Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Investigating the Pathogenic Mechanism of a C-Terminal Desmoplakin (DSP) Mutation in Palmoplantar Keratoderma through Gene Knockdown in HaCaT Keratinocytes and Comparative Quantitative Proteomic Analysis to Identify Dysregulated Signaling Pathways

ABSTRACT: We identified a C-terminal mutation in the Desmoplakin (DSP) gene in a patient with palmoplantar keratoderma (PPK). To explore the pathogenic mechanism, we knocked down DSP expression in human HaCaT keratinocytes and performed a comparative proteomic analysis with normal cells. This study aims to elucidate the role of DSP mutations in PPK pathogenesis.

ORGANISM(S): Homo Sapiens

SUBMITTER: Longnian Li

PROVIDER: PXD070791 | iProX | Fri Nov 14 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

The N6-methyadenosine (m6A) levels in HaCaT-T cells and control HaCaT cells

Project description:Human m6A-mRNA&lncRNA Epitranscriptomic Microarray of arsenite-transformed human keratinocytes (HaCaT-T cells, 1 μM arsenite exposure for 50 passages) compared to its control HaCaT cells (passed for 50 passages without arsenic exposure).

2020-11-08 | GSE161033 | GEO

Protein dataset of immortalized HaCaT cells p53 knock down HaCaT keratinocytes

Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.

2022-04-28 | PXD033538 | Pride

Human keratinocytes HaCaT LC-MSMS_SDS exposure

Project description:We employed human HaCaT cells as a model system to identify cellular proteins that accompany SDS-induced toxicity based on a proteomic approach. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of SDS (25 µg/ml, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to SDS was analyzed by LC-MS/MS approach and quantified using Progenesis LC software. The abundance of 217 proteins (which were identified by multiple peptides, ≥ 2) was altered in keratinocytes exposed to SDS; in which 131 proteins had increased abundance while 86 proteins was down regulated. The Pathview map of 131 up-regulated proteins was built and enhancement of glycolysis/gluconeogenesis was found.

2017-11-03 | PXD007789 | Pride

Taxifolin protects HaCaT keratinocytes from UVB damage

Project description:The photoprotective efficacy and underlying mechanisms of taxifolin against UVB-induced injury were evaluated in human immortalized keratinocytes (HaCaT).

2026-04-06 | PXD073279 | Pride

RNA-seq in human keratinocytes HaCaT cell line

Project description:To figure out the expression level of genes in normal human keratinocytes, we performed RNA-seq analysis in HaCaT cells. Here, we used 4 HaCaT cells as parallel samples.

2023-01-04 | GSE202683 | GEO

Human keratinocytes HaCaT LC-MS/MS

Project description:Triton X-100 has been used as a model substance to study the effects of irritants on the skin. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of Triton X-100, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to Triton X-100 was analyzed by LC-MS/MS approach and quantified using Progenesis LC software.

2017-11-03 | PXD007776 | Pride

HaCaT keratinocytes day3 vs HaCaT keratinocytes day10

Project description:The keratinocyte cell line HaCaT was cultured for three days (proliferation) or for ten days (differentiation). RNA from cells at day3 was compared to RNA from cells at day10. The microarray hybridizations were performed in dye-swap procedure : RNA from cells at day3 was labeled with Cy3 (GSM4674, GSM4675, GSM4682, GSM4683) and then with cy5 (GSM4680, GSM4681). Keywords = cell density differentiation program in human keratinocytes

2003-03-10 | E-GEOD-336 | biostudies-arrayexpress

RNA-seq analysis of HaCaT keratinocytes overexpressing ATF7 under high glucose conditions

Project description:To investigate the downstream transcriptional targets of ATF7 in keratinocytes under high glucose conditions, we performed RNA-sequencing (RNA-seq) analysis in HaCaT human keratinocytes overexpressing ATF7.

2026-07-03 | GSE326162 | GEO

Impact of p53 knockout on protein dataset of HaCaT cells in confluent and subconfluent conditions

Project description:Immortalized keratinocytes HaCaT is popular model for skin research (toxicity, irritation, allergic reactions or interaction of cells). They maintain stable keratinocyte phenotype and respond to keratinocyte differentiation stimuli. However, the programs of stratification and expression of differentiation markers in HaCaT keratinocytes are aberrant. HaCaT cells bear two mutant p53 alleles (R282Q and H179Y) which contain Gain-of-Function (GOV) mutations acquired as a result of spontaneous immortalization (mutp53). At the same time, mutp53 acts as a transcription factor, and also affects interaction of p63 protein with its transcription targets. It is known that proteins of the P53 family play an important role in regulating processes of proliferation and differentiation of human keratinocytes.At the same time, the role of mutp53 in these processes is not fully clear. We present data sets obtained as a result of high-performance proteomic analysis of immortalized HaCaT keratinocytes with p53 knockout in two different states: sub-confluent and confluent, which are characterized by different intensity of cell differentiation processes. As a protocol for proteomic profiling of cells, we used the approach of obtaining LC-MS/MS measurements followed by their processing with Progenesis LC-MS software (Nonlinear Dynamics Ltd.)

2022-02-24 | PXD030700 | Pride

Aberrantly expressed genes in HaCaT keratinocytes chronically exposed to arsenic trioxide

Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5µg/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide

2012-04-12 | GSE37192 | 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