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Effects of Nogo-B receptor overexpression on transcriptomic profiling in the NIH3T3 fibroblast cell line

ABSTRACT: Effects of Nogo-B receptor overexpression on transcriptomic profiling in the NIH3T3 fibroblast cell line

PROVIDER: PRJNA1065490 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27585000_1.fastq.gz	Fastqsanger.gz
	SRR27585000_2.fastq.gz	Fastqsanger.gz
	SRR27584995_1.fastq.gz	Fastqsanger.gz
	SRR27584995_2.fastq.gz	Fastqsanger.gz
	SRR27584996_1.fastq.gz	Fastqsanger.gz

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Effects of Nogo-B receptor overexpression on transcriptomic profiling in the NIH3T3 fibroblast cell line

Project description:Unrestrained receptor tyrosine kinase (RTK) signaling and epigenetic dysregulation are responsible in part for tumorigenesis. Aberrant RTK signaling results in the remodeling of histone modification. As a Ras modulator, NgBR promotes Ras-mediated RTK signaling pathways. Meanwhile, we observed that NgBR overexpression in NIH3T3 cells significantly increased the acetylation of histone H3 and histone H4. To further elucidate the underlying mechanism that NgBR upregulates histone acetylation in tumorigenesis, we carried out RNA-seq analysis to examine the transcriptome alternation in NIH3T3 cells and NgBR-overexpressed NIH3T3 cells (3T3NgBR cells) and revealed that overexpression of NgBR up-regulates ACSS2 expression, but not ACSS1 and ACSS3. Moreover. ACSS2 overexpression abrogated NgBR deficiency-caused decrease of histone acetylation in NIH3T3 cells. Taken together, all the data suggested that NgBR regulates tumorigenesis in NIH3T3 cells via ACSS2-mediated histone acetylation.

2025-05-01 | GSE253418 | GEO

Role of SIRT7 overexpression in mouse fibroblast cells NIH3T3

Project description:Role of SIRT7 overexpression in mouse fibroblast cells NIH3T3

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Identification of Protein Expression Changes During Fibroblast Activation in Response to LAMP2A Overexpression

Project description:Proteomic analysis comparing LAMP2A-TGFβtreated group versus Vector-TGFβ 3 treated group in NIH3T3 fibroblast cells to study the effect of LAMP2A overexpression on protein expression changes During Fibroblast Activation.

2024-09-02 | PXD055463 |

Role of SIRT7 overexpression in mouse fibroblast cells NIH3T3

Project description:Human SIRT7 GFP or GFP alone were overexpressed in NIH3T3 cells.In confluent conditions, SIRT7GFP overexpressing cells but not GFP expressing cells showed presence of distinct compact cellular colonies composed of small sized cells (ST7). Along with this SIRT7GFP overexpressing cells with long and fibroblast morphoogy(LT7) were also present. Single cell clones from these cells were expanded to form ST7 (Small SIRT7GFP expressing) and LT7 (Long SIRT7GFP expressing) lines. RNA from GFP expressing cells (SKGFP), ST7 and LT7 lines was then isolated and applied to microarray analysis to identify gene expression changes in two cell lines

2020-07-14 | GSE148486 | GEO

Mus musculus strain:mouse embryonic fibroblast (MEF) cells line NIH3T3

Project description:Mus musculus strain:mouse embryonic fibroblast (MEF) cells line NIH3T3 Raw sequence reads

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Mus musculus strain:mouse embryonic fibroblast (MEF) cells line NIH3T3

Project description:Mus musculus strain:mouse embryonic fibroblast (MEF) cells line NIH3T3 Raw sequence reads

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Nogo maintains muscle integrity and regulates muscle regeneration via modulating Nogo-A expression

