ArticleProceedings of the National Academy of Sciences of the United States of America2013
A kinase interacting protein (AKIP1) is a key regulator of cardiac stress.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Deep representation learning of electrocardiogram reveals biological insights in cardiac phenotypes and cardiovascular diseases.iScience · 2025Article
- Assessing the Function of Porcine A Kinase-Interacting Protein 1 (AKIP1) In Vitro-A Central Regulator of Oxidative Stress and Mitochondrial Functions.International journal of molecular sciences · 2025Article
- Role of the leucine-rich repeat protein kinase 2 C-terminal tail in domain cross-talk.The Biochemical journal · 2024Article
- A Kinase Interacting Protein 1 regulates mitochondrial protein levels in energy metabolism and promotes mitochondrial turnover after exercise.Scientific reports · 2023Article
- A Kinase Interacting Protein 1 (AKIP1) promotes cardiomyocyte elongation and physiological cardiac remodelling.Scientific reports · 2023Article
- The Tails of Protein Kinase A.Molecular pharmacology · 2022Review
- A-Kinase Interacting Protein 1 Promotes Cell Invasion and StemnessFrontiers in oncology · 2021Article
- The role of miR-320 in glucose and lipid metabolism disorder-associated diseases.International journal of biological sciences · 2021Review
- Article
- A-kinase-interacting protein 1 overexpression correlates with deteriorative tumor features and worse survival profiles, and promotes cell proliferation but represses apoptosis in non-small-cell lung cancer.Journal of clinical laboratory analysis · 2020Article
- Cardiac ischemia-reperfusion injury induces ROS-dependent loss of PKA regulatory subunit RIα.American journal of physiology. Heart and circulatory physiology · 2019Article
- AKIP1 promotes angiogenesis and tumor growth by upregulating CXC-chemokines in cervical cancer cells.Molecular and cellular biochemistry · 2018Article
- Does BCA3 Play a Role in the HIV-1 Replication Cycle?Viruses · 2018Article
- An AP-MS- and BioID-compatible MAC-tag enables comprehensive mapping of protein interactions and subcellular localizations.Nature communications · 2018Article
- MiR-320 regulates cardiomyocyte apoptosis induced by ischemia-reperfusion injury by targeting AKIP1.Cellular & molecular biology letters · 2018Article
- Upregulation of AKIP1 contributes to metastasis and progression and predicts poor prognosis of patients with colorectal cancer.OncoTargets and therapy · 2018Article
- Breast cancer-associated gene 3 interacts with Rac1 and augments NF-κB signaling in vitro, but has no effect on RANKL-induced bone resorption in vivo.International journal of molecular medicine · 2017Article
- Establishment of a prediction model of changing trends in cardiac hypertrophy disease based on microarray data screening.Experimental and therapeutic medicine · 2016Article
- Overexpression of AKIP1 predicts poor prognosis of patients with breast carcinoma and promotes cancer metastasis through Akt/GSK-3β/Snail pathway.American journal of translational research · 2016Article
- Mechanisms of cyclic AMP/protein kinase A- and glucocorticoid-mediated apoptosis using S49 lymphoma cells as a model system.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 2 countries.
Funding
Abstract
cAMP-dependent protein kinase (PKA) regulates a myriad of functions in the heart, including cardiac contractility, myocardial metabolism,and gene expression. However, a molecular integrator of the PKA response in the heart is unknown. Here, we show that the PKA adaptor A-kinase interacting protein 1 (AKIP1) is up-regulated in cardiac myocytes in response to oxidant stress. Mice with cardiac gene transfer of AKIP1 have enhanced protection to ischemic stress. We hypothesized that this adaptation to stress was mitochondrial dependent. AKIP1 interacted with the mitochondrial localized apoptosis inducing factor (AIF) under both normal and oxidant stress. When cardiac myocytes or whole hearts are exposed to oxidant and ischemic stress, levels of both AKIP1 and AIF were enhanced. AKIP1 is preferentially localized to interfibrillary mitochondria and up-regulated in this cardiac mitochondrial subpopulation on ischemic injury. Mitochondria isolated from AKIP1 gene transferred hearts showed increased mitochondrial localization of AKIP1, decreased reactive oxygen species generation, enhanced calcium tolerance, decreased mitochondrial cytochrome C release,and enhance phosphorylation of mitochondrial PKA substrates on ischemic stress. These observations highlight AKIP1 as a critical molecular regulator and a therapeutic control point for stress adaptation in the heart.
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Registered trials
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 Socratic graph.