Ask about this productRelated genes to: TXNIP antibody
- Gene:
- TXNIP NIH gene
- Name:
- thioredoxin interacting protein
- Previous symbol:
- -
- Synonyms:
- VDUP1, EST01027, HHCPA78, THIF, ARRDC6
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: TXNIP antibody
Related articles to: TXNIP antibody
- Childhood obesity is common and associated with adverse health outcomes. Fetal programming via epigenetics is a potential mechanism underlying its pathogenesis. We conducted an epigenome-wide association study (EWAS) on cord blood DNA to identify DNA methylation sites that may mediate the association of maternal body mass index (BMI) with offspring adiposity using data from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study and its follow-up study (HAPO FUS). HAPO was a prospective, multicenter, international observational study that recruited pregnant women between 2000 and 2006 for glucose tolerance testing; cord blood was collected at delivery and newborn anthropometrics were obtained. The HAPO FUS was conducted from 2013 to 2016, where the 10-14 year-old offspring underwent measures of body composition, anthropometrics, and a fasting glucose tolerance test. Eligibility for HAPO FUS included gestational age at delivery ≥ 37 weeks without major neonatal malformations. There were 3,243 samples with cord blood DNA methylation (cbDNAm) data; mean child age at follow-up was 11.5 years. The present study used cord blood DNA to conduct methylation profiling using the Infinium MethylationEPIC 850 K BeadChip. Linear regression models were used to test the association between maternal BMI and cbDNAm levels adjusting for population substructure, cell count, maternal and child co-variates; multiple testing was accounted for using Bonferroni correction. Mediation analysis tested if cbDNAm CpG sites that were associated (Bonferroni P < 0.05) with maternal BMI explained the known association between maternal BMI and child BMI. - Source: PubMed
Publication date: 2026/05/02
Brolly GraceGurra MirandaScholtens Denise MLowe William LHivert Marie-FranceJosefson Jami L - Kidney ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury. This study assessed the renooprotective effects of morin hydrate (MH) and its association with inflammatory and mitochondrial regulatory pathways in an I/R rat model. - Source: PubMed
Publication date: 2026/04/30
Mohanad MarwaEl-Awdan Sally AAboulhoda Basma EAbdAllah HendAhmed Maha A E - Particulate matter (PM) is a complex mixture of airborne solid particles and liquid droplets originating from various environmental sources, and it has been implicated in the initiation, development, and progression of pulmonary inflammation and respiratory diseases. However, the underlying associated molecular mechanisms remain unclear. Franch. & Sav. (AD) is a medicinal herb classified within the Campanulaceae family and genus , with a broad geographic distribution across East Asia, including Korea, Asia, and Russia. In this study, we investigated the mechanisms underlying the effects of AD on PM-induced lung inflammation in both PM-stimulated RAW264.7 cells and PM-exposed mice. Considering that the reactive oxygen species (ROS)-mediated thioredoxin-interacting protein (TXNIP) and NOD-like receptor pyrin domain containing (NLRP3) inflammasome pathway plays a role in PM-induced inflammatory responses, we focused on determining whether AD exerts its anti-inflammatory effects through modulation of this signaling pathway. The anti-inflammatory properties of the methanolic extract of AD were evaluated using PM-stimulated RAW264.7 cells and PM-exposed mice. PM was administered intranasally to mice for 7 days, whereas AD or dexamethasone was orally administered for the same duration. AD treatment significantly attenuated pulmonary inflammation, as evidenced by reduced inflammatory cell counts and decreased cytokine levels in bronchoalveolar lavage fluid. In addition, AD decreased oxidative stress marker (ROS and thiobarbituric acid reactive substances) while increasing glutathione content, leading to suppression of TXNIP/NLRP3 inflammasome expression. Histopathological analysis revealed a marked alleviation of inflammatory responses in lung tissue, characterized by diminished inflammatory cell infiltration and reduced alveolar wall thickening. Collectively, these findings suggest ROS-mediated TXNIP serves as a key regulatory factor, and AD may serve as a potential therapeutic agent for pulmonary inflammation. - Source: PubMed
Publication date: 2026/04/09
Ha Ji-HyeLee Ba-WoolYi Da-HyeJeong Seong-HunKim Ju-HongLee Hyeon JinKim Yun-HyeJeong Ju HwanJang Hyun-JaeKim Woo SikPark Ji-YoungJeong Hyung JaeKwon Hyung-JunKim Tae-WonKo Je-WonLee In-Chul - Chronic kidney disease (CKD) is a worldwide public health issue primarily characterized by glomerulosclerosis and the renal tubulointerstitial fibrosis. Recent studies have shown that TRPC6 is essential in renal interstitial fibrosis, although the precise mechanisms involved are not yet fully understood. - Source: PubMed
Publication date: 2026/04/24
Wei LintingCui ChenkaiLi YanGe PengboLi KeWang HaodongZhao WeihaoWang YinhongZhang JianpengFu Rongguo - Thioredoxin‑interacting protein (Txnip), a member of α‑arrestin superfamily, is best known for inhibiting thioredoxins and glucose transporters, increasing oxidative and metabolic stress. Through these functions, Txnip has emerged as a key contributor to the pathogenesis of heart diseases. Txnip contains C‑terminal PPXY motifs that are conserved among α‑arrestins across diverse species. Nevertheless, the physiological significance of these motifs remains unknown. We demonstrate that mutation of Txnip PPXY motifs to AAXA uncouples Txnip's canonical functions from its cytotoxic effects. While the mutant reduced glutathione levels and glucose uptake to the same extent as wild‑type Txnip, it attenuated cell death. To assess translational relevance, we engineered inducible, cardiomyocyte‑restricted Txnip PPXY‑to‑AAXA knock‑in mice. These mice displayed normal cardiac structure and function at baseline but were strongly protected after myocardial infarction, exhibiting improved left ventricular performance and overall survival. Mechanistically, structural modeling identified the E3 ubiquitin ligase ITCH as the principal PPXY‑binding partner. The PPXY mutation abolished Txnip ubiquitination and stabilized Txnip protein, revealing a paradoxical dissociation between Txnip levels and cardiotoxicity. Transcriptomic profiling uncovered enrichment of PPAR‑α/PGC‑1α-associated pathways, although metabolic assays and untargeted lipidomics did not support these findings. Instead, immediate early genes of the Fos/Jun AP‑1 network were consistently downregulated after ischemic injury, and AP‑1 DNA‑binding activity was diminished in PPXY mutant hearts. These results identify the Txnip PPXY motifs as key regulators of Txnip protein turnover and injury‑responsive transcriptional programs. Disruption of these motifs stabilizes Txnip yet confers cardioprotection, providing evidence that elevated Txnip levels do not invariably drive cardiotoxicity. - Source: PubMed
Publication date: 2026/04/22
Nakayama YoshinobuKitaura AtsuhiroAbdali Syed AmirNguyen Truong DYoshioka Jun