic mechanisms that underlie craniofacial development, and shed light on the embryonic, cellular, and molecular drivers of rare congenital syndromes in humans.
Project description:RNA Evaluation H9 derived neural crest cells microRNA-seq from Mortazavi For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf