ArticleThe Journal of biological chemistry2011
A-kinase anchoring protein (AKAP)-Lbc anchors a PKN-based signaling complex involved in α1-adrenergic receptor-induced p38 activation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- Nanodomain cAMP signaling in cardiac pathophysiology: potential for developing targeted therapeutic interventions.Physiological reviews · 2025Review
- Titin's cardiac-specific N2B element is critical to mechanotransduction during volume overload of the heart.Journal of molecular and cellular cardiology · 2024Article
- Signalling of Adrenoceptors: Canonical Pathways and New Paradigms.Handbook of experimental pharmacology · 2024Review
- Inhibition of importin-7 attenuates ventilator-induced lung injury by targeting nuclear translocation of p38.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Phosphorylation, compartmentalization, and cardiac function.IUBMB life · 2023Article
- AKAP13 couples GPCR signaling to mTORC1 inhibition.PLoS genetics · 2021Article
- Review
- The structure and function of protein kinase C-related kinases (PRKs).Biochemical Society transactions · 2021Review
- A Serum Biomarker Panel of exomiR-451a, exomiR-25-3p and Soluble TWEAK for Early Diagnosis of Rheumatoid Arthritis.Frontiers in immunology · 2021Article
- Review
- Cardiac function modulation depends on the A-kinase anchoring protein complex.Journal of cellular and molecular medicine · 2019Review
- Absence of gravin-mediated signaling inhibits development of high-fat diet-induced hyperlipidemia and atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2019Article
- PKC and PKN in heart disease.Journal of molecular and cellular cardiology · 2019Review
- A-Kinase Anchoring Protein-Lbc: A Molecular Scaffold Involved in Cardiac Protection.Journal of cardiovascular development and disease · 2018Review
- Common functional variants of the glutamatergic system in Autism spectrum disorder with high and low intellectual abilities.Journal of neural transmission (Vienna, Austria : 1996) · 2018Article
- Loss of Protein Kinase Novel 1 (PKN1) is associated with mild systolic and diastolic contractile dysfunction, increased phospholamban Thr17 phosphorylation, and exacerbated ischaemia-reperfusion injury.Cardiovascular research · 2018Article
- Targeting protein-protein interactions in complexes organized by A kinase anchoring proteins.Frontiers in pharmacology · 2015Review
- PRK1/PKN1 controls migration and metastasis of androgen-independent prostate cancer cells.Oncotarget · 2014Article
- The crystal structure of the RhoA-AKAP-Lbc DH-PH domain complex.The Biochemical journal · 2014Article
- The C-terminus of the long AKAP13 isoform (AKAP-Lbc) is critical for development of compensatory cardiac hypertrophy.Journal of molecular and cellular cardiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitogen-activated protein kinases (MAPKs) pathways are highly organized signaling systems that transduce extracellular signals into a variety of intracellular responses. In this context, it is currently poorly understood how kinases constituting these signaling cascades are assembled and activated in response to receptor stimulation to generate specific cellular responses. Here, we show that AKAP-Lbc, an A-kinase anchoring protein (AKAP) with an intrinsic Rho-specific guanine nucleotide exchange factor activity, is critically involved in the activation of the p38α MAPK downstream of α(1b)-adrenergic receptors (α(1b)-ARs). Our results indicate that AKAP-Lbc can assemble a novel transduction complex containing the RhoA effector PKNα, MLTK, MKK3, and p38α, which integrates signals from α(1b)-ARs to promote RhoA-dependent activation of p38α. In particular, silencing of AKAP-Lbc expression or disrupting the formation of the AKAP-Lbc·p38α signaling complex specifically reduces α(1)-AR-mediated p38α activation without affecting receptor-mediated activation of other MAPK pathways. These findings provide a novel mechanistic hypothesis explaining how assembly of macromolecular complexes can specify MAPK signaling downstream of α(1)-ARs.
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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 OpenQuestion graph.