ArticleJournal of molecular and cellular cardiology2012
Embryonic expression of AMPK γ subunits and the identification of a novel γ2 transcript variant in adult heart.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Binding of 14-3-3 stabilises recombinant AMPKγ2-containing complexes.The Biochemical journal · 2026Article
- Pharmacologic AMPK Activation Extends Lifespan inbioRxiv : the preprint server for biology · 2026Article
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- Sexual Dimorphism in Cardiometabolic Diseases: The Role of AMPK.International journal of molecular sciences · 2023Review
- New insights into activation and function of the AMPK.Nature reviews. Molecular cell biology · 2023Review
- The importance of the AMPK gamma 1 subunit in metformin suppression of liver glucose production.Scientific reports · 2020Article
- Characterisation of the developing heart in a pressure overloaded model utilising RNA sequencing to direct functional analysis.Journal of anatomy · 2020Article
- AMP-activated protein kinase: the current landscape for drug development.Nature reviews. Drug discovery · 2019Review
- AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Review
- A novel, de novo mutation in theAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- AMP-Activated Protein Kinase: An Ubiquitous Signaling Pathway With Key Roles in the Cardiovascular System.Circulation research · 2017Review
- Effect of different γ-subunit isoforms on the regulation of AMPK.The Biochemical journal · 2017Article
- AMP-activated protein kinase: a cellular energy sensor that comes in 12 flavours.The FEBS journal · 2016Review
- AMPK: energy sensor and survival mechanism in the ischemic heart.Trends in endocrinology and metabolism: TEM · 2015Review
- Mutation in the γ2-subunit of AMP-activated protein kinase stimulates cardiomyocyte proliferation and hypertrophy independent of glycogen storage.Circulation research · 2014Article
- Localisation of AMPK γ subunits in cardiac and skeletal muscles.Journal of muscle research and cell motility · 2013Article
- AMP-activated protein kinase: a target for drugs both ancient and modern.Chemistry & biology · 2012Review
- AMP-activated protein kinase regulation and biological actions in the heart.Circulation research · 2012Review
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6 authors at 2 institutions in 1 country.
Funding
Abstract
AMP-activated protein kinase (AMPK), the key sensor and regulator of cellular energy status, is a heterotrimeric enzyme with multiple isoforms for each subunit (α1/α 2; β1/β2; γ1/γ2/γ3). Mutations in PRKAG2, which encodes the γ2 regulatory subunit, cause a cardiomyopathy characterized by hypertrophy and conduction abnormalities. The two reported PRKAG2 transcript variants, γ2-short and γ2-long (encoding 328 and 569 amino acids respectively), are both widely expressed in adult tissues. We show that both γ2 variants are also expressed during cardiogenesis in mouse embryos; expression of the γ3 isoform was also detected unexpectedly at this stage. As neither γ2 transcript is cardiac specific nor differentially expressed during embryogenesis, it is paradoxical that the disease is largely restricted to the heart. However, a recently annotated γ2 transcript, termed γ2-3B as transcription starts at an alternative exon 3b, has been identified; it is spliced in-frame to exon 4 thus generating a protein of 443 residues in mouse with the first 32 residues being unique. It is increasingly expressed in the developing mouse heart and quantitative PCR analysis established that γ2-3B is the major PRKAG2 transcript (~60%) in human heart. Antibody against the novel N-terminal sequence showed that γ2-3B is predominantly expressed in the heart where it is the most abundant γ2 protein. The abundance of γ2-3B and its tissue specificity indicate that γ2-3B may have non-redundant role in the heart and hence mediate the predominantly cardiac phenotype caused by PRKAG2 mutations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.