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Transcriptomes of UFMylation gene knockdown in mouse embryonic fibroblast cell (MEF) treated with hypoxia for 24 hours [mouse]

ABSTRACT: Transcriptomes of UFMylation gene knockdown in mouse embryonic fibroblast cell (MEF) treated with hypoxia for 24 hours [mouse]

PROVIDER: PRJNA1139653 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29939013_1.fastq.gz	Fastqsanger.gz
	SRR29939013_2.fastq.gz	Fastqsanger.gz
	SRR29939014_1.fastq.gz	Fastqsanger.gz
	SRR29939014_2.fastq.gz	Fastqsanger.gz
	SRR29939015_1.fastq.gz	Fastqsanger.gz

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Transcriptomes of UFMylation gene knockdown in mouse embryonic fibroblast cell (MEF) treated with hypoxia for 24 hours [mouse]

Project description:To investagate the gene expression profiling of dysUFMylation in MEF under hypoxia, we constructed Ufl1 konckouted-MEF using CRISPR-Cas9 and couducted RNA-seq. mRNAs were isolated and purified using RNeasy Plus Mini Kit (Qiagen). Samples were prepared from three biological replicates.

2025-06-20 | GSE272936 | GEO

Analysis of the transcriptomic profile of WT mouse embryonic fibroblast (MEF WT) and Nf2-knockout mouse embryonic fibroblast (MEF Nf2 KO) cell lines

Project description:Analysis of the transcriptomic profile of WT mouse embryonic fibroblast (MEF WT) and Nf2-knockout mouse embryonic fibroblast (MEF Nf2 KO) cell lines

| PRJNA662370 | ENA

Irradiation response in PKBalpha MEF

Project description:MEF proficient or deficient in PKBalpha, or PKBalpha knockout MEF where PKBalpha expression was reconstituted by stable transfection were subjected to 10Gy gamma-IR treatment. 4 or 24 hours after treatment, gene expression changes were analyzed. Keywords: genotype0-specific stress response in PKBalpha MEF

2008-04-04 | GSE9146 | GEO

Analysis of the transcriptomic profile of WT mouse embryonic fibroblast (MEF WT) and Nf2-knockout mouse embryonic fibroblast (MEF Nf2 KO) cell lines

Project description:Merlin is the tumor suppressor protein encoded by the NF2 gene. The expression of Merlin is remarkably decreased in metastatic breast cancer tissues irrespective of the breast cancer subtype. In order to ascribe clinical relevance, we re-capitulated the loss of Merlin in breast cancer cells. Merlin deficiency elicited a markedly invasive phenotype. In order to overcome the challenge of embryonic lethality of a total Nf2-knockout, we generated a unique mammary-specific Nf2-knockout mouse mammary tumor model. Both, the Nf2-knockout mouse embryonic fibroblasts (MEF) and Merlin-deficient breast tumor cells displayed a robust invasive phenotype. Transcriptomic assessment of Nf2-knockout MEFs revealed notable alterations in glutathione transferase and antioxidant networks indicating a role for Merlin in redox biology. This programmatic alteration resonated with the pathways that emerged from breast tumor cells engineered for Merlin deficiency.

2021-04-14 | GSE157677 | GEO

UFMylation maintains YAP stability to promote vascular endothelial cell senescence

Project description:Endothelial cell senescence is an accomplice for vascular aging, which leads to cardiovascular diseases (CVD). Evidences showed that Hippo- Yes-associated protein (YAP) signaling pathway plays an essential role in aging-associated CVD. However, the exact role of YAP protein in endothelial cell senescence remains not fully clear. Here, we reported that YAP was elevated in senescent human umbilical vein endothelial cells (HUVECs) and inhibition of YAP by either specific siRNAs or inhibitor Verteporfin could attenuate HUVECs senescence. In contrast, overexpression of YAP induces cell senescence. Besides, we found that UFMylation activity and YAP were both elevated in senescent cells. Mechanistically, we found that UFMylation, a newly identified ubiquitin-like modification with essential biological functions, maintains the stability of YAP and further found that YAP is a substrate for UFMylation. Importantly, we found that compound 8.5, an inhibitor of E1 of UFMylation, can attenuate cell senescence with reduced YAP protein and alleviate vascular aging and improve cardiac function in aged mice. Therefore, compound 8.5 may be a potential small molecule for delaying vascular aging. Together, our finding provides molecular mechanism by which UFMylation maintains YAP stability and exerts an important role in promoting cell senescence, and identified that a previously unrecognized UFMylation is a potential therapeutic target for anti-aging.

2025-01-08 | GSE273828 | 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

| PRJNA765330 | ENA

Primary Mouse Hepatocytes treated with 500μM Metformin for 24 hours

Project description:Anaylsis of gene expression in primary mouse hepatocytes treated with 500μM Metformin for 24 hours

2019-12-08 | GSE138087 | GEO

Tet-ZFP36L1 in 6 hours and 24 hours

Project description:Tet-ZFP36L1 in 6 hours and 24 hours

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Ribosomal protein RPL26 is the principal target of UFMylation

Project description:UFM1 is a small, metazoan-specific, ubiquitin-like protein modifier that is essential for embryonic development. Although loss-of-function mutations in UFM1 conjugation are linked to ER stress, neither the biological function nor the relevant cellular targets of this protein modifier are known. Here we show that a largely uncharacterized ribosomal protein, RPL26, is the principal target of UFM1 conjugation. RPL26 UFMylation and deUFMylation is catalyzed by enzyme complexes tethered to the cytoplasmic surface of the ER and UFMylated RPL26 is highly enriched on ER membrane-bound ribosomes and polysomes. Biochemical analysis and structural modeling establish that UFMylated RPL26 and the UFMylation machinery are in close proximity to the SEC61 translocon, suggesting that this modification plays a direct role in cotranslational protein translocation into the ER. These data suggest that UFMylation is a ribosomal modification specialized to facilitate metazoan-specific protein biogenesis at the ER.

2018-12-11 | GSE123539 | GEO

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