Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression signatures in the skin of focal palmoplantar keratoderma (FPPK) patients

ABSTRACT: We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53613 | GEO | 2013/12/24

SECONDARY ACCESSION(S): PRJNA232488

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression signatures in the skin of focal palmoplantar keratoderma (FPPK) patients

Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. From a 37-year-old Chinese male (II-7) and his 12-year-old son (III-7), biopsies from unaffected and affected skin tissues were obtained and their transcriptome profiles were analyzed in order to identify molecular changes related with the pathology of FPPK.

2013-12-24 | E-GEOD-53613 | biostudies-arrayexpress

Gene expression signatures of HaCaT cell lines transfected with mutant TRPV3

Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. To understand the effect of TRPV3 mutation, transcriptome of HaCaT cell lines transfected with mutant TRPV3 were profiled in time-course manner (16, 24 and 40hr).

2013-12-24 | E-GEOD-53615 | biostudies-arrayexpress

Gene expression signatures of 293T cell lines transfected with mutant TRPV3

Project description:We identified a number of affected pathways through transcriptome analysis on the skin biopsy samples of the FPPK patients. Our findings suggest that TRPV3 dysfunction may increase apoptotic activity, inhibit keratinocyte differentiation and disturb the intricate balance between proliferation and differentiation state of keratinocytes in the skin. To understand the effect of TRPV3 mutation, transcriptome of 293T cell lines transfected with mutant TRPV3 were profiled in time-course manner (16, 24 and 40hr).

2013-12-24 | E-GEOD-53614 | biostudies-arrayexpress

Gene expression signatures of HaCaT cell lines transfected with mutant TRPV3

2013-12-24 | GSE53615 | GEO

Gene expression signatures of 293T cell lines transfected with mutant TRPV3

2013-12-24 | GSE53614 | GEO

Molecular effects of different TRPV3 Mutations

2015-12-31 | GSE71236 | GEO

Molecular effects of different TRPV3 Mutations

Project description:To understand the impact of dysfunctional TRPV3 on keratinocyte proliferation and differentiation, we conducted transcriptomic analysis on cells that express cloned different TRPV3 mutations identified in focal palmoplantar keratoderma (FPPK) patients and identified a number of perturbed pathways associated with epidermal cells construction and development. We also analyzed the molecular changes of skin biopsy samples from patients. Our data suggests that TRPV3 dysfunction inhibits keratinocyte differentiation, actives apoptosis pathway resulted in cell death, and disturbs the balance between keratinocyte proliferation and differentiation processes in the skin. To explore the functional impact of the different TRPV3 mutations on cells, we cloned the wild type and mutant TRPV3 clones into expression vector. The wild-type human TRPV3 gene was amplified from cDNA made from a mixture of human tissue total RNA and cloned into pcDNA3.1 (Life Technologies, Carlsbad, CA). The accuracy of the cloned sequence was checked with Sanger sequencing. Quick Change II XL site-directed mutagenesis kit (Agilent, Santa Clara, CA) was used to introduce sequence changes corresponding to mutations observed in patients. The HEK293T cells were transfected using Lipofectamine 2000 (Life Technologies, Carlsbad, CA) according to the manufacturerâs instructions. Cells were also transfected with the same plasmid without insert as control.

2015-12-31 | E-GEOD-71236 | biostudies-arrayexpress

Expression data from human 3D skin models in response to IL-31 treatment

Project description:Atopic dermatitis, a chronic inflammatory skin disease with increasing prevalance, is closely associated with skin barrier defects. A cytokine related to disease severity and inhibition of keratinocyte differentiation is IL-31. To identify its molecular targets, IL-31-dependent gene expression was determined in 3-dimensional organotypic skin models. In this data set we include expression data from human 3D skin models treated with or without IL-31 for 2, 8, 24 and 48 hours. As a source of keratinocytes HaCaT cells were used. These are immortalized primary keratinocytes. Human dermal fibroblasts were derived from a skin biopsy. A total of 8 samples were analyzed. We compared the control vs the IL-31 treated sample for each time point.

2016-02-29 | E-GEOD-76880 | biostudies-arrayexpress

Expression data from human 3D skin models in response to IL-31 treatment

2016-02-29 | GSE76880 | GEO

Transcription profiling of CHUK deleted mouse keratinocytes compared to wild type mouse keratinocytes

Project description:It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKÎ± induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKÎ± deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKÎ± inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKÎ± serves as an innate surveillant. Experiment Overall Design: The differences in gene expression profiles of CHUK deleted mouse keratinocytes compared to wild type mouse keratinocytes were analyzed using two dual-channel agilent microarrays in duplicates.

2009-08-12 | E-GEOD-12111 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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