ArticleJCI insight2019
KIAA0317 regulates pulmonary inflammation through SOCS2 degradation.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Therapeutic targeting of AREL1 in hepatic stellate cells attenuates MASH-related liver fibrosis.Nature communications · 2026Article
- TEAD-independent mechanisms of YAP function in cardiomyocyte cell cycle reentry.Life science alliance · 2026Article
- Phosphoglycerate dehydrogenase-mediated serine reprogramming aggravates macrophage hyperinflammation in murine Pseudomonas aeruginosa pneumonia.Nature communications · 2026Article
- Age-dependent immune responses and resident cell dynamics in young mice following pneumonia.iScience · 2026Article
- NSP7 Molecular Degrader Attenuates Coronaviral Infection Through the β-TrCP1/FBXO5 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibition of virally induced TFEB proteasomal degradation as a host-centric therapeutic approach for coronaviral infection.Science advances · 2025Article
- Leveraging Therapeutic Proteins and Peptides fromInternational journal of molecular sciences · 2024Article
- Neuroinflammation mediates the progression of neonate hypoxia-ischemia brain damage to Alzheimer's disease: a bioinformatics and experimental study.Frontiers in aging neuroscience · 2024Article
- A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence.Immunity & ageing : I & A · 2023Article
- KIAA0317 regulates SOCS1 stability to ameliorate colonic inflammation.The FEBS journal · 2023Article
- Epigenetics as a mediator of genetic risk in osteoarthritis: role during development, homeostasis, aging, and disease progression.American journal of physiology. Cell physiology · 2023Review
- Redefining the catalytic HECT domain boundaries for the HECT E3 ubiquitin ligase family.Bioscience reports · 2022Article
- The Emerging Roles of Tripartite Motif Proteins (TRIMs) in Acute Lung Injury.Journal of immunology research · 2021Review
- An IL-17F.S65L Knock-In Mouse Reveals Similarities and Differences in IL-17F Function in Oral Candidiasis: A New Tool to Understand IL-17F.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
Dysregulated proinflammatory cytokine release has been implicated in the pathogenesis of several life-threatening acute lung illnesses such as pneumonia, sepsis, and acute respiratory distress syndrome. Suppressors of cytokine signaling proteins, particularly SOCS2, have recently been described as antiinflammatory mediators. However, the regulation of SOCS2 protein has not been described. Here we describe a mechanism of SOCS2 regulation by the action of the ubiquitin E3 ligase KIAA0317. KIAA0317-mediated degradation of SOCS2 exacerbated inflammation in vitro, and depletion of KIAA0317 in vivo ameliorated pulmonary inflammation. KIAA0317-knockout mice exhibited resistance to LPS-induced pulmonary inflammation, while KIAA03017 reexpression mitigated this effect. We uncovered a small molecule inhibitor of KIAA0317 protein (BC-1365) that prevented SOCS2 degradation and attenuated LPS- and P. aeruginosa-induced lung inflammation in vivo. These studies show KIAA0317 to be a critical mediator of pulmonary inflammation through its degradation of SOCS2 and a potential candidate target for therapeutic inhibition.
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.