| 1993 |
IL-11 and IL-6 share the common signal transducer gp130; anti-gp130 antibodies abolished IL-11-induced cell proliferation, protein tyrosine phosphorylation, and junB gene expression in TF-1 cells, whereas anti-IL-6R antibody had no effect on IL-11 signaling, demonstrating that IL-11 uses a distinct ligand-binding protein but the same gp130 signal transducer as IL-6. |
Anti-gp130 antibody neutralization, tyrosine phosphorylation assay, gene expression assay in TF-1 cells |
Journal of immunology |
High |
8360477
|
| 1995 |
IL-11 activates JAK tyrosine kinases, MAP kinases, and pp90rsk; pp90rsk was identified as an H7-sensitive kinase critical for primary response gene (JunB, tis11, tis8) expression induced by IL-11; STAT91 tyrosine phosphorylation occurs but is not sufficient alone for primary response gene activation. |
Kinase activity assays, H7 inhibitor studies, gene expression analysis in mouse preadipocytes |
Annals of the New York Academy of Sciences |
Medium |
7545369
|
| 1996 |
The human IL-11 receptor alpha chain (IL-11Rα) absolutely requires gp130 for signaling; expression of IL-11Rα alone in Ba/F3 cells allowed IL-11 binding but no proliferative response, whereas co-expression of IL-11Rα with human gp130 generated high-affinity binding sites and IL-11-dependent proliferation. |
Molecular cloning, receptor transfection in Ba/F3 and M1 cells, radiolabeled IL-11 binding, proliferation assay, macrophage differentiation assay |
Oncogene |
High |
8637716
|
| 1994 |
IL-1α and TGF-β (β1 and β2) are dose-dependent stimulators of IL-11 protein production, mRNA accumulation, and gene transcription in human lung fibroblasts, acting synergistically via largely PKC- and cyclic nucleotide-independent but partially calmodulin-dependent pathways; these regulation pathways are distinct from those governing IL-6. |
ELISA for IL-11 protein, Northern blot for mRNA, nuclear run-on for gene transcription, pharmacological inhibitors (HA1004, staurosporine, phorbol ester, W7, TFP, A23187) |
Journal of immunology |
High |
8133053
|
| 1997 |
A soluble form of the IL-11 receptor alpha chain (sIL-11R) can signal in trans via gp130 (inducing gp130 phosphorylation, STAT3, and SHP-2 phosphorylation) but requires 10–20-fold higher IL-11 concentrations than membrane-bound receptor; sIL-11R can also act as an IL-11 antagonist by competing for limiting gp130 on cells expressing the transmembrane receptor. |
Recombinant protein expression, receptor binding assays (Kd measurements), phosphorylation assays, M1 differentiation assay, Ba/F3 proliferation assay |
Blood |
High |
9373251
|
| 2000 |
IL-11 induces rapid tyrosine phosphorylation of gp130, STAT3 (at 0.1 ng/ml) and STAT1 (at 10 ng/ml), and phosphorylation of p42/p44 MAPKs in HUVECs; at low (STAT3/MAPK-activating) concentrations, IL-11 confers cytoprotection against immune-mediated injury in a protein synthesis- and MEK1-dependent manner without activating NF-κB. |
Western blot for phosphorylation, MEK inhibitor (PD98059), functional cytotoxicity assay with CTL and complement |
Journal of immunology |
Medium |
10725745
|
| 2003 |
In human intestinal subepithelial myofibroblasts, IL-1β and TGF-β1 induce IL-11 secretion via AP-1 (c-Jun) activation and through ERK p42/44 and p38 MAPK pathways; p38 MAPK also mediates IL-11 mRNA stabilization; dominant-negative c-Jun adenovirus blocked IL-11 induction. |
EMSA for AP-1 binding, dominant-negative c-Jun adenovirus, MAP kinase inhibitors (SB-202190, PD-98059, U-0216), ELISA, Northern blot |
American journal of physiology. Gastrointestinal and liver physiology |
High |
12760902
|
| 2004 |
IL-11 protects human microvascular endothelium from alloinjury in vivo by upregulating survivin expression in endothelial cells and keratinocytes; topical survivin antisense oligonucleotide abrogated IL-11-mediated protection, identifying survivin induction as the cytoprotective mechanism. |
