ArticleThe Journal of clinical investigation2001
Proteasomal regulation of betac signaling reveals a novel mechanism for cytokine receptor heterotypic desensitization.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 38 citations in OpenAlex.
- Pro-inflammatory and counter-regulatory modulators of interleukin-5-driven eosinophil programs: a framework for precision medicine in eosinophilic diseases.Frontiers in immunology · 2026Review
- Inhibition of JAK2 Suppresses Myelopoiesis and Atherosclerosis in ApoeCardiovascular drugs and therapy · 2020Article
- Neutrophil GM-CSF receptor dynamics in acute lung injury.Journal of leukocyte biology · 2019Article
- LNK/SH2B3 Loss of Function Promotes Atherosclerosis and Thrombosis.Circulation research · 2016Article
- Eliminative signaling by Janus kinases: role in the downregulation of associated receptors.Journal of cellular biochemistry · 2014Review
- CBL linker region and RING finger mutations lead to enhanced granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling via elevated levels of JAK2 and LYN.The Journal of biological chemistry · 2013Article
- Article
- Competitive regulation of E-cadherin juxtamembrane domain degradation by p120-catenin binding and Hakai-mediated ubiquitination.PloS one · 2012Article
- Three lysine residues in the common β chain of the interleukin-5 receptor are required for Janus kinase (JAK)-dependent receptor ubiquitination, endocytosis, and signaling.The Journal of biological chemistry · 2011Article
- Interleukin-5 and IL-5 receptor in health and diseases.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2011Review
- SRC family kinases accelerate prolactin receptor internalization, modulating trafficking and signaling in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2009Article
- Separate endocytic pathways regulate IL-5 receptor internalization and signaling.Journal of leukocyte biology · 2008Article
- Cross-talk between ICAM-1 and granulocyte-macrophage colony-stimulating factor receptor signaling modulates eosinophil survival and activation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Proteasomes mediate prolactin-induced receptor down-regulation and fragment generation in breast cancer cells.The Journal of biological chemistry · 2005Article
- Cellular level models as tools for cytokine design.Biotechnology progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
IL-5, IL-3, and GM-CSF are hematopoietic cytokines that are key mediators of the allergic inflammatory response. The receptors for these three cytokines consist of a cytokine-specific alpha (Ralpha) chain and a shared common beta (betac) chain. Herein, we demonstrate that agonistic ligation of these receptor subunits rapidly induces proteasomal degradation of the betac, but not the Ralpha, cytoplasmic domain, resulting in termination of signal transduction and yielding a truncated betac isoform ligated to the Ralpha subunit. Proteasomal degradation of the betac cytoplasmic domain was also a prerequisite for endocytosis and lysosomal degradation of the ligated receptor subunits. Moreover, proteasome-dependent termination of signaling induced by one betac-engaging cytokine resulted in cellular desensitization to signal transduction by subsequent stimulation with another betac-engaging cytokine. These data provide the first evidence for ligand-dependent proteasomal degradation of the betac cytoplasmic domain, and they establish a novel mechanism for heterotypic desensitization of shared cytokine receptor signaling.
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.