Project description:Human CD8+CCR7+ T cells from three donors were transduced with CRISPRi and CRISPRa TF gRNA libraries and expanded for 10 days. After 10 days, we used single-cell RNA sequencing (scRNA-seq) to analyze the transcriptomic effects of silencing or activating each gene candidate.
Project description:Human CD8+ T cells from three donors were transduced with lentivirus encoding for BATF3-2A-GFP or GFP and expanded for 10 days. Total RNA was isolated from each sample and submitted for RNA-seq. We then performed gene expression profiling analysis.
Project description:We demonstrated that chemically difined PCL-PVAc-PEG based 3a medium was superior to conventional StemSpan besed medium in expansion of human hematopoietic stem cells. In fact, more phenotypic HSCs (CD34+EPCR+CD90+CD45RA-ITGA3+) were expanded in our culture condition and higher donor chmerism was achieved in transplantation assay using humanized mice. But detail transcriptome profiles of expanded HSCs was unknown and therefore single-cell RNA sequencing was done to reveal it. As a result, expanded cells in our medium had more HSPC featured cells. Interestingly, erythroid/megakaryocyte progenitors was more expanded in our condition. On the other hands, other culture condition made more myeloid progenitor cells but few HSPC featured cells. This result support the idea that our new medium are able to selectively expand HSCs.
Project description:Transcriptome (total RNA) profiling of bovine in vitro cultured expanded blastocysts (EB) comparing control non-treated expanded blastocysts with SAM-treated expanded blastocysts. S-Adenosyl methionine (SAM) is the global methyl donor providing methyl group for variety of biomolecules such as DNA , histone, RNA, lipids and etc. Two-condition experiment, bovine non-treated expanded blastocysts (pools of 10) vs bovine SAM-treated expanded blastocysts. Four biological replicates of each tissue were hybridized to four two-color arrays in a dye-balanced design.
Project description:A Comparative Study of Human Testes and Epididymis through the Proteomics and RNA-seq Methods
<ul><li>Dataset imported into MassIVE from <a href="https://www.iprox.cn/page/project.html?id=IPX0003098000">https://www.iprox.cn/page/project.html?id=IPX0003098000</a> on 12/10/21</li></ul>
Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals miRNA expression profiles were obtained via RNA-seq analysis performed on tissue samples from the liver of 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals.
Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals miRNA expression profiles were obtained via RNA-seq analysis performed on tissue samples from the striatum of 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals.
Project description:Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric alterations. The mutation responsible for this disease is an abnormally expanded and unstable CAG repeat within the coding region of the gene encoding huntingtin (Htt). Knock-in mouse models of HD with human exon 1 containing expanded CAG repeats inserted in the murine huntingtin gene (Hdh) provide a genetic reconstruction of the human causative mutation within the mouse model. The goal of this study is RNA expression profiling by RNA sequencing (RNA-seq) in 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals mRNA expression profiles were obtained via RNA-seq analysis performed on tissue samples from the liver of 2, 6, and 10 month old knock-in mice with CAG lengths of 20, 80, 92, 111, 140, 175 along with littermate control wild-type animals.