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Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2

ABSTRACT: Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2

PROVIDER: PRJNA494414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7956090.fastq.gz	Fastqsanger.gz
	SRR7956091.fastq.gz	Fastqsanger.gz
	SRR7956092.fastq.gz	Fastqsanger.gz
	SRR7956093.fastq.gz	Fastqsanger.gz
	SRR7956094.fastq.gz	Fastqsanger.gz

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Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2 & MCM7

Project description:Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2 & MCM7

| PRJNA494413 | ENA

Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2

Project description:Minichromosome maintenance (MCM) proteins facilitate replication by licensing origins and unwinding the DNA double strand. Interestingly, the number of MCM hexamers greatly exceeds the number of firing origins suggesting additional roles of MCMs. Here we show a hitherto unanticipated function of MCM2 in cilia formation in human cells and zebrafish that is uncoupled from replication. Zebrafish depleted of MCM2 develop ciliopathy-phenotypes including microcephaly and aberrant heart looping due to malformed cilia. In non-cycling human fibroblasts, loss of MCM2 promotes transcription of a subset of genes, which cause cilia shortening and centriole overduplication. Chromatin immunoprecipitation experiments show that MCM2 binds to transcription start sites of cilia inhibiting genes. We propose that such binding may block RNA polymerase II-mediated transcription. Depletion of a second MCM (MCM7), which functions in complex with MCM2 during its canonical functions, reveals an overlapping cilia-deficiency phenotype likely unconnected to replication, although MCM7 appears to regulate a distinct subset of genes and pathways. Our data suggests that MCM2 and 7 exert a role in ciliogenesis in post-mitotic tissues.

2018-10-20 | GSE120766 | GEO

Comparison of the transcriptomes of hTERT-immortalized and wild type marmoset fibroblasts by next-generation RNA sequencing.

Project description:Neuborn marmoset fibroblasts were immortalized by piggyBac transposition of hTERT expression cassette. The gene expression of the resulting one polyclonal and two monoclonal immortalized cell lines were then compared with the wild type cells used for their derivation.

2018-10-29 | GSE114965 | GEO

miRNA Expression in Senescent and Immortalized BJ fibroblasts

Project description:Limited data exists regarding changes of microRNA (miRNA) expression during senescence in human cells and no reports correlate telomerase expression with regulation of senescence-related miRNAs. We used miRNA microarrays to provide a detailed account of miRNA profiles for early passage and senescent human foreskin (BJ) fibroblasts as well as early and late passage immortalized fibroblasts (BJ-hTERT) that stably express the human telomerase reverse transcriptase subunit hTERT. The revelation that miRNA expression changes with extended passaging in BJ-hTERT cells will contribute to a comprehensive understanding of the connections between telomerase expression, senescence and processes of cellular aging.

2010-06-05 | GSE22134 | GEO

Genome-wide expression analysis of human hTert immortalized fibroblasts after donwregulation of MCM7

2018-10-20 | GSE120767 | GEO

Genome-wide expression analysis of human hTert immortalized fibroblasts after donwregulation of MCM7

Project description:Genome-wide expression analysis of human hTert immortalized fibroblasts after donwregulation of MCM7

| PRJNA494415 | ENA

Genome-wide expression analysis of human hTert immortalized fibroblasts after downregulation of MCM2 & MCM7

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-10-20 | GSE120768 | GEO

Expression data for hTERT-immortalized human Sertoli cell line versus original primary human Sertoli cells

Project description:Primary human Sertoli cells (hSerCs) were immortalized by transducing human TERT into the genome to produce human TERT-immortalized human Sertoli cells (hTERT hSerCs). Total RNA was isolated from both primary hSerCs and hTERT hSerCs and submitted for Affymetrix gene analysis. Gene expression differences of common Sertoli cell marker genes and xenobiotic transporters was preferentially assessed between each cell type.

2020-09-23 | GSE158400 | GEO

Fibroblasts hTERT-BJ1: Control vs Colpvp

Project description:Fibroblasts hTERT-BJ1: Control vs Colpvp

| PRJNA1093089 | ENA

Mutated RNA component of the telomerase induces apoptosis via GADD45-? in hTERT-overexpressing primary fibroblasts

Project description:Mutant template human telomerase RNAs (MT-hTers) have been shown to induce apoptosis in various cancerous cells that have high telomerase activity. However, the exact mechanisms by which MT-hTers inhibit the growth of cancer cells and affect normal somatic cells remain largely unknown. To determine the effects of MT-hTers on normal cells, MT-hTer-47A and -AU5 were introduced into IMR90 primary lung fibroblasts that have very low endogenous hTERT levels. Growth of IMR90 cells following MT-hTers infection was not impaired, however, cell proliferation of IMR90 wild-type hTERT (WT-hTERT) cells under MT-hTers-47A and -AU5 treatment was inhibited and increased cell death was observed. FACS analysis also showed that these cells underwent apoptosis. Confocal microscopy revealed that MT-hTers induced DNA damage foci, i.e., 53BP1 and ?-H2AX, in immortalized IMR90 WT-hTERT cells. Microarray analysis of the IMR90 WT-hTERT MT-hTer-47A and -AU5 versus IMR90 MT-hTer-47A and -AU5 revealed that GADD45-? was significantly elevated, and this result was further confirmed following RT-PCR and real time PCR assays. Moreover, we have showed that MT-hTers induce ATM phosphorylation at Ser 1981 in IMR90 WThTERT cells, and Western analysis revealed high levels of phospho p53 expression in these cells following activation of ATM. Our results also suggest that p53-dependent apoptosis in MT-hTers-infected IMR90 WT-hTERT cells could be due to a decreased expression of TRF2. Taken together, we propose a model that MT-hTers induce DSBs-like damages and trigger programmed cell death in IMR90 WT-hTERT cells following ATM-mediated phosphorylation of p53, which in turn upregulate GADD45-?, ultimately leading to apoptosis. MT-hTer-47A and -AU5 were introduced into IMR90 primary lung fibroblasts and immortalized IMR90 WT-hTERT cells. Through microarray analysis, gene expression of MT-hTer-infected IMR90 WT-hTERT cells were compared against MT-hTer-infected IMR90 control cells.

2011-05-28 | E-GEOD-24975 | biostudies-arrayexpress

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