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STAT3 secretion defect results in development abnormally

ABSTRACT: STAT3 secretion defect results in development abnormally

PROVIDER: PRJNA511761 | ENA |

REPOSITORIES: ENA

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STAT3 secretion defect results in development abnormally

Project description:Total RNA from embryos (12 days) of STAT3mut/mut, STAT3mut/wt and STAT3wt/wt mice which come from the same womb were extracted using TRIzol reagent (Invitrogen) following the manufacturer’s protocols. RNA quantity, quality and integrity were analyzed with NanoDrop ND-1000 and standard denaturing agarose gel electrophoresis. Sample labeling and array hybridization were performed according to the Agilent One-Color Microarray-Based Gene Expression Analysis protocol of Agilent Technology. The Whole Mouse Genome Oligo Microarray (Agilent 4*44k) represents all known genes and transcripts in the mouse genome (Kyoto Encyclopedia of Genes and Genomes, KEGG). All the microarray experiments were performed by Kangchen Biotechnology Limited (Shanghai, China).

2018-12-26 | GSE124348 | GEO

STAT3 induces breast cancer growth and progression via IL-6, STC1 and MMP13 secretion by Cancer Associated Fibroblasts

Project description:In the tumor microenvironment, Cancer Associated Fibroblasts (CAFs) become activated by cancer cells and increase their secretory activity to produce soluble factors that contribute to tumor cells proliferation, invasion and dissemination to distant organs. The pro-tumorigenic transcription factor STAT3 and its canonical inducer, the pro-inflammatory cytokine IL-6 act conjunctly in a positive feedback loop that maintains high levels of IL-6 secretion and STAT3 activation in both tumor and stromal cells. Here, we demonstrate that STAT3 is essential for the pro-tumorigenic functions of murine breast cancer CAFs both in vitro and in vivo, and identify a STAT3 signature significantly enriched for genes encoding for secreted proteins. Among those, IL-6, ANGPTL4, STC-1 and MMP13 were validated as STAT3-dependent mediators of CAF pro-tumorigenic functions by different approaches. CAFs activities were moreover impaired by IL-6 Receptor blocking antibodies and by MMP13 inhibition, supporting the feasibility of a therapeutic approach based on inhibiting STAT3-induced CAF-secreted proteins. The usefulness of such an approach is supported by the observation that an equivalent CAF-STAT3 signature in humans is expressed at high levels in breast cancer stromal cells and characterizes patients with a shorter disease specific survival, including those with basal-like disease.

2021-12-31 | GSE178081 | GEO

MKL1 deficiency results in a severe neutrophil motility defect due to impaired actin polymerization

Project description:MKL1 deficiency results in a severe neutrophil motility defect due to impaired actin polymerization

| PRJNA555994 | ENA

Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity

Project description:This SuperSeries is composed of the following subset Series: GSE34886: Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity [expression profiling] GSE34887: Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity [MRE-seq] Refer to individual Series

2012-01-04 | E-GEOD-34267 | biostudies-arrayexpress

Expression profiling of STAT3-regulated genes in U937-derived macrophages

Project description:We used RNA-Seq assay to characterize STAT3-regulated gene expression patterns in U937-derived macrophages. We wanted to determine how STAT3 activation involves in function, differentiation, cytokine secretion of macrophages.

2023-10-26 | GSE231829 | GEO

A Bartonella effector acts as signaling hub for intrinsic STAT3 activation to trigger anti-inflammatory responses

Project description:Chronically infecting pathogens avoid clearance by the innate immune system by promoting premature transition from an initial pro-inflammatory response towards an anti-inflammatory tissue-repair response. STAT3, a central regulator of inflammation, controls this transition and thus is targeted by numerous chronic pathogens. Here we show that BepD, an effector of the chronic bacterial pathogen Bartonella henselae targeted to infected host cells, establishes an exceptional pathway for canonical STAT3 activation, thereby impairing secretion of pro-inflammatory TNF-α and stimulating secretion of anti-inflammatory IL-10. Tyrosine phosphorylation of EPIYA-related motifs in BepD facilitates STAT3 binding and activation via c-Abl-dependent phosphorylation of Y705. The tyrosine-phosphorylated scaffold of BepD thus represents a signaling hub for intrinsic STAT3 activation that is independent from canonical STAT3 activation via transmembrane receptor-associated Janus kinases. We anticipate that our findings on a molecular shortcut to STAT3 activation will inspire new treatment options for chronic infections and inflammatory diseases.

2020-02-12 | PXD017119 | Pride

Oral STAT3 Inhibitor, TTI-101, in Patients With Advanced Cancers

Project description:Many patients have cancers that have increased activity of a protein called STAT3 that contributes critically to the development and growth of their cancer. Despite our knowledge of STAT3’s importance to cancer, scientists and doctors have not developed a drug that targets it and that patients can take to treat their cancer more effectively than treatments that are now available. Tvardi Therapeutics, Incorporated has developed a compound, TTI-101, which can be given by mouth and acts as a direct inhibitor of STAT3. Administration of TTI-101 to mice demonstrated that it blocked growth of cancers of the breast, head and neck, lung, and liver and it was safe when administered at high doses to mice, rats, and dogs. In this application, Tvardi is proposing to further develop TTI-101 for treatment of solid tumors for which the prognosis is dismal. The investigators will determine how safe it is when administered to patients with cancer, determine whether an adequate dose can be administered to patients with cancer that will block STAT3 in their cancer, and determine whether treatment with TTI-101 leads to reduced growth of their cancer.

| 2247646 | ecrin-mdr-crc

A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance

Project description:A human mutation in STAT3 promotes type 1 diabetes through a defect in CD8+ T cell tolerance

| PRJNA725474 | ENA

Neural tube closure defect

Project description:Neural tube closure defect

| PRJNA704672 | ENA

Trophoblast epithelial-mesenchymal transition (EMT) in abnormally invasive placenta (AIP)

Project description:Comparison of genes associated with the EMT between cytotrophoblast cells (CTB) and extravillous trophoblast cells (EVT) from normal third trimester placenta and abnormally invasive placenta (AIP)

2018-01-01 | GSE104350 | GEO

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