Entry Detail



General Information

Database ID:TRD04445
Confidence:Median
Contents:>> tsRNA Information
>> tsRNA Association Statistics
>> Disease Information
>> Disease Association Statistics
>> Evidence Support
>> Reference



tsRNA Information

tsRNA Name:tiRNA-Gln-TTG-001
tsRNA Type:N/A
Amino acid and Anticodon:GlnTTG
Sequence:N/A
Related Target:N/A
Predicted Target:N/A
External Links:
MINTbase ID:N/A
tRFdb ID:N/A



tsRNA Association Statistics

Total Associated Disease Number:27
More Information
Network:
(Display the first 15 nodes)



Disease Information

 MeSHDisease Ontology
Disease ID:D009205DOID:820
Disease Name:Myocarditismyocarditis
Category:MeSHDisease Ontology
Type:Cardiovascular Diseasesdisease of anatomical entity
Define:Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.An extrinsic cardiomyopathy that is characterized as an inflammation of the heart muscle.
Alias:CarditisMyocardial inflammation



Disease Association Statistics

Total Associated tsRNA Number:58
More Information
Network:
(Display the first 15 nodes)



Evidence Support

Strong Evidence:RT-PCR
Weak Evidence:High-throughput sequencing



Reference

[1] PubMed ID:34114472
Disease Name:Myocarditis
Tissue:Heart
Dysfunction Pattern:Up-Regulation
Validated Method:RT-PCR//High-throughput sequencing
Description:tiRNA-Gln-TTG-001 was overexpressed in children with FM during acute phase, and the generation and extracellular release of tiRNA-Gln-TTG-001 were higher after myocarditis-mimicked activity in vitro.
Comparision:FM-A VS Control
Mechanism:The potential target genes of tiRNA-Gln-TTG-001 were found to be related to myotube differentiation and metabolism, and Ras, MAPK, PI3K-Akt signaling pathways may exert crucial influence on the pathogenesis and progression of FM.