RNA-sequencing profiling of mRNAs in A549 cells with TIF1γ overexpression or TAF15 knockdown
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ABSTRACT:
PROVIDER: PRJNA863643 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20715327_1.fastq.gz | Fastqsanger.gz | |||
| SRR20715327_2.fastq.gz | Fastqsanger.gz | |||
| SRR20715328_1.fastq.gz | Fastqsanger.gz | |||
| SRR20715328_2.fastq.gz | Fastqsanger.gz | |||
| SRR20715329_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the target gene regulated by TIF1γ and TAF15, we established stable TIF1γ-overexpressing and TAF15-silencing A549 cells separately, and total RNA was extracted and subjected to RNA sequencing analysis. Following that, differentially expressed genes were employed for further investigation.
2022-10-19 | GSE210093 | GEO
Project description:TAF15, a DNA and RNA-binding protein primarily localized in the nucleus, has been reported to be associated with the aging process and neurodegenerative diseases accompanied by cognitive decline. However, its role in regulating learning and memory remains unclear. Here, we discovered that TAF15 accumulates in the hippocampus of aged mice, and TAF15 overexpressing in hippocampal neurons led to spatial learning and memory impairments in young mice. These finding are further supported by the significant reduction of dendritic spines density and synaptic proteins level. Further studies revealed that overexpression of TAF15 is likely to reduce the number of dendritic spines by inhibiting the expression of Npas4 (among the most rapidly induced immediate-early genes) and its target gene Nptx2. Notably, the expression of Npas4 and Nptx2 in the hippocampus of aged mice is also downregulated. Additionally, we demonstrated that TAF15 binds to the core promoter of Npas4 gene and inhibits its transcription, and neuronal depolarization induces the dissociation of TAF15 from Npas4 promoter. Together, these findings uncover a direct role of TAF15 in regulating spatial learning and memory formation, which may provide new insights into aging-related cognitive deficits.
2024-12-18 | GSE244954 | GEO
Project description:TAF15 (formerly TAFII68) is a member of the TET family of RNA and DNA binding proteins whose genes are frequently translocated in sarcomas. Consistent with a functional role in cell viability, TAF15 depletion had a growth-inhibitory effect and increased apoptosis. Interestingly, one of the genes affected by TAF15 depletion is CDKN1A/p21, a key regulator of cell cycle. Here we show that TAF15 down-regulates CDKN1A/p21 expression through a pathway involving miRNAs.
2012-12-21 | GSE34470 | GEO
Project description:KEAP1 overexpressed and NRF2 siRNA knockdown A549 NSCLC cells were used to identify downstream genes of NRF2 pathway separately and by combinatorial analysis. We used triplicate microarrays of transfected A549 cells with mKeap1-GFP for overexpression, siRNAs targeting NRF2 for knockdown and siGFP as control respectively. As a result, we identified several genes which are involved in cancer metabolic functions in these cells. We used microarrays to identify the gene downregulated in both KEAP1 overexpressed and NRF2 siRNA knockdown A549 NSCLC cells and found a subset of downregulated genes which are involved in metabolic functions.
2017-08-02 | GSE94393 | GEO
Project description:TAF15 (formerly TAFII68) is a member of the TET family of RNA and DNA binding proteins whose genes are frequently translocated in sarcomas. Consistent with a functional role in cell viability, TAF15 depletion had a growth-inhibitory effect and increased apoptosis. Interestingly, one of the genes affected by TAF15 depletion is CDKN1A/p21, a key regulator of cell cycle. Here we show that TAF15 down-regulates CDKN1A/p21 expression through a pathway involving miRNAs. We performed a gene expression profiling upon TAF15 knock down by RNA interference.Total RNAs purified from four biological replicates of HeLa GL3 luc cells transfected either with si-TAF15 or control si-LUC were hybridized to the array.
2012-12-21 | E-GEOD-34470 | biostudies-arrayexpress
Project description:TAF15 overexpression impairs memory in mice by inhibiting the transcription of Npas4
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Project description:TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3â untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease. RNA-seq, CLIP-seq and arrays in mouse and human against TAF15 knockdowns This Series represents array sample(s).
2016-07-05 | E-GEOD-77699 | biostudies-arrayexpress
Project description:TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3’ untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease.
2016-07-05 | GSE77699 | GEO
Project description:Frontotemporal dementia (FTD) is the most common form of dementia after Alzheimer's disease and results from frontotemporal lobar degeneration (FTLD). The pathological hallmarks of FTLD are neuronal inclusions of specific, abnormally assembled proteins1. In the majority of cases, the inclusions contain amyloid filament assemblies of TAR DNA-binding protein 43 (TDP-43) or tau, with distinct filament structures characterising different FTLD subtypes2,3. The presence, identities and structures of amyloid filaments in the remaining ~10% of FTLD cases are unknown, but are widely believed to be composed of the protein fused in sarcoma (FUS). As such, these cases are commonly referred to as FTLD-FUS. Here, we used cryogenic electron microscopy (cryo-EM) to determine the structures of amyloid filaments extracted from the prefrontal and temporal cortices of four individuals with FTLD-FUS. Unexpectedly, we found abundant amyloid filaments of the FUS homologue TATA-binding protein-associated factor 15 (TAF15), rather than of FUS itself. The filament fold is formed from residues 7 to 99 in the low-complexity domain (LCD) of TAF15 and was identical between individuals. The formation of TAF15 amyloid filaments with a characteristic fold in FTLD establishes TAF15 proteinopathy in neurodegenerative disease. Furthermore, we found TAF15 filaments with the same fold in the motor cortex and brainstem of two of the individuals, who also showed changes associated with amyotrophic lateral sclerosis (ALS), suggesting that TAF15 proteinopathy may underlie a disease spectrum of FTLD and ALS. The structure of TAF15 amyloid filaments provides a basis for the development of model systems of neurodegenerative disease, as well as for the design of diagnostic and therapeutic tools targeting TAF15 proteinopathy.
2023-12-07 | PXD044821 | Pride
Project description:TDP-43, FUS, and TAF15 are implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. We integrate CLIP-seq and RNA Bind-N-Seq technologies to discover that TAF15 binds to ~4,900 RNAs enriched for GGUA motifs. In the mouse brain, TAF15 and FUS, but not TDP-43, exhibit strikingly similar RNA binding profiles, yet they alter the expression of distinct mRNA populations upon their individual depletions. TAF15 has a minimal role in alternative splicing and instead affects RNA turnover, consistent with an enrichment of TAF15 binding sites in 3â?? untranslated regions. In human stem cell-derived motor neurons, loss of both TAF15 and FUS affected mRNAs distinct from those altered by loss of either protein alone, revealing redundant roles for TAF15 and FUS in maintaining mRNA levels. Furthermore, concomitant rather than individual depletion of TAF15 and FUS more closely resembles RNA profiles of motor neurons derived from FUS R521G ALS patients or from late-stage, sporadic ALS patients. Our study reveals convergent and divergent mechanisms by which FUS, TAF15 and TDP-43 affects RNA metabolism in neurological disease. RNA-seq, CLIP-seq and arrays in mouse and human against TAF15 knockdowns This Series represents RNA-seq sample(s).
2016-07-05 | E-GEOD-77702 | biostudies-arrayexpress