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Small RNA-seq gene expression profile of the SUM159PT breast cancer cell line, upon overexpression of the microRNA responsive elements of candidate TDMD triggers (ABCA1, HADHB, TRAF6)

ABSTRACT: small RNA-seq gene expression profile of the SUM159PT breast cancer cell line, upon overexpression of the microRNA responsive elements of candidate TDMD triggers (ABCA1, HADHB, TRAF6)

PROVIDER: PRJNA992423 | ENA |

REPOSITORIES: ENA

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small RNA-seq gene expression profile of the SUM159PT breast cancer cell line, upon overexpression of the microRNA responsive elements of candidate TDMD triggers (ABCA1, HADHB, TRAF6)

Project description:We investigate the potential of candidate microRNA responsive elements (MRE, contained in the 3'UTR of candidate transcripts) to trigger target-dependent microRNA degradation (TDMD). To this purpose, we over-expressed the MRE by delivering a lentiviral construct in SUM159PT cells and we profiled microRNAs by small RNA sequencing 7 days after the infection.

2024-12-31 | GSE236781 | GEO

SUM159PT

Project description:SUM159PT

| PRJNA922598 | ENA

Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy [bulkRNA-seq]

Project description:Glaucoma is an optic neuropathy characterized by progressive degeneration of retinal ganglion cells (RGCs) and visual loss. Previous studies have reported that the variation of the ATP-binding cassette transporter 1 (ABCA1) gene is linked to a higher risk of glaucoma in humans, but the pathological mechanisms remain unknown. Here we report that ABCA1 loss, especially in astrocytes, causes optic neuropathy. ABCA1 was mainly expressed in astrocytes rather than neurons, and that knockout of Abca1 gene under GFAP promoter (Glia-KO) caused age-associated RGC degeneration and ocular dysfunction without affecting intraocular pressure, a major risk factor for glaucoma. Glia-KO mice showed age-associated changes in astrocyte reactivity accompanied by the accumulation of cholesterol, a major substrate of ABCA1. Single-cell RNA sequencing revealed that Abca1 deficiency causes astrocyte-triggered inflammation and increased sensitivity of RGCs against excitotoxicity. Altogether, these findings suggest that astrocytic dysfunction caused by ABCA1 loss triggers age-associated optic neuropathy-like pathology.

2022-07-11 | GSE207928 | GEO

Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy [scRNA-seq]

2022-07-11 | GSE207929 | GEO

Transcription profiling of livers from mice overexpress ABCA1 in LDL receptor -/- genetic background to characterize the effects of ABCA1 overexpression.

Project description:Changes in the transcript profile due to ABCA1 expression in murine liver samples was evaluated in LDL receptor -/- genetic backgrounds. Experiment Overall Design: Case (ABCA1-transgenic) versus control (wild-type) design with 4 biological replicates per condition

2007-11-13 | E-GEOD-5496 | biostudies-arrayexpress

Homo sapiens strain:SUM159PT

Project description:SUM159PT cell line transcriptome

| PRJNA224979 | ENA

RNA-sequencing of hepatocyte specific ABCA1 deletion mice

Project description:ATP binding cassette transporter A1 (ABCA1) regulates cellular cholesterol efflux. We characterized the gene expression changes following hepatocyte specific ABCA1 deletion in mice. We report that genes and pathways related to lipogenesis were downregulated in mice with hepatocyte specific ABCA1 deletion compared to floxed controls.

2017-06-06 | GSE96093 | GEO

ABCA1-eRNA as a novel Epigenetic Regulator, promotes cholesterol efflux, Attenuates Macrophage Inflammation and Severity of Coronary Artery Disease [ABCA1 RNA-seq]

Project description:Enhancer RNAs (eRNAs) are emerging as powerful regulators of various biological processes, but the underlying epigenetic regulatory mechanisms of these molecules in cholesterol homeostasis remain elusive. Using an integrated genomic screen, we identified an intragenic super-enhancer derived long noncoding RNA embedded in the ATP-binding cassette transporter A1 (ABCA1) gene, named ABCA1-seRNA, which is required for activation of RXRα/LXR mediated gene expression. Deficiency of ABCA1-seRNA abolished cholesterol efflux, promotes Macrophage Inflammation, and that haven been causally Susceptibility to Coronary heart disease. Mechanistically, ABCA1-seRNA affects cholesterol efflux by interaction with MED23 and recruitment RXR and LXR to mediate ABCA1 transcription in cis. Furthermore, ABCA1-seRNA repression inflammatory response and attenuated macrophage M1 polarization and migration through ubiquitination of a NF-B subunit P65. Our results suggest that super-enhancer derived long noncoding RNA, as a novel Epigenetic Regulator, are critical components to maintain cholesterol homeostasis and inflammation restriction, represent an attractive therapeutic target to reduce Atherosclerotic cardiovascular disease (ASCVD).

2024-12-01 | GSE192939 | GEO

Ribosome profiling on SUM159PT cells grown in vitro or in vivo

Project description:SUM159PT cells were grown either in vitro (in culture) or in vivo (mouse), after which RPL10a tagged with GFP was used to perform extraction by immoprecipitation and subsequent ribosome profiling

2016-02-17 | GSE74512 | GEO

Misfolded SOD1 binds the ubiquitin ligase TRAF6

Project description:Amyotrophic lateral sclerosis (ALS) is a fatal disease, characterized by the selective loss of motor neurons. Mutations in Cu/Zn superoxide dismutase (SOD1) are the second most common cause of ALS and it is now well accepted that they result in a gain of toxicity due to protein misfolding. We previously demonstrated in the SOD1G93A rat model that misfolded SOD1 exists as distinct conformers and deposits on mitochondrial subpopulations. Here, using SOD1G93A rats coupled with conformation-restricted antibodies for misfolded SOD1 (AMF7-63 and B8H10), we identified the interactomes of the mitochondrial pools of misfolded SOD1. This strategy identified binding partners that uniquely interacted with either AMF7-63- or B8H10-reactive SOD1 conformers as well as a high proportion of interactors common to both conformers. Of this latter set, we identified the E3 ubiquitin ligase TNF receptor-associated factor 6 (TRAF6) and determined that exposure of the SOD1 functional loops facilitates this interaction. However, this conformational criterion is not universally fulfilled by all SOD1 mutants and differentiates TRAF6-interacting from non-interacting SOD1 mutants. Functionally, TRAF6 stimulates mutant SOD1 polyubiquitination and aggregation. While TRAF6 E3 ubiquitin ligase activity is required for the former, it is dispensable for the latter, indicating that the polyubiquitination and aggregation of mutant SOD1 mediated by TRAF6 are independent events. We propose that misfolded SOD1 binding to TRAF6 may be relevant to ALS disease.

2020-02-24 | PXD015279 | Pride

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