Project description:Gene expression analysis of whole heart samples obtained from CAR wild type and knockout mouse E10.5 embryos. We used the microarray to detect any gene expression changes in the E10.5 embronic heart due to the global deletion of CAR.
Project description:An increasing number of studies, including mutant expression profiling and comparative transcriptomic analyses, require reference RNA-seq data collections in mice. Particularly, to complement previous profiling data sets based on arrays, a full RNA-seq developmental series will be required for whole embryos. E10.5 is a key reference stage as it represents the early organogenesis stage. Here, we have performed high-throughput sequencing of total RNA form whole mice embryos at embryonic stage E10.5.
Project description:Mouse Wdr74-knockout embryos were generated using the CRISPR-Cas9 system. Embryos from the 4-cell stage to the morula stage were collected and treated with acidic Tyrode's solution to remove the zona pellucida. We used 50 embryos per sample at each developmental stage and identified the proteome of mouse Wdr74-knockout embryos by label-free quantification.
Project description:An increasing number of studies, including mutant expression profiling and comparative transcriptomic analyses, require reference RNA-seq data collections in mice. Particularly, to complement previous profiling data sets based on arrays, a full RNA-seq developmental series will be required for whole embryos. E10.5 is a key reference stage as it represents the early organogenesis stage. Here, we have performed high-throughput sequencing of total RNA form whole mice embryos at embryonic stage E10.5. Sequencing of the total RNA of whole embryos of mouse at embryonic stage E10.5.
Project description:We used microarrays to identify Pax3 targets during myogenesis in the mouse embryo Mouse embryos were genotyped Pax3GFP/+ or Pax3PAX3-FKHR/GFP and dissected at E10.5 under a fluorescent binocular. The forelimb buds were dissected and dissociated and GFP positive cells were then sorted by flow cytometry before RNA extraction and hybridization on Affymetrix microarrays. We also sorted GFP negative cells.
Project description:Comparison of pooled Dll1tm1Gos and wildtype E10.5 embryo samples. 4 dual-color DNA-chip hybridizations on a non-commercial cDNA chip and 9 dual-color hybridisations on a commercial chip (Atlas Glass Mouse 1) of cDNAs from a pool of embryos were made. Keywords: other
Project description:Steroids enriched within the lung tumor microenvironment suppress the cytotoxic activity of tumor-infiltrating NK cells and intensify hypoxic stress. To model these conditions in vitro, CEACAM5-specific CAR-NK cells and NR3C1-knockout CAR-NK cells were exposed to hydrocortisone (1 µM), hypoxia-mimicking CoCl₂ (100 µM), or their combination. NK cells were treated for 24 hours, followed by a 6-hour co-culture with A549 lung cancer cells to activate NK-cell effector programs. After co-culture, NK cells were isolated to high purity and subjected to bulk RNA sequencing to characterize transcriptional changes driven by steroid signalling, hypoxia, and glucocorticoid receptor deficiency. This dataset includes multiple treatment groups: untreated CAR-NK cells, hypoxia-treated CAR-NK cells, combined hypoxia + hydrocortisone–treated CAR-NK cells, and corresponding NR3C1-knockout CAR-NK cell groups under identical conditions.
Project description:To investigate the role of the Smchd1 protein in epigenetic silencing of autosomal loci, we carried out a comparative microarray gene expression analysis of wild-type and Smchd1-/- female embryos at E10.5. Embryos were collected at E10.5 after natural mating, sexed and genotyped. Total RNAs were extracted from three individual wild-type and three Smchd1-/- female embryos and cRNAs prepared from these samples was hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 array.
Project description:In this study, we delved into deciphering the glycosylation patterns and precise localization of glycosylation sites within CAR-T proteins. Specifically, we focused on samples derived from human T cells that underwent gene knockout of AAVS1 and SPPL3, two critical genes that could potentially influence CAR-T function. To ensure accuracy and precision, we employed optimal tribrid orbitrap mass spectrometry settings for glycosylation landscapes of the CAR-T proteins. By analyzing these data, we aimed to gain a deeper understanding of how AAVS1 and SPPL3 knockout impacted the glycosylation profiles and ultimately the function and efficacy of CAR-T cells in immunotherapy applications.
Project description:CEACAM5-specific CAR NK-92 cells were engineered to target CEACAM5-expressing lung tumor cells. To study their transcriptional response during tumor engagement, parental NK-92 cells, CEACAM5-CAR NK-92 cells, hydrocortisone-treated CAR NK-92 cells, NR3C1-knockout (cortisol-resistant) CAR NK-92 cells, and hydrocortisone-treated NR3C1-knockout CAR NK-92 cells were co-cultured with CEACAM5⁺ A549 lung cancer cells for 16 hours. Following co-culture, NK-92–derived effector cells were isolated by flow cytometry and processed for bulk RNA sequencing. This dataset captures transcriptional programs associated with CAR activation, hydrocortisone exposure, and glucocorticoid receptor deficiency in NK-92–based effector cells responding to CEACAM5⁺ tumor targets.