Human skin graft/SCID mouse alloinjury model, intradermal IL-11 injection, survivin antisense oligonucleotide, immunohistochemistry |
Journal of immunology |
Medium |
14734714
|
| 2005 |
IL-11Rα (IL-11 receptor alpha) is required for IL-13-induced inflammation, fibrosis, hyaluronic acid accumulation, myofibroblast accumulation, alveolar remodeling, mucus metaplasia, and respiratory failure in mice; IL-13 stimulates CC chemokines, MMPs, mucin genes, and gob-5 via IL-11Rα-dependent pathways. |
IL-11Rα null mutant mice crossed to IL-13-overexpressing transgenic mice, histology, gene expression analysis |
Journal of immunology |
High |
15699166
|
| 2008 |
IL-11 promotes chronic gastric inflammation and associated tumorigenesis via excessive STAT3 and STAT1 activation; gp130(Y757F/Y757F) mice lacking IL-11Rα showed normal gastric STAT3 activation and failed to develop gastric tumors; reducing STAT3 activity (genetically or with antisense oligonucleotides) normalized gastric IL-11 expression. |
Genetic mouse models (gp130 mutant, IL-11Rα knockout, STAT3/STAT1 reduction), STAT3 antisense oligonucleotides, histology, immunohistochemistry |
The Journal of clinical investigation |
High |
18431520
|
| 2008 |
Endogenous IL-11 signaling via IL-11Rα is required for antigen-induced Th2 eosinophilic inflammation, mucus production, and IL-13 production in the murine lung; an antagonistic IL-11 mutein reduced OVA-induced inflammation, mucus responses, and IL-13 production. |
IL-11Rα null mutant mice, OVA sensitization/challenge model, IL-11 mutein antagonist administration, BAL and lung analysis |
American journal of respiratory cell and molecular biology |
High |
18617680
|
| 2009 |
IL-17F induces IL-11 expression in bronchial epithelial cells via the Raf1-MEK1/2-ERK1/2-MSK1-CREB signaling pathway; siRNA knockdown of MSK1 inhibited CREB activation and IL-11 expression; Th2 cytokines (IL-4, IL-13) augmented this response. |
MEK inhibitors (PD-98059, U0126), Raf1 dominant-negative mutant overexpression, MSK1 inhibitors (Ro-31-8220, H89), MSK1 and CREB siRNA, phosphorylation assays |
American journal of physiology. Lung cellular and molecular physiology |
High |
19251839
|
| 2009 |
IL-11 signaling via IL-11Rα is required for uterine stromal decidualization; a PEGylated IL-11 antagonist administered to mice during early decidualization blocked IL-11 action in decidual cells (reducing cyclin D3 expression) and completely abolished pregnancy; IL-11 antagonist reduced STAT3 phosphorylation in human endometrial cells. |
In vivo PEGylated IL-11 antagonist administration in mice, immunohistochemistry for cyclin D3, STAT3 phosphorylation assay in HES cells |
Biology of reproduction |
Medium |
19144959
|
| 2009 |
IL-11 regulates autoimmune demyelination via immunoregulation (modulation of CD11c+ APC-mediated lymphocyte activation, reducing T effector cytokine production) and direct neuroprotection (reducing oligodendrocyte progenitor apoptosis and potentiating mitosis); IL-11Rα-null mice showed exacerbated EAE severity. |
IL-11Rα null mutant mice in EAE model, exogenous IL-11 treatment, T cell/APC co-culture cytokine assays, oligodendrocyte progenitor culture apoptosis/mitosis assays |
Journal of immunology |
High |
19734214
|
| 2011 |
Mutations in IL11RA that render the receptor unable to mediate IL-11 signaling cause a human syndrome of craniosynostosis, maxillary hypoplasia, delayed tooth eruption, and supernumerary teeth; cell-transfection experiments confirmed the p.Arg296Trp mutation causes loss of IL-11 signaling function. |
Homozygosity mapping, mutational analysis, cell transfection signaling assay, Il11ra null mouse phenotyping |
American journal of human genetics |
High |
21741611
|
| 2013 |
IL-11 is a hypoxia-inducible, VHL-regulated gene in human cancer cells; HIF-1 and AP-1 cooperatively mediate transcriptional activation of the IL-11 promoter; autocrine IL-11 production under hypoxia increases anchorage-independent growth via IL-11Rα-triggered STAT1-dependent signaling; IL-11 silencing abrogated hypoxia-induced tumor growth. |
Luciferase reporter assays for IL-11 promoter (HIF-1/AP-1 mutagenesis), siRNA knockdown of IL-11 and STAT1, VHL reconstitution, xenograft tumor models |
The Journal of clinical investigation |
High |
23549086
|
| 2015 |
IL-11 induces differentiation of CD11b+CD14+ monocytic myeloid-derived suppressor cells (MDSCs) from PBMCs via STAT3 phosphorylation through the IL-11Rα/gp130/JAK/STAT3 pathway; MDSC generated in the presence of IL-11 expressed higher arginase-1 and suppressed T cell proliferation. |
PBMC culture with IL-11, flow cytometry, STAT3 phosphorylation assay, T cell co-culture suppression assay |
Scientific reports |
Medium |
28781374
|
| 2016 |
HMGA2 directly binds the IL-11 promoter and induces its transcriptional activity; IL-11 downstream of HMGA2 modulates cell migration and invasion through pSTAT3-dependent signaling in colorectal cancer cells. |
Chromatin immunoprecipitation-PCR, luciferase reporter assay, HMGA2 overexpression/silencing, invasion assays |
Carcinogenesis |
Medium |
26964871
|
| 2017 |
IL-11 is the dominant TGFβ1-induced transcript in primary human fibroblasts and is required for TGFβ1's pro-fibrotic effect; IL-11 and IL-11Rα are expressed specifically in fibroblasts and drive non-canonical, ERK-dependent autocrine signaling required for fibrogenic protein synthesis; fibroblast-specific Il11 transgene expression or IL-11 injection causes heart and kidney fibrosis, while Il11ra1 deletion protects against fibrosis. |
Integrated imaging-genomics of human fibroblasts, fibroblast-specific transgenic mice, Il11ra1 knockout mice, ERK pathway assays, organ histology and function |
Nature |
High |
29160304
|
| 2017 |
Stromal/fibroblast loss of LKB1 induces IL-11 production and activation of the JAK/STAT3 pathway in tumor epithelia; JAK1/2 inhibitor ruxolitinib dramatically decreased polyposis in LKB1-deficient mice, placing IL-11-JAK/STAT3 downstream of LKB1 loss in gastrointestinal tumorigenesis. |
Mesenchymal Lkb1 conditional knockout mice, lineage tracing, immunohistochemistry, ruxolitinib treatment |
The Journal of clinical investigation |
High |
29202476
|
| 2018 |
Autocrine JAK2 activation by IL-11 (via FRA1-mediated IL-11 expression induced by elevated ROS) mediates platinum drug resistance in ovarian cancer via JAK2-STAT5 signaling; JAK2 inhibitor or anti-IL-11 antibody overcomes resistance in vitro and in vivo. |
qHTCS screen, genomic sequencing, anti-IL-11 antibody, JAK2 inhibitor (LY2784544), in vitro and xenograft models |
Oncogene |
Medium |
29662190
|
| 2020 |
TGFβ1-induced IL-11 upregulation in fibroblasts drives pulmonary fibrosis via a TGF-β1/IL-11/MEK/ERK (TIME) signaling axis; anti-IL-11 antibody or MEK inhibitor PD98059 blocked senescence-associated collagen deposition; cytoplasmic p16INK4a accumulation in senescent fibroblasts upregulated MEK/ERK by inhibiting nuclear translocation of pERK1/2. |
Bmi-1 knockout mouse model, anti-IL-11 antibody, MEK inhibitor, p16INK4a/Bmi-1 double knockout, pulmonary fibroblast and AT2 cell culture |
Experimental & molecular medicine |
Medium |
31959867
|
| 2020 |
Fibroblast-specific IL-11Rα signaling drives chronic (but not acute) lung inflammation following bleomycin injury; conditional knockout of Il11ra1 in adult fibroblasts reduced ERK activation in fibroblasts and STAT3 phosphorylation in immune cells, and diminished NF-κB phosphorylation and pro-inflammatory gene activation. |
Fibroblast-specific Il11ra1 conditional knockout (loxP/Cre), bleomycin lung injury model, neutralizing anti-IL-11 antibodies, ERK/STAT3/NF-κB western blotting |
