TXNIP_PIG TXNIP ELISA tesk kit
- Known as:
- TXNIP_PIG TXNIP Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15150
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TXNIP_PIG TXNIP ELISA tesk kit
Related genes to: TXNIP_PIG TXNIP ELISA tesk kit
- 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_PIG TXNIP ELISA tesk kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: TXNIP_PIG TXNIP ELISA tesk kit
- Diabetic kidney disease (DKD) is a major cause of renal failure and end-stage renal disease. Pyroptosis, a Gasdermin-dependent inflammatory form of programmed cell death, has been implicated in DKD progression. Metformin has shown renoprotective effects in DKD; however, the underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/08/19
Shi ShuyuWang BingZhou YangLi QiHou YushengZhang XinyiWang Qiuyue - Music-based interventions have shown promise in aiding recovery in individuals with brain damage (BD), including acquired and traumatic brain injury (ABI and TBI). To investigate the underlying molecular mechanisms, we conducted a study integrating transcriptomic and epigenomic data. We compared gene expression changes driven by musical stimuli in healthy individuals exposed to music with transcriptomic data from TBI patients, identifying 154 common differentially expressed genes (DEGs) affected in TBI and impacted by music, including , . These genes are notably involved in synaptic plasticity, and neurodegenerative processes. Epigenomic analysis revealed that 92 of these DEGs also exhibited significant differential methylation in TBI samples, particularly in genes associated with neurodevelopment, neuroinflammation, and mood regulation. Pathway enrichment and cross-validation in independent datasets of TBI patients highlighted the cGMP-PKG signaling pathway, a key regulator of memory and plasticity. Co-expression network analysis further revealed six gene modules significantly associated with TBI, including modules centered on and genes, previously implicated in neuroinflammation and epilepsy, two conditions commonly associated with TBI. Interestingly, several hub genes from these modules also showed sensitivity to musical stimuli, suggesting that music may target biologically relevant networks involved in TBI pathology. These findings reveal intriguing molecular parallels between signatures associated with TBI and the biological response to music exposure, providing a proof-of-concept for future investigation. This molecular insight suggests a potential role for music as a biologically grounded component of neurorehabilitation. However, future studies should directly assess transcriptomic and epigenomic responses to music-based interventions in BD patients. - Source: PubMed
Publication date: 2026/08/19
Gómez-Carballa AlbertoPischedda SaraMallah Nour El ZahraaNowak WiktorMartinón-Torres FedericoNavarro LauraSalas Antonio - Microplastics are ubiquitous in the atmosphere and may be inhaled into the respiratory system to cause adverse health effects. Photoaging of microplastics in the atmosphere is inevitable, which changes their toxic effects greatly, yet the impacts and underlying mechanisms remain poorly understood. In this study, poly(vinyl chloride) microplastics (PVC-MPs), commonly detected in the atmosphere, were selected to investigate the effects of photoaging on pulmonary toxicological responses at 7 days after a single intratracheal instillation in a mouse model. Photoaging enhanced the abundance of oxygen-containing functional groups on the particle surface, surface hydrophilicity, and oxidative potential. Upon a short-term intratracheal exposure, photoaged PVC-MPs (A-PVC) induced more severe pulmonary inflammation and epithelial barrier dysfunction than the virgin PVC-MPs (V-PVC), as evidenced by increased protein leakage and lactate dehydrogenase release in bronchoalveolar lavage fluid and disruption of tight junction proteins. Transcriptomic analysis revealed enrichment of the NOD-like receptor signaling pathway and activated TXNIP-NLRP3 inflammasome axis. In vitro tests with BEAS-2B cells indicated that more A-PVC was adsorbed on the cell membrane, likely due to increased membrane affinity than V-PVC, thus triggering excessive ROS generation and leading to TXNIP-dependent NLRP3 activation and tight junction disruption. Inhibition of ROS, TXNIP, or NLRP3 attenuated inflammasome activation and preserved barrier integrity. These findings demonstrate that environmental photoaging exacerbated short-term pulmonary toxicity of PVC-MPs through a ROS-TXNIP-NLRP3-mediated inflammatory amplification axis. - Source: PubMed
Liu XinweiZhao JiayiZhang YinqingZhu Lingyan - Ulcerative colitis (UC) involves recurrent colonic mucosal inflammation and impaired epithelial repair. Current therapies are limited due to safety concerns. The TXNIP-NLRP3 inflammasome axis serves as a critical link between oxidative stress and inflammation in UC. The present study evaluated the protective role of dimethyl itaconate (DMI), a cell-permeable itaconate derivative, in a chronic dextran sulfate sodium (DSS)-induced ulcerative colitis model with verapamil as a positive control. - Source: PubMed
Publication date: 2026/08/17
Tiwari PriyankaAabis MohammadKumar VinodJena Gopabandhu - Cardiovascular disease (CVDs) and atherosclerosis remain a major causes of morbidity and mortality worldwide. Endothelial dysfunction is a central driver of atherosclerosis, which is significantly accelerated in diabetes mellitus through hyperglycemia-induced oxidative stress, oxidized low-density lipoprotein (oxLDL) accumulation, and NLRP3 inflammasome activation. Phenolic acids, a class of plant-derived polyphenols, have gained attention as vasoprotective agents due to their antioxidant and anti-inflammatory properties. Among them, rosmarinic acid and salvianolic acid have gained attention, yet no previous review has systematically compared their distinct molecular mechanisms. This review addresses the gap by summarizing the pathophysiological mechanisms linking endothelial dysfunction to atherosclerotic progression and comparing how rosmarinic acid and salvianolic acid modulate oxidative stress, nitric oxide signaling, inflammatory responses, and NLRP3 inflammasome activation. Rosmarinic acid primarily exerts its effects through the p38 MAPK-FOXO1-TXNIP and AMPK/eNOS pathways, while salvianolic acid mainly acts via the PKM2/PKR and NF-ĸB/NLRP3 signaling pathways. Despite these findings, clinical evidence remains limited, primarily limited to Phase 1 pharmacokinetic studies and mixed-extract trials, leaving compound-specific efficacy in humans unverified. This review highlights these translational gaps and suggests prioritizing clinical trials of purified compounds, bioavailability optimization, and dose-standardization studies to advance rosmarinic acid and salvianolic acid toward clinical application in diabetic atherosclerosis. - Source: PubMed
Publication date: 2026/07/24
Won YaeramKim Hye Jung