ArticleThe Journal of experimental medicine2011
E3 ubiquitin ligase CHIP facilitates Toll-like receptor signaling by recruiting and polyubiquitinating Src and atypical PKC{zeta}.
Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 93 citations in OpenAlex.
- CHIP/STUB1 suppresses the transcription and latent reactivation of HIV-1 via the TRAF6-NF-κB-HIV-LTR axis.PLoS pathogens · 2025Article
- The E3 ubiquitin ligase STUB1 inhibits Senecavirus A replication by mediating VP1 ubiquitination and proteasomal degradation.Journal of virology · 2025Article
- The E3 ubiquitin ligase TRIM56 promotes aggregation and activation of Src protein through Lys63-linked polyubiquitination in hepatocellular carcinoma.Cell death & disease · 2025Article
- CHIP promotes CAD ubiquitination and degradation to suppress the proliferation and colony formation of glioblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Polyphenols alleviate metabolic disorders: the role of ubiquitin-proteasome system.Frontiers in nutrition · 2024Review
- STUB1-mediated ubiquitination regulates the stability of GLUD1 in lung adenocarcinoma.iScience · 2023Article
- E3 ligase HECTD3 promotes RNA virus replication and virus-induced inflammation via K33-linked polyubiquitination of PKR.Cell death & disease · 2023Article
- Chaperone-assisted E3 ligase CHIP: A double agent in cancer.Genes & diseases · 2022Review
- CHIP ameliorates cerebral ischemia-reperfusion injury by attenuating necroptosis and inflammation.Aging · 2021Article
- CHIP promotes the activation of NF-κB signaling through enhancing the K63-linked ubiquitination of TAK1.Cell death discovery · 2021Article
- CHIP-dependent regulation of the actin cytoskeleton is linked to neuronal cell membrane integrity.iScience · 2021Article
- CHIP and BAP1 Act in Concert to Regulate INO80 Ubiquitination and Stability for DNA Replication.Molecules and cells · 2021Article
- TRIM41 is required to innate antiviral response by polyubiquitinating BCL10 and recruiting NEMO.Signal transduction and targeted therapy · 2021Article
- Conserved and Unique Roles of Chaperone-Dependent E3 Ubiquitin Ligase CHIP in Plants.Frontiers in plant science · 2021Review
- Neurodevelopmental Disorders (NDD) Caused by Genomic Alterations of the Ubiquitin-Proteasome System (UPS): the Possible Contribution of Immune Dysregulation to Disease Pathogenesis.Frontiers in molecular neuroscience · 2021Review
- Article
- The ubiquitin system: orchestrating cellular signals in non-small-cell lung cancer.Cellular & molecular biology letters · 2020Review
- The E3 ubiquitin ligase CHIP in normal cell function and in disease conditions.Annals of the New York Academy of Sciences · 2020Review
- PKCζ facilitates lymphatic metastatic spread of prostate cancer cells in a mice xenograft model.Oncogene · 2019Article
- Control of mTOR signaling by ubiquitin.Oncogene · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The carboxyl terminus of constitutive heat shock cognate 70 (HSC70)-interacting protein (CHIP, also known as Stub1) is a U box-containing E3 ubiquitin ligase that is important for protein quality control. The role of CHIP in innate immunity is not known. Here, we report that CHIP knockdown inhibits Toll-like receptor (TLR) 4- and TLR9-driven signaling, but not TLR3-driven signaling; proinflammatory cytokine and type 1 interferon (IFN) production; and maturation of antigen-presenting cells, including macrophages and dendritic cells. We demonstrate that CHIP can recruit the tyrosine kinase Src and atypical protein kinase C ζ (PKCζ) to the TLR complex, thereby leading to activation of IL-1 receptor-associated kinase 1, TANK-binding kinase 1, and IFN regulatory factors 3 and 7. CHIP acts as an E3 ligase for Src and PKCζ during TLR signaling. CHIP-mediated enhancement of TLR signaling is inhibited by IFNAR deficiency or expression of ubiquitination resistant mutant forms of Src or PKCζ. These findings suggest that CHIP facilitates the formation of a TLR signaling complex by recruiting, ubiquitinating, and activating Src and PKCζ.
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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.