FASEB journal |
High |
32656894
|
| 2021 |
IL-11 drives fibrogenesis in fibroblasts through ERK/mTOR/P70RSK protein translation rather than STAT3; recombinant human IL-11 increases pSTAT3 in Il11ra1-null fibroblasts (indicating STAT3 activation by rhIL11 is IL-11Rα-independent); STAT3 inhibition causes ER stress and cell death; IL-11 selectively promotes Collagen 1 synthesis via an EPRS-regulated ribosome stalling mechanism; nintedanib causes dose-dependent ER stress. |
Il11ra1 null fibroblasts, ERK/mTOR/P70RSK inhibitors, STAT3 inhibitors, ER stress assays, ribosome stalling analysis, nintedanib/pirfenidone drug studies |
Frontiers in molecular biosciences |
High |
34651016
|
| 2021 |
IL-11 deletion (Il11-/-) places Il11 activity upstream of IL-6 in the bleomycin lung injury model; Il11-/- mice are protected from pulmonary fibrosis and show lesser ERK, STAT3, and NF-κB activation with reduced Il1b, Timp1, Ccl2 and IL-6 expression; unlike Il11ra1-/- mice, Il11-/- mice do not have craniosynostosis or long bone mass changes. |
Il11 knockout mice generation, bleomycin lung injury, ERK/STAT3/NF-κB assays, hematological profiling, bone phenotyping |
Scientific reports |
High |
34239012
|
| 2021 |
IL-11 stimulates ERK activation leading to fibrogenesis in dermal fibroblasts independently of STAT3, TGFβ upregulation, and SMAD2/3 phosphorylation; TGFβ isoforms induce IL-11 secretion from dermal fibroblasts creating an autocrine loop; ERK inhibition phenocopied anti-IL-11 antibody in preventing TGFβ-induced HDF-to-myofibroblast transformation. |
IL-11 neutralizing antibody, IL11RA siRNA, ERK inhibitor, STAT3/SMAD2/3 western blotting, myofibroblast transformation assays, HDF cultures from SSc patients |
Rheumatology |
High |
33590875
|
| 2021 |
The MAFF-BACH1 heterodimer directly transcriptionally activates IL-11 expression (identified by ChIP-seq and RNA-seq), leading to STAT3 signaling activation; IL-11 inhibition suppresses tumor metastasis to similar levels as MAFF inhibition in breast cancer. |
ChIP-seq, RNA-seq, IL-11 inhibition, in vivo metastasis models |
Nature communications |
High |
34262028
|
| 2021 |
IL-11 stimulation of fibroblasts causes transient STAT3 phosphorylation and sustained ERK activation, triggering a proinflammatory transcriptional program including robust IL-33 upregulation (38-fold); STAT3 inhibition (but not MEK/ERK inhibition) prevented IL-11-induced IL33 expression; IL-11 stimulated a proinflammatory secretome including IL8, IL6, MCP1, CCL20, CXCL1/5/6. |
RNA sequencing time course, proteomic secretome analysis, STAT3 and MEK/ERK inhibitors, primary human kidney/lung/skin fibroblasts |
International journal of molecular sciences |
High |
36012165
|
| 2021 |
The rhomboid intramembrane protease RHBDL2 cleaves the IL-11 receptor between Ala-370 and Ser-371 in the extracellular domain (proximal to the plasma membrane), generating soluble IL-11R (sIL-11R) capable of IL-11 trans-signaling; RHBDL2 can cleave IL-11R within the early secretory pathway; the human mutation IL-11R-A370V prevents RHBDL2-mediated cleavage but does not impede classical IL-11 signaling. |
RHBDL2 overexpression, cleavage site mapping, transmembrane domain mutagenesis, IL-11 trans-signaling assays, subcellular localization studies |
FASEB journal |
High |
33566379
|
| 2021 |
Species-matched IL-11 is hepatotoxic rather than hepatoprotective; IL-11 secreted from APAP-damaged hepatocytes triggers an autocrine loop of NOX4-dependent cell death downstream of mitochondrial dysfunction; hepatocyte-specific deletion of Il11ra1 or germline deletion of Il11 protected against APAP-induced liver injury with reduced JNK and ERK activation. |
Hepatocyte-specific Il11ra1 conditional knockout, Il11 germline knockout, anti-IL-11RA neutralizing antibody, NOX4 pathway analysis, JNK/ERK western blotting, APAP liver injury model |
