RGD Reference Report - Alternative splicing of the primary Fas transcript generating soluble Fas antagonists is suppressed in the failing human ventricular myocardium. - Rat Genome Database

Send us a Message
Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   
Search RGD Grant Resources Citing RGD About Us Contact Us
Genes Variants Community Projects QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data
OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) Variant Visualizer Multi-Ontology Enrichment (MOET) Gene-Ortholog Location Finder (GOLF) InterViewer (Protein-Protein Interactions) PhenoMiner (Quatitative Phenotypes) Gene Annotator OLGA (Gene List Generator) AllianceMine GViewer (Genome Viewer)
Aging & Age-Related Disease Cancer & Neoplastic Disease Cardiovascular Disease Coronavirus Disease Developmental Disease Diabetes Hematologic Disease Immune & Inflammatory Disease Infectious Disease Liver Disease Neurological Disease Obesity & Metabolic Syndrome Renal Disease Respiratory Disease Sensory Organ Disease
Find Models   new Genetic Models Autism Models Rat PhenoMiner (Quantitative Phenotypes) Chinchilla PhenoMiner Expected Ranges (Quantitative Phenotype) PhenoMiner Term Comparison Hybrid Rat Diversity Panel Phenotypes Phenotypes in Other Animal Models Animal Husbandry Strain Medical Records Phylogenetics Strain Availability Calendar Rats 101 Submissions Photo Archive
Pathways
Rat Community Forum Directory of Rat Laboratories Video Tutorials News RGD Publications RGD Presentations Archive Nomenclature Guidelines Resource Links Laboratory Resources Employment Resources

Alternative splicing of the primary Fas transcript generating soluble Fas antagonists is suppressed in the failing human ventricular myocardium.

Authors: Schumann, H  Morawietz, H  Hakim, K  Zerkowski, HR  Eschenhagen, T  Holtz, J  Darmer, D 
Citation: Schumann H, etal., Biochem Biophys Res Commun. 1997 Oct 29;239(3):794-8.
RGD ID: 8686420
Pubmed: PMID:9367848   (View Abstract at PubMed)
DOI: DOI:10.1006/bbrc.1997.7555   (Journal Full-text)

Apoptosis of cardiomyocytes has been proposed as a factor contributing to severe heart failure. Since the trigger for apoptotic cellular suicide in nonischemic myocardium is unknown, we analyzed in human myocardial tissue the expression of the apoptosis-inducing membrane receptor Fas/APO-1 and of its alternatively spliced soluble isoforms which antagonize Fas by binding of the Fas ligand. Using reverse transcription polymerase chain reaction (RT-PCR) we found mRNA for Fas and 5 isoforms in nonfailing left ventricles, whereas Fas and only one isoform (FasExo6Del) were detectable in failing left ventricles. Standard calibrated, competitive RT-PCR revealed no significant increase of Fas mRNA in failing compared to nonfailing ventricles. However, the mRNA for FasExo6Del, expressed nearly on the same level as Fas in nonfailing ventricles, was decreased about 3-fold in failing ventricles. We propose that this altered expression of the Fas system renders the myocardium more susceptible for Fas-mediated apoptosis in end-stage heart failure.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
congestive heart failure  IEP 8686420mRNA:splice variant:heart left ventricle (human)RGD 
congestive heart failure  ISOFAS (Homo sapiens)8686420; 8686420mRNA:splice variant:heart left ventricle (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Fas  (Fas cell surface death receptor)

Genes (Mus musculus)
Fas  (Fas cell surface death receptor)

Genes (Homo sapiens)
FAS  (Fas cell surface death receptor)


Additional Information