ArticlePloS one2013
Thioredoxin-interacting protein gene expression via MondoA is rapidly and transiently suppressed during inflammatory responses.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Adipocyte/Tumor cell crosstalk via IGF-1/TXNIP axis promotes malignancy and endocrine resistance in breast cancer.Cell communication and signaling : CCS · 2025Article
- D-mannose alleviates intervertebral disc degeneration through glutamine metabolism.Military Medical Research · 2024Article
- Sulforaphane acutely activates multiple starvation response pathways.Frontiers in nutrition · 2024Article
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- Thioredoxin-Interacting Protein (TXNIP) with Focus on Brain and Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Oroxindin inhibits macrophage NLRP3 inflammasome activation in DSS-induced ulcerative colitis in mice via suppressing TXNIP-dependent NF-κB pathway.Acta pharmacologica Sinica · 2020Article
- Intracellular Cryptococcus neoformans disrupts the transcriptome profile of M1- and M2-polarized host macrophages.PloS one · 2020Article
- Tumor necrosis factor induces rapid down-regulation of TXNIP in human T cells.Scientific reports · 2019Article
- Cytokines Regulate β-Cell Thioredoxin-interacting Protein (TXNIP) via Distinct Mechanisms and Pathways.The Journal of biological chemistry · 2016Article
- Reactive oxygen species and mitochondria: A nexus of cellular homeostasis.Redox biology · 2015Review
- New Insight Into Metformin Action: Regulation of ChREBP and FOXO1 Activities in Endothelial Cells.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Article
- Transcription factor Ets1 regulates expression of thioredoxin-interacting protein and inhibits insulin secretion in pancreatic β-cells.PloS one · 2014Article
- TXNIP deficiency exacerbates endotoxic shock via the induction of excessive nitric oxide synthesis.PLoS pathogens · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whereas accumulating evidence indicates that a number of inflammatory genes are induced by activation of nuclear factor-κB and other transcription factors, less is known about genes that are suppressed by proinflammatory stimuli. Here we show that expression of thioredoxin-interacting protein (Txnip) is dramatically suppressed both in mRNA and protein levels upon stimulation with lipopolysaccharide in mouse and human macrophages. In addition to lipopolysaccharide, a Toll-like receptor 4 ligand, stimulation with other Toll-like receptor ligands such as CpG DNA also suppressed Txnip expression. Not only the Toll-like receptor ligands, but also other proinflammatory stimulators, such as interleukin-1β and tumor necrosis factor-α elicited the similar response in fibroblasts. Suppression of Txnip by lipopolysaccharide is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei and dissociation of the MondoA:Mlx complex that bound to the carbohydrate-response elements in the Txnip promoter in unstimulated cells. Lipopolysaccharide-mediated decrease of nuclear MondoA was inhibited in the presence of 2-deoxyglucose. Furthermore, blockage of glyceraldehyde-3-phosphate dehydrogenase by iodoacetate alleviated the suppression of Txnip mRNA by lipopolysaccharide, suggesting the involvement of glucose-metabolites in the regulation. Since Txnip is implicated in the regulation of glucose metabolism, this observation links between inflammatory responses and metabolic regulation.
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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.