ArticleThe Journal of biological chemistry2012
Constitutively active mutant gp130 receptor protein from inflammatory hepatocellular adenoma is inhibited by an anti-gp130 antibody that specifically neutralizes interleukin 11 signaling.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Beyond fibrosis: Emerging role of IL-11 in regulating innate and adaptive immune cell plasticity.Molecular biology reports · 2026Review
- Nonoperative Management of Hepatic Adenomas: A Review.Journal of gastrointestinal cancer · 2026Review
- Interleukin-6 serves as a critical factor in various cancer progression and therapy.Medical oncology (Northwood, London, England) · 2024Review
- The IL6-like Cytokine Family: Role and Biomarker Potential in Breast Cancer.Journal of personalized medicine · 2021Review
- Capture and display of antibodies secreted by hybridoma cells enables fluorescent on-cell screening.mAbs · 2019Article
- IL-23R Signaling Plays No Role in Myocardial Infarction.Scientific reports · 2018Article
- Zac1 regulates IL-11 expression in osteoarthritis.Oncotarget · 2018Article
- IL-6/IL-12 Cytokine Receptor Shuffling of Extra- and Intracellular Domains Reveals Canonical STAT Activation via Synthetic IL-35 and IL-39 Signaling.Scientific reports · 2017Article
- Synthetic Deletion of the Interleukin 23 Receptor (IL-23R) Stalk Region Led to Autonomous IL-23R Homodimerization and Activation.Molecular and cellular biology · 2017Article
- Potential therapeutic implications of IL-6/IL-6R/gp130-targeting agents in breast cancer.Oncotarget · 2016Review
- Lack of gp130 expression in hepatocytes attenuates tumor progression in the DEN model.Cell death & disease · 2015Article
- Alternative intronic polyadenylation generates the interleukin-6 trans-signaling inhibitor sgp130-E10.The Journal of biological chemistry · 2014Article
- Inhibition of protein kinase II (CK2) prevents induced signal transducer and activator of transcription (STAT) 1/3 and constitutive STAT3 activation.Oncotarget · 2014Article
- Intracellular signaling prevents effective blockade of oncogenic gp130 mutants by neutralizing antibodies.Cell communication and signaling : CCS · 2014Article
- Biochemical and functional analyses of gp130 mutants unveil JAK1 as a novel therapeutic target in human inflammatory hepatocellular adenoma.Oncoimmunology · 2013Article
- Interleukin-6 contributes to CNS axon regeneration upon inflammatory stimulation.Cell death & disease · 2013Article
- Targeting the tumor microenvironment: JAK-STAT3 signaling.JAK-STAT · 2013Review
- Molecular classification of hepatocellular adenomas.International journal of hepatology · 2013Article
- Interleukin-6 controls recycling and degradation, but not internalization of its receptors.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ligand-independent constitutively active gp130 mutants were described to be responsible for the development of inflammatory hepatocellular adenomas (IHCAs). These variants had gain-of-function somatic mutations within the extracellular domain 2 (D2) of the gp130 receptor chain. Cytokine-dependent Ba/F3 cells were transduced with the constitutively active variant of gp130 featuring a deletion in the domain 2 from Tyr-186 to Tyr-190 (gp130ΔYY). These cells showed constitutive phosphorylation of signal transducer and activator of transcription-3 (STAT3) and cytokine-independent proliferation. Deletion of the Ig-like domain 1 (D1) of gp130, but not anti-gp130 mAbs directed against D1, abolished constitutive activation of gp130ΔYY, highlighting that this domain is involved in ligand-independent activation of gp130ΔYY. Moreover, soluble variants of gp130 were not able to inhibit the constitutive activation of gp130ΔYY. However, the inhibition of constitutive activation of gp130ΔYY was achieved by the anti-gp130 mAb B-P4, which specifically inhibits gp130 signaling by IL-11 but not by other IL-6 type cytokines. IL-11 but not IL-6 levels were found previously to be up-regulated in IHCAs, suggesting that mutations in gp130 are leading to IL-11-like signaling. The mAb B-P4 might be a valuable tool to inhibit the constitutive activation of naturally occurring gp130 mutants in IHCAs and rare cases of gp130-associated hepatocellular carcinoma.
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