ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Pin1-FADD interactions regulate Fas-mediated apoptosis in activated eosinophils.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Expression patterns of serum miR-27a-3p and activating transcription factor 3 in children with bronchial asthma and their correlations with airway inflammation.The clinical respiratory journal · 2025Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- The mechanisms of Pin1 as targets for cancer therapy.Frontiers in immunology · 2024Review
- MiR-21 attenuates FAS-mediated cardiomyocyte apoptosis by regulating HIPK3 expression.Bioscience reports · 2023Article
- Pin1 and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Targeting Pin1 for Modulation of Cell Motility and Cancer Therapy.Biomedicines · 2021Review
- Roles of peptidyl-prolyl isomerase Pin1 in disease pathogenesis.Theranostics · 2021Review
- [Effects of artesunate on eosinophil apoptosis and expressions of Fas and Bcl-2 proteins in asthmatic mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Eosinophil accumulation predicts response to melanoma treatment with immune checkpoint inhibitors.Oncoimmunology · 2020Article
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- Wentong decoction cures allergic bronchial asthma by regulating the apoptosis imbalance of EOS.Chinese medicine · 2018Article
- Dissecting the inflammatory twitch in allergically inflamed mice.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Article
- Landscape of Pin1 in the cell cycle.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- A computational model of unresolved allergic inflammation in chronic asthma.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Determinants of eosinophil survival and apoptotic cell death.Apoptosis : an international journal on programmed cell death · 2015Review
- Mitochondria in the center of human eosinophil apoptosis and survival.International journal of molecular sciences · 2014Review
- Regulation of spontaneous eosinophil apoptosis-a neglected area of importance.Journal of cell death · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Abnormally long-lived eosinophils (Eos) are the major inflammatory component of allergic responses in the lungs of active asthmatics. Eos recruited to the airways after allergen exposure produce and respond to IL-5 and GM-CSF, enhancing their survival. Prosurvival signaling activates Pin1, a peptidyl-prolyl cis-trans isomerase that binds to Bax and prevents its activation. How long-lived Eos, despite the continued presence of GM-CSF or IL-5, eventually undergo apoptosis to end allergic inflammation remains unclear. In this study, we show that Pin1 location, activity, and protein interactions are jointly influenced by Fas and the prosurvival cytokine IL-5. Fas signaling strongly induced the phosphorylation of FADD at Ser(194) and Pin1 at Ser(16), as well as their nuclear accumulation. Phospho-mimic Ser(194)Glu FADD mutants accelerated Eos apoptosis compared with wild-type or Ser(194)Ala mutants. Downstream of FADD phosphorylation, caspase 8, 9, and 3 cleavage, as well as Eos apoptosis induced by Fas, were reduced by constitutively active Pin1 and enhanced by Pin1 inhibition. Pin1 was activated by IL-5, whereas simultaneous IL-5 and anti-Fas treatment modestly reduced peptidyl isomerase activity but induced Pin1 to associate with FADD after its phosphorylation at Ser(194). Mechanistically, Pin1-mediated isomerization facilitated the subsequent dephosphorylation of Ser(194) FADD and maintenance of cytoplasmic location. In vivo-activated bronchoalveolar Eos obtained after allergen challenge showed elevated survival and Pin1 activity that could be reversed by anti-Fas. Therefore, our data suggest that Pin1 is a critical link between FADD-mediated cell death and IL-5-mediated prosurvival signaling.
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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.