ArticleInflammatory bowel diseases2015
Protective Role of β-arrestin2 in Colitis Through Modulation of T-cell Activation.
Article in Inflammatory bowel diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Sodium butyrate regulates macrophage polarization by TGR5/β-arrestin2 in vitro.Molecular medicine (Cambridge, Mass.) · 2025Article
- Loss of β-arrestin2 aggravated condylar cartilage degeneration at the early stage of temporomandibular joint osteoarthritis.BMC musculoskeletal disorders · 2024Article
- MicroencapsulatedNutrients · 2023Article
- GRK2 Mediates Macrophage Polarization by Regulating EP4-cAMP-pCREB Signaling in Ulcerative Colitis and the Therapeutic Effect of Paroxetine on Mice with DSS-Induced Colitis.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Deficiency of β-arrestin2 exacerbates inflammatory arthritis by facilitating plasma cell formation.Acta pharmacologica Sinica · 2021Article
- β-arrestin2 regulating β2-adrenergic receptor signaling in hepatic stellate cells contributes to hepatocellular carcinoma progression.Journal of Cancer · 2021Article
- Article
- Beneficial effects of Lactobacillus reuteri 6475 on bone density in male mice is dependent on lymphocytes.Scientific reports · 2019Article
- SYK-CARD9 Signaling Axis Promotes Gut Fungi-Mediated Inflammasome Activation to Restrict Colitis and Colon Cancer.Immunity · 2018Article
- G protein-coupled receptor kinase-2-deficient mice are protected from dextran sodium sulfate-induced acute colitis.Physiological genomics · 2018Article
- β-arrestin2 functions as a key regulator in the sympathetic-triggered immunodepression after stroke.Journal of neuroinflammation · 2018Article
- Pyrin Inflammasome Regulates Tight Junction Integrity to Restrict Colitis and Tumorigenesis.Gastroenterology · 2018Article
- Poly(I:C) Priming Exacerbates Cecal Ligation and Puncture-Induced Polymicrobial Sepsis in Mice.Inflammation · 2018Article
- Role of G protein-coupled receptor kinase-6 inPhysiological genomics · 2017Article
- G-protein-coupled receptor kinase-2 is a critical regulator of TNFα signaling in colon epithelial cells.The Biochemical journal · 2017Article
- Non-Hematopoietic β-Arrestin1 Confers Protection Against Experimental Colitis.Journal of cellular physiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
β-arrestin2 (β-arr2), identified as a scaffolding protein in G-protein-coupled receptor desensitization, is a negative regulator of inflammation in polymicrobial sepsis. In this study, we wanted to investigate the role of β-arr2 in intestinal inflammation, a site of persistent microbial stimulation. In the absence of β-arr2, mice exhibited greater extent of mucosal inflammation determined by cellular infiltration and expression of inflammatory mediators even under homeostatic conditions. Furthermore, β-arr2-deficient mice were more susceptible to dextran sulfate sodium-induced colitis as demonstrated by greater body weight loss, higher disease activity index, and shortened colon as compared with wild-type mice. We also show that T cells from β-arr2 knockout mice exhibit altered activation status under both basal and colitic conditions, implicating their involvement in disease induction. Further assessment of the role of β-arr2 in intrinsic T-cell differentiation confirmed its importance in T-cell polarization. Using the T-cell transfer model of colitis, we demonstrate that T-cell-specific β-arr2 is important in limiting colitic inflammation; however, it plays a paradoxical role in concurrent systemic wasting disease. Together, our study highlights a critical negative regulatory role of β-arr2 in intestinal inflammation and demonstrates a distinct role of T-cell-specific β-arr2 in systemic wasting disease.
Indexed as
Identifiers
What OpenQuestion holds
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.