Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [RNA-seq]

ABSTRACT: To understand induction of cornification genes during lineage appropriate (keratinocyte differentiation) and inappropriate (fibroblast senescence) conditions , we generated histone modification and gene expression datasets. Then we compared keratinocyte's datasets with fibroblast senescence ones in this study.

ORGANISM(S): Homo sapiens

PROVIDER: GSE180361 | GEO | 2021/10/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [ChIP-seq]

Project description:To understand induction of cornification genes during lineage appropriate (keratinocyte differentiation) and inappropriate (fibroblast senescence) conditions , we generated histone modification and gene expression datasets. Then we compared keratinocyte's datasets with fibroblast senescence ones in this study.

2021-10-23 | GSE180358 | GEO

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

Project description:To understand induction of cornification genes on lineage appropriate (keratinocyte differentiation) and inappropriate (fibroblast senescence) conditions , we generated histone modification and gene expression dataset. Then we compared these keratinocyte's dataset with our previous fibroblast senescence dataset in the study.

2021-01-04 | GSE130457 | GEO

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

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

2021-10-23 | GSE180469 | GEO

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

Project description:Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

| PRJNA540290 | ENA

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

Project description:Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence

| PRJNA748372 | ENA

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [RNA-seq]

Project description:Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [RNA-seq]

| PRJNA747991 | ENA

Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [ChIP-seq]

Project description:Aberrant gene expression leakage from linage-specific heterochromatic loci during senescence [ChIP-seq]

| PRJNA747981 | ENA

Transcriptomic study from total RNA extract from reconstructed Human Epidermis (RHE) at 3 time points and quatriplicats under Afatinib (100 nm) exposure versus vehicle

Project description:Effect of EGFR inhibitors on the epidermis Epidermal Growth Factor inhibitors (EGFRi) used in oncology therapy modify the keratinocyte differentiation processes, impairing proper skin barrier formation and leading to Cutaneous Adverse Drug Reactions (CADR). To uncover the molecular signatures associated with CADRs, we applied phospho-proteomic and transcriptomic assays on Reconstructed Human Epidermis (RHE) tissues exposed to a therapeutically relevant concentration of afatinib, a second EGFRi generation. Following drug exposure, we observed an increased expression of gene families involved in keratinocyte differentiation, senescence, oxidative stress and alterations in the epidermal immune-related markers. Furthermore, our results show that afatinib may interfere with Vitamin D3 (VD3) metabolism, acting via CYP27A1 and CYP24A1 to regulate calcium concentration through the PI3K/AKT pathway. Consequently, basal layer keratinocytes switch from a pro-proliferating to a pro-differentiative program, characterized by upregulation of biomarkers associated with increased keratinization, cornification, Th2 response and decreased innate immunity. Such effects may increase the skin susceptibility to cutaneous penetration of irritants and pathogens.

2022-02-23 | GSE167246 | GEO

Retinoblastoma protein regulates carcinogen susceptibility at heterochromatic cancer driver loci.

Project description:Carcinogenic insult, such as UV light exposure, creates DNA lesions that evolve into mutations if left unrepaired. These resulting mutations can contribute to carcinogenesis and drive malignant phenotypes. Susceptibility to carcinogens (i.e., the propensity to form a carcinogen-induced DNA lesion) is regulated by both genetic and epigenetic factors. Importantly, carcinogen susceptibility is a critical contributor to cancer mutagenesis. It is known that mutations can be prevented by tumor suppressor regulation of DNA damage response pathways; however, their roles carcinogen susceptibility have not yet been reported. In this study, we reveal that the retinoblastoma (RB1) tumor suppressor regulates UV susceptibility across broad regions of the genome. In particular, centromere and telomere-proximal regions exhibit significant increases in UV lesion susceptibility when RB1 is deleted. Several cancer-related genes are located within genomic regions of increased susceptibility, including telomerase reverse transcriptase, TERT, thereby accelerating mutagenic potential in cancers with RB1 pathway alterations. These findings reveal novel genome stability mechanisms of a tumor suppressor and uncover new pathways to accumulate mutations during cancer evolution.

| S-EPMC8739494 | biostudies-literature

Physical and functional CSL-p53 interactions underlie control of cancer stromal cell evolution [ChIP-seq]

Project description:Senescence of stromal fibroblasts has been linked to establishment of cancer associated fibroblasts (CAF) and aging-associated increase of tumors. However, in clinically occurring carcinomas, density and proliferation of CAFs are frequently increased rather than decreased. We previously showed that genetic deletion or down-modulation of the canonical Notch effector CSL/RBP-J? in skin dermal fibroblasts is sufficient for CAF activation with consequent development of multifocal keratinocyte tumors. We now show that CSL deletion or knockdown induces senescence of primary fibroblasts derived from dermis, oral mucosa, breast and lung. CSL functions in these cells as a constitutive direct repressor of multiple senescence- and CAF-effector genes. At the same time, it physically interacts with p53, repressing its activity, and p53 activation provides a failsafe mechanism against compromised CSL function. Concomitant loss of CSL and p53 overcomes fibroblast senescence, enhances expression of CAF effector genes and, in vivo, promotes tumour and stromal cell expansion. Together, the findings support a CAF activation/stromal evolution model under convergent CSL/p53 control. Examination of genome-wide CSL binding sites in primary human dermal fibroblasts usinf two different antibodies against CSL

2015-08-24 | E-GEOD-59942 | biostudies-arrayexpress

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