Entry Detail

General Information

Database ID: LDA0003707
Species: Homo sapiens
Confidence Score: 0.731059
Contents: >> ncRNA Information
>> ncRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference
Causality: Yes
Clinical Significance: Unknown

 


ncRNA Information

Reference Genome Note: GRCh38 for human lncRNAs; GRCm39 for mouse lncRNAs; mRatBN7.2 for rat lncRNAs; hg19 for human circRNAs; mm9 for mouse circRNAs.

ncRNA Symbol:DACH1
Full Name:dachshund family transcription factor 1
Category:LncRNA
Species:Homo sapiens
Synonyms:DACH
Chromosome:13
Strand:-
Coordinate:
Start Site(bp):71437966End Site(bp):71867204
External Links:
Ensembl ID:ENSG00000276644
Ensembl Transcript ID:N/A
Entrez Gene:1602.0
NONCODE ID:N/A
RefSeq Accession:N/A

 

ncRNA Association Statistics

Total Associated Disease Number:2   
More Information
Causal Disease Number:2
Network:
Top Causal Diseases:
Pulmonary Fibrosis  (Score: 0.731059)
Pulmonary Fibrosis  (Score: 0.731059)
More Information

 

 

Disease Information

 Disease OntologyMeSH
Disease ID:DOID:3770D011658
Disease Name:pulmonary fibrosisPulmonary Fibrosis
Category:Disease OntologyMeSH
Type:Respiratory Tract Diseases
Define:An interstitial lung disease that is characterized by destruction, scarring, and thickening of the interstitial lung tissues and progressive pulmonary function loss in a restrictive pattern, has_symptom progressive shortness of breath, fatigue, and chronic cough, possibly has_material_basis_in exposure to certain chemicals, autoimmune conditions, and radiation.A process in which normal lung tissues are progressively replaced by FIBROBLASTS and COLLAGEN causing an irreversible loss of the ability to transfer oxygen into the bloodstream via PULMONARY ALVEOLI. Patients show progressive DYSPNEA finally resulting in death.
Alias:Fibrosis of lungPulmonary Fibrosis//Fibrosis, Pulmonary//Pulmonary Fibroses//Fibroses, Pulmonary//Alveolitis, Fibrosing//Alveolitides, Fibrosing//Fibrosing Alveolitides//Fibrosing Alveolitis//Idiopathic Diffuse Interstitial Pulmonary Fibrosis

 

Disease Association Statistics

Total Associated ncRNA Number:64   
More Information
Causal ncRNA Number:16
Network:
Top Causal ncRNAs:
H19  (Score: 0.731059)
DACH1  (Score: 0.731059)
Rmrp  (Score: 0.731059)
circANKRD42  (Score: 0.731059)
Zfas1  (Score: 0.731059)
hsa_circ_0026344  (Score: 0.731059)
hsa_circ_0044226  (Score: 0.731059)
MIR99AHG  (Score: 0.731059)
H19  (Score: 0.731059)
DACH1  (Score: 0.731059)
More Information

 

Evidence Support

Strong Evidence:In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//FISH//IHC//EdU Staining//IF
Weak Evidence:

 

Reference

[1] PubMed ID:36176913
Disease Name:Pulmonary Fibrosis
Sample: lungs of IPF patients, mouse model of lung fibrosis
Dysfunction Pattern:Interaction(SRSF1/CTNNB1 )
Validated Method:In Vivo Experiment//RNA Pull-Down//Western Blot//Transfection//Wound Healing Assay//qRT-PCR//FISH//IHC//EdU Staining//IF
Description:Here we report that lncRNA DACH1 (dachshund homolog 1) is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis. Mechanistically, LncDACH1 binding to the serine/arginine-rich splicing factor 1 (SRSF1) protein decreases its activity and inhibits the accumulation of Ctnnb1. Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts. Furthermore, loss of LncDACH1 promoted proliferation, differentiation, and extracellular matrix (ECM) deposition in mouse lung fibroblasts, whereas such effects were abolished by silencing of Ctnnb1. In addition, a conserved fragment of LncDACH1 alleviated hyperproliferation, ECM deposition and differentiation of MRC-5 cells driven by TGF-β1.
Causality:Yes
Causal Description:LncDACH1 knockout mice develop spontaneous pulmonary fibrosis, whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation, collagen deposition and differentiation of mouse lung fibroblasts. Similarly, forced expression of LncDACH1 not only prevented bleomycin (BLM)-induced lung fibrosis, but also reversed established lung fibrosis in a BLM model.
Clinical-realted Application: