ArticleBiochemistry2011
β-arrestin-2 regulation of the cAMP response element binding protein.
Article in Biochemistry, 2011. 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, 25 citations in OpenAlex.
- Histamine HPharmaceuticals (Basel, Switzerland) · 2026Article
- A unique melanocortin-4-receptor signaling profile for obesity-associated constitutively active variants.Journal of molecular endocrinology · 2023Article
- Antibiotic Disruption of the Gut Microbiota Enhances the Murine Hepatic Dysfunction Associated With a High-Salt Diet.Frontiers in pharmacology · 2022Article
- β-Arrestin2 deficiency attenuates oxidative stress in mouse hepatic fibrosis through modulation of NOX4.Acta pharmacologica Sinica · 2021Article
- Resveratrol restores intracellular transport in cystic fibrosis epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- HDAC6 depletion improves cystic fibrosis mouse airway responses to bacterial challenge.Scientific reports · 2019Article
- Acetyl-CoA carboxylase inhibition regulates microtubule dynamics and intracellular transport in cystic fibrosis epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Clinically-approved CFTR modulators rescue Nrf2 dysfunction in cystic fibrosis airway epithelia.The Journal of clinical investigation · 2019Article
- Orphan GPR61, GPR62 and GPR135 receptors and the melatonin MTScientific reports · 2017Article
- Multifaceted role of β-arrestins in inflammation and disease.Genes and immunity · 2015Review
- The emerging roles of β-arrestins in fibrotic diseases.Acta pharmacologica Sinica · 2015Review
- PAF enhances MMP-2 production in rat aortic VSMCs via a β-arrestin2-dependent ERK signaling pathway.Journal of lipid research · 2013Article
- Reduced caveolin-1 promotes hyperinflammation due to abnormal heme oxygenase-1 localization in lipopolysaccharide-challenged macrophages with dysfunctional cystic fibrosis transmembrane conductance regulator.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- β-Arrestin recruitment and G protein signaling by the atypical human chemokine decoy receptor CCX-CKR.The Journal of biological chemistry · 2013Article
- β-Arrestins in the immune system.Progress in molecular biology and translational science · 2013Review
- Regulatory role of β-arrestin-2 in cholesterol processing in cystic fibrosis epithelial cells.Journal of lipid research · 2012Article
- Molecular pathways for intracellular cholesterol accumulation: common pathogenic mechanisms in Niemann-Pick disease Type C and cystic fibrosis.Archives of biochemistry and biophysics · 2011Review
- Role of β and α1-adrenoceptors in pancreatic regulation of glucose homeostasis, apoptosis, and fibrosis in dexamethasone-treated rats: A new insight into β-arrestin2 crosstalk with cAMP, PKA-ERK1/2-CREB, and PKB-FOXO1 signaling pathways.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Previous work demonstrated that cystic fibrosis (CF) cells exhibit an increase in cAMP-mediated signaling as a characteristic response to lost CFTR function. Evidence for increased cAMP-mediated signaling in CF included increased phosphorylation of the cAMP response element binding protein (CREB) and elevated β-arrestin-2 (βarr2) expression. However, subsequent studies reveal that CREB activation in CF cells is independent of protein kinase-A (PKA). The goal of this study is to test the hypothesis that elevated βarr2 expression leads to increased CREB activation in a PKA-independent mechanism. βarr2-GFP expressing tracheal epithelial cells (βarr2-GFP) exhibit an increase of pCREB content and subsequent CRE activation compared to GFP expressing control cells. βarr2 activation of the ERK cascade represents a candidate mechanism leading to CREB activation. ERK exhibits increased activation in βarr2-GFP cells compared to cont-GFP cells, and ERK inhibition diminishes CRE activation in both GFP and βarr2-GFP cells. To test directly whether CREB regulation in CF is βarr2-dependent, nasal epithelium excised from wt mice (Cftr +/+; βarr2 +/+), CF mice (Cftr -/-; βarr2 +/+), and DKO mice (Cftr -/-; βarr2 -/-) were analyzed for pCREB protein content. Removal of βarr2 expression from CF mice reduces both pCREB and pERK content to wt levels. These data indicate that CF-related CREB regulation is mediated directly through βarr2 expression via the ERK pathway.
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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.