Science translational medicine |
High |
34108253
|
| 2021 |
IL-11 suppresses host CD4+ T cell-mediated antitumor responses; adoptive bone marrow transfer and in vivo CD4+ T cell depletion showed the tumor-promoting activity of IL-11 is mediated through suppression of CD4+ T cells; IL11Rα-deficient CD4+ T cells showed elevated IFNγ and TNFα expression; IL-11 potently suppressed IFNγ, TNFα, IL-6, and IL-12p70 production by CD4+ T cells in vitro. |
Adoptive bone marrow transfer, in vivo T cell depletion, Il11ra conditional knockout, in vitro cytokine suppression assays, RNAscope, syngeneic tumor models |
Cancer immunology research |
High |
33906864
|
| 2021 |
IL-11 stimulation of renal tubular epithelial cells (TECs) induces ERK- and p90RSK-mediated GSK3β inactivation, SNAI1 upregulation, and pro-inflammatory gene expression; TEC-specific deletion of Il11ra1 reduces pathogenic signaling and protects from renal injury-induced inflammation, fibrosis, and failure; anti-IL-11 therapy promotes TEC proliferation and parenchymal regeneration in chronic kidney disease. |
TEC-specific Il11ra1 conditional knockout, anti-IL-11 neutralizing antibody, ERK/p90RSK/GSK3β/SNAI1 pathway assays, acute and chronic kidney injury mouse models |
Nature communications |
High |
36470928
|
| 2022 |
IL-11 stimulates an ERK/P90RSK axis that phosphorylates LKB1 at S325 and S428, causing LKB1 inactivation, which in turn inhibits AMPK and activates mTOR; this IL-11/ERK/LKB1/AMPK/mTOR axis drives myofibroblast transformation in stromal cells and mesenchymal transition in hepatocytes and epithelial cells; metformin-stimulated AMPK activation inhibits IL-11-induced phenotypes. |
Phospho-LKB1 site-specific analysis (S325, S428), AMPK/mTOR assays, metformin treatment, genetic manipulation of IL-11 in fatty liver disease mouse model, multiple cell types |
iScience |
High |
35992082
|
| 2022 |
In Marfan syndrome aortic VSMCs, IL-11 is upregulated and drives ERK-dependent collagen secretion, MMP2/9 expression, aortic dilation, fibrosis, and inflammation; genetic deletion of Il11ra1 or therapeutic anti-IL11RA antibody (X209) reduced aortic pathology and ERK/COL1A1/MMP2/9 expression. |
Fbn1C1041G/+ Marfan mouse model, Il11-EGFP reporter, Il11ra1 knockout crossed to MFS mice, anti-IL11RA antibody X209, echocardiography, histology, immunoblotting |
Circulation research |
High |
35135328
|
| 2022 |
IL-11 activates pancreatic stellate cells (PSCs), which specifically express IL11RA in the pancreas, causing transient STAT3 phosphorylation and sustained ERK activation leading to PSC-to-myofibroblast transformation; IL-6 stimulation caused sustained STAT3 phosphorylation without ERK activation or PSC transformation; TGFβ, CTGF, and PDGF induced IL-11 secretion from PSCs via autocrine IL-11 activity; anti-IL11RA antibody prevented PSC activation. |
PSC culture with IL-11 vs IL-6, ERK/STAT3 assays, anti-IL11RA neutralizing antibody, pancreatic duct ligation mouse model, NF-κB signaling analysis |
International journal of molecular sciences |
High |
35408908
|
| 2023 |
IL-11 in monocytes induces NLRP3 inflammasome activation (upregulating NFKB1, NLRP3, IL1B by scRNA-seq); IL-11R+ monocytes in CSF of MS patients upregulate NLRP3 inflammasome genes, complement, IL-18, and migratory genes (VEGFA/B); anti-IL-11 mAb in EAE mice decreased NFκBp65+, NLRP3+, and IL-1β+ monocytes in the CNS. |
Single-cell RNA sequencing of IL-11-stimulated PBMCs, IL-11R+-sorted CSF cells, anti-IL-11 mAb treatment in EAE mice |
PNAS |
High |
37339207
|
| 2023 |
IL-11-induced renal tubular epithelial cell EMT is dependent on sequential activation of STAT3 and ERK1/2 signaling and upregulation of metadherin (MTDH); micheliolide (MCL) competitively inhibits IL-11 binding to IL-11Rα1, suppressing STAT3/ERK1/2-metadherin pathways and inhibiting IL-11-induced EMT and fibrosis. |
