ArticleNature communications2012
CYLD negatively regulates transforming growth factor-β-signalling via deubiquitinating Akt.
Article in Nature communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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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.
The trial behind it
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Who cites it
86 citing papers in PubMed, 147 citations in OpenAlex.
- Targeted DNA triplex-forming oligonucleotide liposome for pulmonary fibrosis gene therapy.Cell reports. Medicine · 2026Article
- Targeting noncanonical nuclear factor kappa B signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha.The British journal of dermatology · 2026Article
- Cleavage-Resistant CYLD Protects Against Autoimmune Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CYLD Limits Neutrophil-Driven Psoriatic Inflammation.Inflammation · 2026Article
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- The Role of the PI3K/Akt/mTOR Pathway in Atherosclerosis: Mechanisms, Therapeutic Potential, and Emerging Targeted Treatments.Current atherosclerosis reports · 2025Review
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- CYLD links the TRAF6/sNASP axis to TLR4 signaling in sepsis-induced acute lung injury.Cellular and molecular life sciences : CMLS · 2025Article
- Cyld restrains the hyperactivation of synovial fibroblasts in inflammatory arthritis by regulating the TAK1/IKK2 signaling axis.Cell death & disease · 2024Article
- CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.Cell death & disease · 2024Article
- Deficiency of the Deubiquitinase UCHL1 Attenuates Pulmonary Arterial Hypertension.Circulation · 2024Article
- Roles of ubiquitin-specific proteases in inflammatory diseases.Frontiers in immunology · 2024Review
- SP1-activated USP27X-AS1 promotes hepatocellular carcinoma progression via USP7-mediated AKT stabilisation.Clinical and translational medicine · 2024Article
- Inactivation of Tumor Suppressor CYLD Inhibits Fibroblast Reprogramming to Pluripotency.Cancers · 2023Article
- Targeting the deubiquitinaseOncology reports · 2023Review
- CYLD in health and disease.Disease models & mechanisms · 2023Review
- Interfering with the Ubiquitin-Mediated Regulation of Akt as a Strategy for Cancer Treatment.International journal of molecular sciences · 2023Review
- Down-regulated cylindromatosis enhances NF-κB activation and aggravates inflammation in HBV-ACLF patients.Emerging microbes & infections · 2022Article
- Potential use of EGFR-targeted molecular therapies for tumor suppressor CYLD-negative and poor prognosis oral squamous cell carcinoma with chemoresistance.Cancer cell international · 2022Article
- Cylindromatosis drives synapse pruning and weakening by promoting macroautophagy through Akt-mTOR signaling.Molecular psychiatry · 2022Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 11 institutions in 4 countries.
Funding
Abstract
Lung injury, whether induced by infection or caustic chemicals, initiates a series of complex wound-healing responses. If uncontrolled, these responses may lead to fibrotic lung diseases and loss of function. Thus, resolution of lung injury must be tightly regulated. The key regulatory proteins required for tightly controlling the resolution of lung injury have yet to be identified. Here we show that loss of deubiquitinase CYLD led to the development of lung fibrosis in mice after infection with Streptococcus pneumoniae. CYLD inhibited transforming growth factor-β-signalling and prevented lung fibrosis by decreasing the stability of Smad3 in an E3 ligase carboxy terminus of Hsc70-interacting protein-dependent manner. Moreover, CYLD decreases Smad3 stability by deubiquitinating K63-polyubiquitinated Akt. Together, our results unveil a role for CYLD in tightly regulating the resolution of lung injury and preventing fibrosis by deubiquitinating Akt. These studies may help develop new therapeutic strategies for preventing lung fibrosis.
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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.