Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene signatures detect damaged LSECs in all chronic liver diseases.

ABSTRACT: Gene signatures detect damaged LSECs in all chronic liver diseases.

PROVIDER: PRJNA748010 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15192264_1.fastq.gz	Fastqsanger.gz
	SRR15192264_2.fastq.gz	Fastqsanger.gz
	SRR15192265_1.fastq.gz	Fastqsanger.gz
	SRR15192265_2.fastq.gz	Fastqsanger.gz
	SRR15192266_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

Gene signatures detect damaged LSECs in all chronic liver diseases.

Project description:Transcriptional alterations in LSECs from healthy and damaged livers were determined using RNA Sequencing. Models include acute liver injury (1 ip injection of CCl4) with different timepoints during recovery. Illumina NextSeq 500 High was used for sequencing.

2021-10-08 | GSE180366 | GEO

Gene Signatures Detect Damaged Liver Sinusoidal Endothelial Cells in Chronic Liver Diseases

Project description:Liver sinusoidal endothelial cells have a gatekeeper function in liver homeostasis by permitting substrates from the bloodstream into the space of Disse and regulating hepatic stellate cell activation status. Maintenance of LSEC's highly specialized phenotype is crucial for liver homeostasis. During liver fibrosis and cirrhosis, LSEC phenotype and functions are lost by processes known as capillarization and LSEC dysfunction. LSEC capillarization can be demonstrated by the loss of fenestrae (cytoplasmic pores) and the manifestation of a basement membrane. Currently, no protein or genetic markers can clearly distinguish healthy from damaged LSECs in acute or chronic liver disease. Single cell (sc)RNA sequencing efforts have identified several LSEC populations in mouse models for liver disease and in human cirrhotic livers. Still, there are no clearly defined genesets that can identify LSECs or dysfunctional LSEC populations in transcriptome data. Here, we developed genesets that are enriched in healthy and damaged LSECs which correlated very strongly with healthy and early stage- vs. advanced human liver diseases. A damaged LSEC signature comprised of Fabp4/5 and Vwf/a1 was established which could efficiently identify damaged endothelial cells in single cell RNAseq data sets. In LSECs from an acute CCl4 liver injury mouse model, Fabp4/5 and Vwf/a1 expression is induced within 1–3 days while in cirrhotic human livers these 4 genes are highly enriched in damaged LSECs. In conclusion, our newly developed gene signature of damaged LSECs can be applicable to a wide range of liver disease etiologies, implicating a common transcriptional alteration mechanism in LSEC damage.

| S-EPMC8564042 | biostudies-literature

Distinct Interferon Signatures and Cytokine Patterns Define Additional Systemic Autoinflammatory Diseases

Project description:Distinct Interferon Signatures and Cytokine Patterns Define Additional Systemic Autoinflammatory Diseases

| PRJNA595006 | ENA

Distinct Interferon Signatures and Cytokine Patterns Define Additional Systemic Autoinflammatory Diseases

Project description:Distinct Interferon Signatures and Cytokine Patterns Define Additional Systemic Autoinflammatory Diseases

| PRJNA595007 | ENA

Detect-seq on transfected HEK293T cells [Detect-seq data]

Project description:Detect-seq on transfected HEK293T cells [Detect-seq data]

| PRJNA727322 | ENA

Tumor genetic heterogeneity analysis of chronic sun-damaged melanomas

Project description:Tumor genetic heterogeneity analysis of chronic sun-damaged melanomas

| PRJNA579371 | ENA

Proteins enriched on damaged lysosomes in 293T

Project description:Lysosomal membrane permeabilization (LMP) or lysosomal membrane damage is commonly associated with aging and age-related diseases. In searching for cellular mechanisms in response to LMP, we used a proteomic approach to identify proteins enriched on damaged lysosomes. This unbiased approach identified a new phosphoinositide signaling pathway triggered by LMP to mediate rapid lysosomal repair. Specifically, LMP induces fast lysosomal recruitment of PI4K2A which generates high levels of the lipid messenger phosphatidylinositol-4-phosphate (PtdIns4P) on damaged lysosomes. Lysosomal PtdIns4P in turn recruits multiple oxysterol-binding protein (OSBP)-related protein (ORP) family members, including ORP9, ORP10, and ORP11, to orchestrate extensive membrane contact sites (MCSs) between damaged lysosomes and the endoplasmic reticulum (ER). The ORPs subsequently catalyze robust ER-to-lysosomal transport of phosphatidylserine (PS), which is critical for rapid lysosomal repair. The lipid transporter ATG2 is also recruited to damaged lysosomes, activated by PS, and is essential for rapid lysosomal repair. Our findings identify a phosphoinositide-dependent membrane tethering and lipid transport (PITT) pathway essential for the maintenance of lysosomal membrane integrity, with important implications for a wide range of diseases characterized by impaired lysosomal function.

2022-09-07 | PXD028852 | Pride

Fragment ends of circulating microbial DNA as signatures for infectious diseases

Project description:Fragment ends of circulating microbial DNA as signatures for infectious diseases

| EGAS00001006321 | EGA

Whole genome-derived tiled peptide arrays detect pre-diagnostic autoantibody signatures in non-small cell lung cancer

Project description:Investigation of whole genome-derived tiled peptide arrays to identify epitopes associated with autoantibody reactivity in NSCLC as a potential means for early detection. Arrays consisted of 2,781,902 tiled peptides representing 20,193 proteins encoded in the human genome. The detailed analysis in this study is further described in Yan et al. Whole genome-derived tiled peptide arrays detect pre-diagnostic autoantibody signatures in non-small cell lung cancer. Cancer Res. 2019 Feb 5. pii: canres.1536.2018

2019-03-11 | GSE128077 | GEO

Qualitative differences in diseases-associated mutants reveal molecular signatures and aberrant signaling-crosstalk

Project description:Qualitative differences in diseases-associated mutants reveal molecular signatures and aberrant signaling-crosstalk

| PRJNA697974 | ENA