IL-11 stimulation of RTECs, STAT3/ERK inhibitors, MCL competitive binding assay, UUO mouse model, dimethylaminomicheliolide (DMAMCL) in vivo |
The American journal of pathology |
Medium |
37673330
|
| 2024 |
As mice age, IL-11 upregulates across tissues to regulate an ERK-AMPK-mTORC1 axis governing cellular and organismal aging pathologies; deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity, and frailty; anti-IL-11 treatment of aged mice improves metabolism and muscle function; genetic deletion of Il11 extended lifespan by 24.9% on average. |
Il11 and Il11ra1 knockout mice, anti-IL-11 antibody administration from 75 weeks, ERK/AMPK/mTORC1 pathway assays, lifespan studies in both sexes |
Nature |
High |
39020175
|
| 2024 |
ALKBH5-mediated m6A demethylation of IL-11 mRNA increases IL-11 mRNA stability and protein levels in cardiac macrophages, driving macrophage-to-myofibroblast transition (MMT) under hypertensive stress; macrophage-specific ALKBH5 knockout inhibited MMT and cardiac fibrosis; IL-11 overexpression in macrophages reversed the ALKBH5-deficient phenotype. |
RNA immunoprecipitation sequencing, macrophage-specific ALKBH5 knockout, lineage tracing, parabiosis, single-cell transcriptomics, siRNA targeting ALKBH5 and IL11RA1 in monocytes |
Nature communications |
High |
38443404
|
| 2024 |
IL-11 functions as a ligand of EGFR in brain metastasis from EGFR-mutated NSCLC; IL-11 secreted from reactive astrocytes binds EGFR on tumor cells activating downstream signaling to upregulate PDL1 and promote CD8+ T cell apoptosis; IL-11 also signals via its canonical IL-11Rα/gp130 receptor; combined gp130 and EGFR inhibition suppressed brain metastasis growth. |
Co-culture of astrocytes and tumor cells, EGFR binding/activation assays, PDL1 expression analysis, in vivo brain metastasis models, gp130 and EGFR inhibitors |
Advanced science |
Medium |
38696655
|
| 2016 |
IL-11R1 (but not IL-11R2 or IL-6R) promotes transcytosis of IL-11 across polarized epithelial cell barriers; basolaterally supplied IL-11 is transported to the apical side in an IL-11R1-dependent, intracellular domain-dependent manner; synthetic transfer of the IL-11R1 intracellular domain to IL-6R confers transcytotic activity on IL-6. |
Polarized cell transcytosis assays, domain swap experiments (IL-11R1 intracellular domain transferred to IL-6R), comparison of IL-11R1 vs IL-11R2 vs IL-6R |
Cell reports |
High |
27425614
|
| 2020 |
A homozygous variant in IL6ST (p.R281Q/p.R279Q in mice) causes selective loss of IL-11 signaling without affecting IL-6, IL-27, OSM, LIF, CT-1, CLC, and CNTF signaling; this selectivity phenocopies aspects of IL-11Rα deficiency (craniosynostosis, teeth abnormalities, reduced litter size). |
In vitro transfected cell line signaling assays, primary patient-derived cells, genome-edited mouse model (Il6st p.R279Q) |
Bone research |
High |
32566365
|
| 2021 |
piR-2158 acts as a transcriptional repressor of IL-11 by competing with AP-1 transcription factor subunit FOSL1 to bind the IL-11 promoter; STAT3 signaling mediates piR-2158-IL-11 regulation of cancer cell stemness, tumor growth, and angiogenesis in breast cancer. |
RNA-seq, ChIP-seq, luciferase reporter assays, FOSL1 competition assays, STAT3 signaling assays |
Theranostics |
Medium |
37153732
|
| 2024 |
Autocrine IL-11/IL-11RA signaling in docetaxel-resistant prostate cancer activates JAK1/STAT4 pathway; activated pSTAT4 translocates to the nucleus, binds CBP at the c-MYC promoter, and amplifies c-MYC transcription; disruption of IL-11/IL-11RA or JAK1/STAT4 reduces pSTAT4 nuclear binding to CBP and restores docetaxel sensitivity. |
Single-cell secretion profiling, ChIP-seq for pSTAT4, Co-IP of pSTAT4 and CBP, luciferase reporter assay, IL-11/IL-11RA inhibition in prostate cancer cells |
Journal of experimental & clinical cancer research |
Medium |
38429845
|