ArticleProceedings of the National Academy of Sciences of the United States of America1999
Autoregulation of pituitary corticotroph SOCS-3 expression: characterization of the murine SOCS-3 promoter.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed.
- SOCS1 and SOCS3 as key checkpoint molecules in the immune responses associated to skin inflammation and malignant transformation.Frontiers in immunology · 2024Review
- Epicardial Adipose Tissue-Derived Leptin Promotes Myocardial Injury in Metabolic Syndrome Rats Through PKC/NADPH Oxidase/ROS Pathway.Journal of the American Heart Association · 2023Article
- Mechanisms of reduced leptin-mediated satiety signaling during obesity.International journal of obesity (2005) · 2022Article
- Simplifying cell fate map by determining lineage history of core pathway activation during fate specification.Trends in developmental biology · 2022Article
- Hypothalamic Regulation of Corticotropin-Releasing Factor under Stress and Stress Resilience.International journal of molecular sciences · 2021Review
- Transcriptomics identifies STAT3 as a key regulator of hippocampal gene expression and anhedonia during withdrawal from chronic alcohol exposure.Translational psychiatry · 2021Article
- Binge-like ethanol drinking activates anaplastic lymphoma kinase signaling and increases the expression of STAT3 target genes in the mouse hippocampus and prefrontal cortex.Genes, brain, and behavior · 2021Article
- Article
- Lyssavirus P-protein selectively targets STAT3-STAT1 heterodimers to modulate cytokine signalling.PLoS pathogens · 2020Article
- Phospho-Ser727 triggers a multistep inactivation of STAT3 by rapid dissociation of pY705-SH2 through C-terminal tail modulation.International immunology · 2020Article
- Steroid receptor coactivator-1 modulates the function of Pomc neurons and energy homeostasis.Nature communications · 2019Article
- Stat3 Regulates Liver Progenitor Cell-Driven Liver Regeneration in Zebrafish.Gene expression · 2018Article
- SOCS3 Suppression Promoted the Recruitment of CD11bFrontiers in immunology · 2018Article
- Mesoderm-specific Stat3 deletion affects expression of Sox9 yielding Sox9-dependent phenotypes.PLoS genetics · 2017Article
- Effect of Cytokine Signaling 3 Gene Polymorphisms in Childhood Obesity.Journal of clinical research in pediatric endocrinology · 2016Article
- STAT3 signaling in immunity.Cytokine & growth factor reviews · 2016Review
- Leptin signalling pathways in hypothalamic neurons.Cellular and molecular life sciences : CMLS · 2016Review
- Single administration of recombinant IL-6 restores the gene expression of lipogenic enzymes in liver of fasting IL-6-deficient mice.British journal of pharmacology · 2016Article
- Transcriptional repression of SOCS3 mediated by IL-6/STAT3 signaling via DNMT1 promotes pancreatic cancer growth and metastasis.Journal of experimental & clinical cancer research : CR · 2016Article
- STAT1 deficiency redirects IFN signalling toward suppression of TLR response through a feedback activation of STAT3.Scientific reports · 2015Article
21 more citing papers are in PubMed but not listed here.
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3 authors.
Funding
Abstract
Pituitary corticotroph SOCS-3 is a novel intracellular regulator of leukemia inhibitory factor (LIF)-mediated proopiomelanocortin gene expression and adrenocorticotropic hormone (ACTH) secretion, inhibiting LIF-activated Janus kinase-signal transducers and activators of transcription (STAT) signaling in a negative autoregulatory loop. We now demonstrate in corticotroph AtT-20 cells that LIF-stimulated endogenous SOCS-3 mRNA expression is blocked in stable transfectants of SOCS-3 wild type or in dominant negative STAT-3 mutants, respectively. We characterized approximately 3.8-kb genomic 5' sequence of murine SOCS-3, including approximately 2.9-kb sequence upstream of the transcription start site (+1), which was determined by 5' rapid amplification of cDNA ends and RNase protection assay. Different 5' constructs were cloned into the pGL3Basic vector, and luciferase activity was assayed in transiently transfected ACTH-secreting corticotroph AtT-20 cells. A STAT-1/STAT-3 binding element, located at nucleotides -72 to -64, was essential for LIF stimulation of SOCS-3 promoter activity. LIF induced 10-fold increased luciferase activity in a wild-type construct spanning -2757 to +929 bases. However, deletion or point mutation of the STAT-1/STAT-3 binding element abrogated LIF action (2- to 3-fold). Electrophoretic mobility-shift assay analysis confirmed specific binding of STAT-1 and STAT-3 to this region. These results characterize the genomic 5' region of murine SOCS-3 and identify an important STAT-1/STAT-3 binding element therein. Thus, LIF-stimulated SOCS-3 gene expression is at least in part mediated by STAT-3 and STAT-1. The cytokine inhibitor SOCS-3 acts in a negative loop to autoregulate its own gene expression, thus limiting its accumulation in the corticotroph cell. These results demonstrate a mechanism for corticotroph plasticity with rapid "on" and "off" ACTH induction in response to neuro-immuno-endocrine stimuli, such as LIF.
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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.