Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cardiomyocyte Specific Deletion of ADAR1 Causes Severe Cardiac Dysfunction and Increased Lethality

18 Mar 2020

Abstract excerpt

Background: Adenosine deaminase acting on RNA 1 (ADAR1) is a double-stranded RNA-editing enzyme that is involved in several functions including the deamination of adenosine to inosine, RNA interference (RNAi) mechanisms and microRNA (miRNA) processing, rendering ADAR1 essential for life. Methods and Results: To investigate whether maintenance of ADAR1 expression is required for normal myocardial homeostasis, we...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to RNA regulation and disease
Share to RNA Research and Splicing
Share to Viral Infections and Immunology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 32258062
DOI: 10.3389/fcvm.2020.00030

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cardiomyocyte Specific Deletion of ADAR1 Causes Severe Cardiac Dysfunction and Increased LethalityPMID 32258062Read ↗

Stress-induced apoptosis associated with null mutation of ADAR1 RNA editing deaminase gene.Semantic proximity Read ↗

Modulation of ADAR mRNA expression in patients with congenital heart defectsSemantic proximity Read ↗

CREG1 promotes autophagy and protects the heart against nutritional stress-induced injury and age-associated hypertrophy, fibrosis and diastolic dysfunctionSemantic proximity Read ↗

PKR and the Integrated Stress Response drive immunopathology caused by ADAR1 mutationSemantic proximity Read ↗

Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis.Semantic proximity Read ↗

RNA Editing Therapeutics: Advances, Challenges and Perspectives on Combating Heart DiseaseSemantic proximity Read ↗

Cardiomyocytes Deficiency of SENP1 Promotes Myocardial Fibrosis via Paracrine ActionSemantic proximity Read ↗

m6A demethylase ALKBH5 attenuates doxorubicin-induced cardiotoxicity via posttranscriptional stabilization of Rasal3Semantic proximity Read ↗

Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction.Semantic proximity Read ↗

miRNA signature of unfolded protein response in H9c2 rat cardiomyoblastsSemantic proximity Read ↗

Exploiting the hypoxia sensitive non-coding genome for organ-specific physiologic reprogramming.Semantic proximity Read ↗

ALKBH5 mediated RNA N6-methyladenosine demethylation protects against myocardial I/R induced injury via FSP1 dependent inhibition of ferroptosisSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.