Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of Terc deficiency on differentiation and maturation of OCs during aging [bone slices]

ABSTRACT: The effect of Terc deficiency on differentiation and maturation of OCs during aging [bone slices]

PROVIDER: PRJNA929930 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23285601_1.fastq.gz	Fastqsanger.gz
	SRR23285601_2.fastq.gz	Fastqsanger.gz
	SRR23285603_1.fastq.gz	Fastqsanger.gz
	SRR23285603_2.fastq.gz	Fastqsanger.gz
	SRR23285606_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

The effect of Terc deficiency on differentiation and maturation of OCs during aging

Project description:The effect of Terc deficiency on differentiation and maturation of OCs during aging

| PRJNA933588 | ENA

The effect of Terc deficiency on differentiation and maturation of OCs during aging [bone slices]

Project description:Aging alters the bone function and elevates osteoporosis disability in diseases such as fractures. Understanding how aging alters bone marrow cellular differentiation could help us identify potential anti-aging targets to restore cellular homeostasis.

2024-09-18 | GSE224119 | GEO

The effect of Terc deficiency on differentiation and maturation of OCs during aging

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

2024-09-20 | GSE225030 | GEO

Post-transcriptional manipulation of TERC reverses molecular hallmarks of telomere disease

Project description:The telomerase RNA component (TERC) is a critical determinant of cellular self renewal. Poly(A)-specific ribonuclease (PARN) is required for post-transcriptional maturation of TERC. PARN mutations lead to incomplete 3â² end processing and increased destruction of nascent TERC RNA transcripts, resulting in telomerase deficiency and telomere diseases. Here, we determined that overexpression of TERC increased telomere length in PARN-deficient cells and hypothesized that decreasing post-transcriptional 3â² oligo-adenylation of TERC would counteract the deleterious effects of PARN mutations. Inhibition of the noncanonical poly(A) polymerase PAP-associated domainâcontaining 5 (PAPD5) increased TERC levels in PARN-mutant patient cells. PAPD5 inhibition was also associated with increases in TERC stability, telomerase activity, and telomere elongation. Our results demonstrate that manipulating post-transcriptional regulatory pathways may be a potential strategy to reverse the molecular hallmarks of telomere disease. mRNA sequencing of induced pluripotent stem cells and 293 cell line.

2016-08-02 | E-GEOD-81507 | biostudies-arrayexpress

Post-transcriptional manipulation of TERC reverses molecular hallmarks of telomere disease

Project description:The telomerase RNA component (TERC) is a critical determinant of cellular self renewal. Poly(A)-specific ribonuclease (PARN) is required for post-transcriptional maturation of TERC. PARN mutations lead to incomplete 3′ end processing and increased destruction of nascent TERC RNA transcripts, resulting in telomerase deficiency and telomere diseases. Here, we determined that overexpression of TERC increased telomere length in PARN-deficient cells and hypothesized that decreasing post-transcriptional 3′ oligo-adenylation of TERC would counteract the deleterious effects of PARN mutations. Inhibition of the noncanonical poly(A) polymerase PAP-associated domain–containing 5 (PAPD5) increased TERC levels in PARN-mutant patient cells. PAPD5 inhibition was also associated with increases in TERC stability, telomerase activity, and telomere elongation. Our results demonstrate that manipulating post-transcriptional regulatory pathways may be a potential strategy to reverse the molecular hallmarks of telomere disease.

2016-08-02 | GSE81507 | GEO

Poly(A)-specific ribonuclease (PARN) mediates 3' end maturation of the telomerase RNA component

Project description:Mutations in the poly(A) ribonuclease (PARN) gene cause telomere diseases including familial idiopathic pulmonary fibrosis (IPF) and dyskeratosis congenita (DC)1,2, but how PARN deficiency impacts telomere maintenance is unclear. Here, using somatic cells and induced pluripotent stem (iPS) cells from DC patients with PARN mutations, we show that PARN is required for the 3′ end maturation of the telomerase RNA component (TERC). Patient cells as well as immortalized cells in which PARN is disrupted show decreased levels of TERC. Deep sequencing of TERC RNA 3′ termini reveals that PARN is required for removal of posttranscriptionally acquired oligo(A) tails that target nuclear RNAs for degradation. Diminished TERC levels and the increased oligo(A) forms of TERC are normalized by restoring PARN, which is limiting for TERC maturation in cells. Our results reveal a novel role for PARN in the biogenesis of TERC, and provide a mechanism linking PARN mutations to telomere diseases. mRNA sequencing of fibroblasts, induced pluripotent stem cells, and 293 cell line.

2015-09-08 | E-GEOD-71709 | biostudies-arrayexpress

The target gene investigation in osteoclats (OCs) treated with mmu-miR-5112 enriched in EVs from OCs with prostate cancer (PCa) cells [target_EV-miR-5112]

Project description:Bone metastatic lesions of PCa contain areas of bone destruction and formation that are directed by OCs and osteoblasts (OBs), respectively. OC-derived EVs are reported to maintain normal bone homeostasis; however, there is no study investigating the role of EVs from OCs in the presence of PCa. We identified mmu-miR-5112 enriched in EVs from OCs co-cultured with several PCa cell lines. NGS analyses were performed to investigate predicted target genes of EV-mmu-miR-5112 in OCs.

2024-06-06 | GSE268550 | GEO

Poly(A)-specific ribonuclease (PARN) mediates 3' end maturation of the telomerase RNA component

2015-09-08 | GSE71709 | GEO

The gene expression profiles of maturing osteoclasts (OCs) co-cultured with prostate cancer (PCa) cell lines.

Project description:Bone metastatic lesions of PCa contain areas of bone destruction and formation that are directed by OCs and osteoblasts (OBs), respectively. Bone resorption induced by OCs is a necessary priming event for tumor progression in PCa bone metastasis.; however, the characteristics of OCs affected by PCa have not been fully elucidated. Here, we performed NGS analysis to investigate the characteristics of OCs in the presence of PCa.

2024-06-06 | GSE268422 | GEO

Expression data between WT and G3/4 Terc KO mouse ESCs during differentiation

Project description:Mammalian telomeres are formed by tandem repeats of the TTAGGG sequence, and shorten with each round of cell division in the absence of telomerase. Telomere shortening and dysfunction has been implicated in the pathology of several age-related diseases and premature ageing syndromes. Telomerase is important for telomere length maintenance. Telomerase RNA component, also known as TERC, is a component of telomerase. Terc knockout leads to telomerase deficiency and telomere shortening. Heterozygous telomerase-deficient (Terc+/-) mice were housed and bred for homozygous generation. ESC lines were generated with high efficiency from wild-type (WT, Terc+/+), heterozygous (Het, Terc+/-) and early- to late-generation (G1, G3 and G4) Terc-/- mouse blastocysts. Telomeres were shorter in Terc+/- ES cells than in WT ES cells, and further shortened from G1 to G4 Terc-/- ES cells. We took advantage of ES cell lines with various telomere lengths to investigate roles of telomere length on differentiation capacity of ES cells. We found that telomere length, but not telomerase activity, is required for differentiation of ES cells into epidermis. We performed microarray analysis to investigate differential gene expression profile at genome-wide levels between WT and G3/G4 Terc-/- (KO) mouse ES cells and during differentiation in vitro of WT and G4 Terc-/- mouse ES cells.

2016-01-29 | GSE77362 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data