Project description:Nogo, also called RTN4, functions through three isoforms including Nogo-A, -B, and -C. Although Nogo-A is a well-known CNS inhibitor and the level of Nogo-A is increased in muscles of ALS patients, its role in the regulation of skeletal muscle homeostasis and regeneration is still vague. In this study, we analyzed various pathological muscle condition of human and mouse model, and discovered significant increase of Nogo-A and myogenic factors. To understand the role of Nogo in skeletal muscle, muscle transcripts from Nogo+/+ and Nogo-/- mouse were analyzed and observed intensified gene expression involved in adipocyte differentiation and lipid metabolism, and reduced gene expression related to muscle differentiation and structure organization suggesting muscle disorder from muscle replacement with fat deposition. Skeletal muscle structure from Nogo null mice displayed dystrophic phenotypes including impaired myofiber structure and immune cell infiltrations, and dysregulated homeostatic features such as higher level of MyoD, procaspase 3, CHOP, and AKT compared to wild-type muscle. Notexin-injured Nogo deficient muscle resulted higher level of immune cell infiltration but defective in IL-6 production, a well-known myokine from immune cells, and abnormally upregulated regenerative muscle fibers than normal muscle. Therefore we hypothesized that increased Nogo-A in pathological conditions may regulate muscle regeneration. Then differentiating C2C12 cells and induced myogenic stem cells(iMSC) showed upregulated Nogo-A and Myogenin, and Nogo-A silencing in C2C12 cells abrogated the capability to differentiate into myotubes. In conclusion, Nogo functions to maintain muscle homeostasis and integrity, and altered Nogo-A expression in pathological muscle condition mediates muscle regeneration. These understanding suggests Nogo-A as a novel differentiation target for the treatment of myopathies at clinical set.

2019-05-31 | GSE131955 | GEO

Effect of Nogo deficiency on the insulin signaling pathway

Project description:The elevation of Nogo-B expression in T2DM mice and Nogo-B knockdown alleviated diabetic symptoms in db/db mice prompted us to further investigate the involvement of Nogo-B in the insulin signaling pathway and T2DM. The three isoforms of Nogo are derived from various RNA splicing events, so deleting Nogo-B exons 2-4 results in the deficiency of other Nogo members, resulting in Nogo knockout (Nogo-/-) mice. As the liver is the key organ in the systemic response to insulin and controls glucose and lipid metabolism, we conducted RNA-seq of livers isolated from 8-week-old Nogo-/- mice and WT littermates.

2023-07-24 | GSE236979 | GEO

Nogo-A modulates gene expression to fine-tune enamel development

Project description:Nogo-A is a major player in neural development and regeneration, and it is the target of several clinical trials. However, its functions outside the nervous system are mostly unknown. We observed that Nogo-A is expressed in dental epithelial cells, responsible for the formation of enamel, and we showed that the deletion of Nogo-A in transgenic mouse models leads to the formation of defective enamel. We observed that Nogo-A directly interacts with molecules important for gene expression regulation, and its deletion perturbs their cellular localization. As a result, Nogo-A deletion induces overexpression of genes involved in cell differentiation and enamel production. Mechanistically, we demonstrated that intracellular Nogo-A, and not cell surface Nogo-A, is responsible for gene expression modulation. Taken together, our results indicate a new role for Nogo-A as regulator of enamel formation and suggest a new possible cell-autonomous function in regulating gene expression and cell differentiation.

2024-06-20 | PXD030386 | Pride

Effects of Nogo-A deletion in the dental epithelium of the continuously growing mouse incisor

Project description:Nogo-A is a major player in the regulation of neural development and regeneration, and it is the target of several clinical trials. Despite its high clinical relevance, the functions of Nogo-A outside the central nervous system are mostly unknown. In this work, we investigated the role of Nogo-A in tooth development in mouse transgenic models. We observed that Nogo-A is expressed in ameloblasts, the cells responsible for the formation of enamel. We show that the deletion of Nogo-A in the dental epithelium leads to the formation of defective enamel. By RNA sequencing we showed that this phenotype is associated with the overexpression of clusters of genes involved in cell differentiation and production of enamel.

2022-01-01 | GSE160829 | GEO

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