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Bulk mRNAseq in control and Cnp-Cre_RelA cKO mouse spinal cords

ABSTRACT: Bulk mRNAseq in control and Cnp-Cre_RelA cKO mouse spinal cords

PROVIDER: PRJNA1248979 | ENA |

REPOSITORIES: ENA

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Bulk mRNAseq in control and Cnp-Cre_RelA cKO mouse spinal cords

Project description:We sequenced mRNA extracted from the cerebral cortices including hippocampi of mice at postnatal day 14 (P14) and compared the gene expression levels between the control group and the RelA conditional knockout (Cnp-Cre; RelA cKO) group.

2025-07-04 | GSE294303 | GEO

scRNAseq from spinal cords

Project description:scRNAseq from spinal cords

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Transcriptome of murine lumbar spinal cord at E12.5 in control and DOT1L cKO through Wnt1cre2 (B6.Cg-E2f1Tg(Wnt1-cre)2Sor/J, Jackson Laboratory #022501)

Project description:DOT1L has a proven function in the cortical and cerebellar development of the mouse model, but has never been studied in the developing spinal cord. Here, we created a transgenic mouse line for Dot1l conditional knock-out in the spinal cord over neurogenesis. We investigated the changes in the trascriptome by performing bulk RNAseq of lumbar spinal cords in controls and Dot1l-cKO. The DEG analysis of cKO littermates revealed a higher degree of differentiation profile as opposed to the controls, concurrent with decreased cell proliferation and altered axonal projection and interneuron migration, supporting the importance of DOT1L activity in the developing spinal cord.

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mRNAseq in control (WT) and Nes:Cre_Qk cKO

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CLIPseq of hnRNP A1 from the spinal cords of mice with experimental autoimmune encephalomyelitis

Project description:Experimental autoimmune encephalomyelitis (EAE) is a mouse model for multiple sclerosis (MS) a chronic autoimmune disease of the central nervous system. We have observed dysfunction of the RNA binding protein hnRNP A1 in neurons from the brains of patients with MS, and the spinal cords of mice with EAE. Here, we sought to characterize the consequences of EAE-induced dysfunction of hnRNP A1 on the RNAs it binds by using CLIPseq to establish both the normal central nervous system RNA binding profile of hnRNP A1 in the spinal cords of naive mice, and any alterations to the binding profile of hnRNP A1 in the spinal cords of mice with EAE.

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scRNAseq from spinal cords of SOD1-G93A and WT mice

Project description:We prepared spinal cords from SOD1-G93A and WT mice treated with vehicle or the RIPK1 inhibitor Nec-1s, which were single cell RNA sequenced using the DropSeq protocol.

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Genome wide analysis of upper spinal cords with training after spinal cord hemisection injury

Project description:The goal of this study is to elucidate the influence of treadmill training on transcriptome of the upper lumbar spinal cord after thoracic spinal cord hemisection. mRNA profiles of spinal cords at 23 days-post injury with/without treadmill training were generated. The expression levels of 650 genes in the trained animal were increased ( > 2-fold) compared to untrained animals. Our study represents the detailed analysis of transcriptomes of spinal cord distal to the hemisected lesion after treadmill training, with biologic replicates, generated by RNA-seq technology.

2019-01-15 | GSE115156 | GEO

Genome wide analysis of lower spinal cords with training after spinal cord hemisection injury

Project description:The goal of this study is to elucidate the influence of treadmill training on transcriptome of the lower lumbar spinal cord after thoracic spinal cord hemisection. mRNA profiles of spinal cords at 23 days-post injury with/without treadmill training were generated. The expression levels of 650 genes in the trained animal were increased ( > 2-fold) compared to untrained animals. Our study represents the detailed analysis of transcriptomes of spinal cord distal to the hemisected lesion after treadmill training, with biologic replicates, generated by RNA-seq technology.

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Human expression data from iPSCs, motor neurons derived from iPSCs and ESCs, and fetal spinal cords

Project description:We compare transcriptomic profiles of human induced pluripotent stem cells (iPSCs), motor neurons (MNs) in vitro differentiated from iPSCs or human ESCs containing a HB9::GFP reporter for MNs, and human fetal spinal cords. The purpose of this comparison is to assess the extent of molecular similarities between in vitro differentiated MNs and in vivo fetal or adult spinal cord MNs. Data for adult spinal cord MNs are published from other studies: GSE3526, GSE19332, GSE20589, and GSE40438. Human induced pluripotent stem cells, pluripotent stem cell derived motor neurons, and fetal spinal cords for RNA extraction and hybridization on Affymetrix arrays.

2016-06-26 | E-GEOD-75701 | biostudies-arrayexpress

Gene expression in experimentally injured and control mouse spinal cords

Project description:This laboratory works on selectins and their carbohydrate ligands in lymphocyte homing and inflammation. The lab also studies heparin-degrading endosulfatases and their roles in regulating the interactions of growth factors and morphogens with proteoglycans. The purpose of the experiment is to examine gene expression profiles in spinal cords of injured as a function of time after a contusion injury. The tissue will be generated in the lab of Linda Noble, Professor in the Department of Neurological Surgery at UCSF who is an expert on the pathogenesis of spinal cord injury. Wild-type male C57B/6 mice (8-10 weeks of age) were used. Injuries were produced by contusion. Spinal cords from control mice (uninjured) and experimental (injured) mice were processed (4 and 7 days after injury). A 3 mm length of spinal cord (centered at the injury) and a 3 mm segment from a distant site were isolated from each animal. Tissue from 3 mice were pooled for each sample. Three replicate samples per treatment group were processed for RNA. Thus, a total of 18 RNA samples were hybridized to 18 gene chips. The analysis will determine whether specific glycosylation changes accompany spinal cord injury. Of particular interest are changes in the sulfation profile of proteoglycan GAG chains (e.g., chondroitin sulfate) and in the appearance of potential carbohydrate ligands for infiltrating leukocytes bearing L-selectin or other endogenous lectins.

2011-02-17 | E-GEOD-27359 | biostudies-arrayexpress

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