Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

UCHL1 aggravates skin fibrosis through an IGF-1-induced AKT/mTOR/ HIF-1α pathway in keloid

ABSTRACT: To investigate the function of UCHL1 in keloids, we established primary dermal fibroblasts in which the target gene has been overexpressed by lentiviral transfection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211150 | GEO | 2022/11/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1

2013-01-30 | GSE43884 | GEO

Genes regulated by UCHL1 in ovarian cancer cells

Project description:UCHL1 is related to apoptosis and proliferation in cancers and we sought to identify genes regulated by UCHL1 UCHL1 was knocked down in A2780 (A2780-shUCHL1). A2780-shUCHL1 and A2780-control were cultured in RPMI and total RNA was extracted and hybridizated on Affymetrix.GeneChip.HG-U133_Plus_2

2013-01-30 | E-GEOD-43884 | biostudies-arrayexpress

Hypoxia and HIF-1α Regulate Collagen Production in Keloids

Project description:Keloids are reactive or spontaneous fibroproliferative dermal tumors characterized by the exaggerated and uncontrolled accumulation of extracellular collagen. Current approaches to mitigate keloidogenesis are largely procedural in nature. However, a better understanding of its biological drivers may lead to novel targeted treatments for keloids. Through whole-genome expression analysis, we found that a HIF-1α transcriptional footprint is preferentially upregulated (activation score=2.024; p=1.05E-19) in keloid fibroblasts (KFs) compared to normal dermal fibroblasts (NFs). We verified that HIF-1α protein is more strongly expressed in keloid specimens compared to normal skin (p=0.035) and that hypoxia (1% O2) leads to increased collagen, especially in the extracellular compartment. Collagen levels were uniformly reduced by selective HIF-1α inhibitor CAY10585. Our results indicate that collagen secretion may be intimately linked to a hypoxic microenvironment within keloid tumors and that HIF-1α blockade could be a novel avenue of treatment for these tumors.

2020-02-22 | GSE145725 | GEO

Ubiquitin C-terminal hydrolase isozyme L1 (UCHL1) is associated with shelterin complex at interstitial telomeric sites

Project description:Ubiquitin C-terminal hydrolase isozyme L1 (UCHL1) is primarily expressed in neuronal cells and neuroendocrine cells. It is a multifunctional protein involved in deubiquitination, ubiquitination, and ubiquitin homeostasis. UCHL1 has been associated with various diseases, including many cancers, but its specific roles are disputed and still generally undetermined. Herein, we demonstrate that UCHL1 is associated with genomic DNA in certain prostate cancer cell lines, including DU 145 cells derived from a brain metastatic site, and in HEK293T embryonic kidney cells with a neuronal lineage. Chromatin immunoprecipitation and sequencing revealed that UCHL1 localizes to TTAGGG repeats at telomeres and interstitial telomeric sequences, as do TRF1 and TRF2, components of the shelterin complex. A weak or transient interaction between UCHL1 and the shelterin complex was confirmed by immunoprecipitation and proximity ligation assays. UCHL1 and TERF2IP, also a component of the shelterin complex, were bound to the nuclear scaffold. UCHL1 may play a role in regulating gene expression by affecting the stabilization of the shelterin proteins or influencing nuclear targeting. As several shelterin proteins (TRF1, TRF2, POT1 and TERF2IP) are ubiquitinated, UCHL1 may have a role in regulating the stability of these proteins. UCHL1 may also regulate the nuclear location of shelterin-associated genomic regions.

2018-02-23 | GSE97111 | GEO

Differential gene expression in UCHL1 silenced ovarian cancer cells

Project description:We report dysregulated genes upon silencing UCHL1 in high-grade serous ovarian cancer cell line, Kuramochi.

2024-03-15 | GSE168935 | GEO

Keloid-specific gene expression profiling for accurate diagnostic and therapeutic applications.

Project description:Scars are a heterogeneous disease including normotrophic scars, hypertrophic scars, and keloids. Of these lesions, keloids are a distinct subtype from any other type of scar because clinically, it causes pain, itching, or tenderness, causing life discomfort and characteristically irreversible. Therefore, for accurate diagnosis and treatment of keloids, it is essential to identify keloid-specific genes. However, in previous studies, keloids were compared with controls such as scar-free normal skin. In these studies, general scar-related genes were likely to be chosen rather than keloid-specific genes. In this study, we acquired transcriptomic profiles of normotrophic scars, hypertrophic scars, and keloids from formalin-fixed paraffin-embedded human skin samples using high-throughput RNA-sequencing techniques. We compared the transcriptome profile of keloids with those of other scar lesions to select for highly accurate keloid-specific genes and pathways. The results revealed that genes related with several biological processes such as sensory/visual perception are upregulated strongly in keloids, whereas genes related with activation of immune response were downregulated remarkably in keloids. Furthermore, the biological process of extracellular matrix organization was highlighted in both hypertrophic scars and keloids. In conclusion, our study provides insight into the pathogenesis of keloids distinct from other scar lesions as well as potential keloid-specific biomarkers.

2021-11-23 | GSE188952 | GEO

Canagliflozin Modulates Hypoxia-Induced Metastasis, Angiogenesis and Glycolysis by Decreasing HIF-1α Protein Synthesis via AKT/mTOR Pathway.

Project description: Not available

| S-EPMC8704642 | biostudies-literature

WTD Attenuating Rheumatoid Arthritis <i>via</i> Suppressing Angiogenesis and Modulating the PI3K/AKT/mTOR/HIF-1α Pathway.

Project description: Not available

| S-EPMC8502817 | biostudies-literature

Schwann cells contribute to keloid formation

Project description:Due to limited availability of proper models to study keloid development, the underlying pathomechanisms of this severe skin disease is still poorly understood. Here we performed single-cell sequencing of keloids and identified the occurrence of a so far unrecognized keloidal Schwann cell population, remaining in the scar tissue after wound healing. In contrast to normal skin, keloidal Schwann cells possess a repair-like phenotype and high cellular plasticity. Our data reveal that keloidal Schwann cells directly contribute to the formation of the extracellular matrix and affect M2 polarization of macrophages. Indeed, we show that macrophages in keloids predominantly display a M2 polarization and produce factors inhibiting Schwann cell differentiation. Our data suggest that this cross-talk contribute to the infinite growth of keloids and that targeting Schwann cells might represent a novel treatment option for keloids.

2022-03-16 | GSE181316 | GEO

The impact of transgenic Uchl1 on gene expression in germinal center B-cells from ImHABCL6 mice

Project description:This study seeks to understand the mechanisms behind enhanced lymphomagenesis observed in ImHABCL6/Uchl1 mice compared with ImHABCL6 alone. As the lymphomas arise from germinal center (GC) B-cells, we reasoned that transgenic Uchl1 altered the gene expression patterns in GC B-cells from these animals. We therefore isolated pre-malignant GC B-cells and examined the gene expression patterns to identify pathways affected by the addition of Uchl1.

2016-01-12 | GSE76706 | GEO

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