TXNIP_RAT Txnip ELISA tesk kit
- Known as:
- TXNIP_RAT Txnip Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15152
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TXNIP_RAT Txnip ELISA tesk kit
Related genes to: TXNIP_RAT 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
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- Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease driven by metabolic stress, inflammation, and fibrosis, with limited effective therapies. Thioredoxin-interacting protein (TXNIP) links hyperglycemia and oxidative stress to NLRP3 inflammasome activation, but the epigenetic mechanisms sustaining TXNIP induction in diabetic MASH remain unclear. Bromodomain-containing protein 4 (BRD4) is an epigenetic reader that promotes inflammatory transcription through chromatin engagement. Here, we examined whether BRD4-associated regulation of TXNIP contributes to diabetic MASH and evaluated LT052, a BD1-biased BET bromodomain inhibitor with preferential BRD4 BD1 activity, in a streptozotocin-accelerated dietary rat model. Diabetic MASH caused severe steatohepatitis, fibrosis, insulin resistance, oxidative stress, NF-κB activation, TXNIP induction, and NLRP3 inflammasome activation. These changes were accompanied by increased BRD4 occupancy at the TXNIP promoter and elevated total hepatic histone H3 acetylation (Ac-H3K9). LT052 markedly improved liver histopathology, metabolic control, redox balance, and inflammatory outcomes, while reducing TXNIP expression, inflammasome activation, and downstream pyroptotic signaling. Mechanistically, LT052 reduced BRD4 occupancy at the TXNIP promoter and decreased total hepatic Ac-H3K9 without altering total BRD4 expression or nuclear BRD4 immunostaining, consistent with reduced BRD4-associated promoter engagement rather than altered BRD4 abundance or localization. Integrated analyses showed broad, dose-dependent improvement across MASH-relevant endpoints. These findings support further investigation of BD1-biased BET inhibition with LT052 as a therapeutic strategy for diabetic MASH. - Source: PubMed
Publication date: 2026/07/16
Hamad Rabab SSaber SamehElmorsy Elsayed AAmer Maha MAli Mohamed A MEissa HananFarrag Alshaimaa AAbuoHashish Norhan AhmedHamed ShereenAbdelaziz Mahmoud AAlalawy Adel IAlsirhani Alaa MuqbilAlRashidi Aljazi AbdullahShahin Mona IAlgarallah Danah MElmowafy RashaElmetwally Ahmed Abdel-MonemShata AhmedAbd Elzaher Mohamed A SAbdel-Hamed Mohamed R - Papillary thyroid cancer (PTC) exhibits marked biological heterogeneity, ranging from indolent tumors to more advanced forms characterized by angioinvasion, multifocality, and metastatic spread. Despite extensive molecular characterization at the tissue level, the clinical relevance of circulating omics-derived proteins in reflecting disease aggressiveness remains insufficiently explored. This study evaluated postoperative serum levels of selected thyroid cancer tissue omics-derived proteins, such as Malectin (MLEC), Thioredoxin-Interacting Protein (TXNIP), Nephronectin (NPNT), Fibronectin-1 (FN1), and Alpha-1-Acid Glycoprotein (ORM1), in relation to clinicopathological features of aggressive PTC. Serum concentrations of the analyzed proteins were measured using ELISA. The study group comprised 79 patients with histopathologically confirmed angioinvasive, multifocal, or metastatic PTC, while the reference group included 25 patients with very low-risk, non-invasive PTC. Subgroup analyses included angioinvasive PTC, multifocal PTC, and an advanced PTC category comprising patients with coexisting aggressive features, including angioinvasion, multifocality, and metastatic disease. Group comparisons were performed using the Mann-Whitney U test with false discovery rate (FDR) correction and effect size estimation. Exploratory univariable logistic regression and ROC curve analyses were subsequently performed to quantify the direction and strength of the associations and to assess discriminatory performance. Among the evaluated serum markers, only postoperative NPNT concentrations were significantly lower in patients with angioinvasive, multifocal, and advanced PTC compared with the reference group (angioinvasive: median 2.21 ng/mL vs. 2.78 ng/mL, p < 0.01, FDR = 0.01; multifocal: median 2.13 ng/mL, p = 0.01, FDR = 0.04; advanced: median 2.01 ng/mL, p = 0.01, FDR = 0.02). In contrast, serum levels of MLEC, TXNIP, FN1, and ORM1 did not differ significantly between aggressive and non-invasive PTC subgroups after correction for multiple testing. Exploratory univariable logistic regression analyses confirmed an inverse association between NPNT levels and aggressive clinicopathological features (OR range: 0.33-0.42), while ROC analyses indicated moderate discrimination (AUC approximately 0.72-0.73). An additional exploratory LASSO model incorporating NPNT and lipid parameters yielded an apparent AUC of 0.81; however, this result requires cautious interpretation because the model was not externally validated. Reduced postoperative serum NPNT levels are associated with histopathological features of more advanced PTC. Although these findings do not establish NPNT as a clinically applicable or validated biomarker, they suggest an association between postoperative NPNT concentrations and aggressive clinicopathological PTC phenotypes. The proposed links with extracellular matrix-related pathways and lipid metabolism remain hypothetical. Further prospective and preoperative studies are warranted to clarify the biological and clinical significance of NPNT in thyroid cancer progression. - Source: PubMed
Publication date: 2026/07/17
Buczyńska-Backiel AngelikaKościuszko MariaAdamska AgnieszkaSiewko KatarzynaDzięcioł JanuszSzelachowska MałgorzataPopławska-Kita AnnaKrętowski Adam Jacek - Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy associated with adverse maternal and fetal outcomes. Nevertheless, the molecular mechanism of placental dysfunction in GDM are still not clear, especially the role of ferroptosis and its interplay with oxidative stress, inflammation, and angiogenesis. - Source: PubMed
Monisha SMilan K LAnuradha MRamkumar K M - The current study examines the role of testosterone and androgen deprivation in regulating mitochondrial quality control, autophagy, and apoptosis during CCl-induced chronic liver injury. Male rats were allocated to Sham, CCl, TP + CCl (testosterone-treated), and Cas + CCl (castrated) groups for 4, 8, and 12 weeks, validated through in vitro assays. Mitochondrial function (MitoTracker, MFN2), lysosomal integrity (LAMP1), autophagy markers (LC3B, Beclin-1, p62/SQSTM1), apoptosis regulators (Bcl-2, cleaved caspase-3), and mTOR signaling were assessed by qRT-PCR, immunohistochemistry, and immunofluorescence. CCl exposure caused progressive increases in cellular stress and fibrotic markers (α-SMA, TGF-β1, and TXNIP), progressive mitochondrial dysfunction, impaired mitochondrial-lysosomal coordination, reduced Beclin-1 and LC3B, p62 accumulation, and a shift toward an anti-apoptotic Bcl-2 imbalance. Testosterone treatment restored mitochondrial membrane potential in vitro, normalized MitoTracker and MFN2 expression, preserved LAMP1 levels, and partially sustained mitochondrial-lysosomal coupling. TP also enhanced Beclin-1 and LC3B, reduced p62 accumulation, and sustained mTOR activity, consistent with improved autophagic flux. Moreover, TP-lowered Bcl-2 was associated with controlled cleaved caspase-3 activation, suggesting selective clearance of damaged hepatocytes rather than widespread apoptosis. In contrast, Cas + CCl animals showed exaggerated mitochondrial impairment, persistent p62 accumulation, reduced LC3B and mTOR signaling, and a pro-apoptotic cleaved caspase-3 profile. Together, these findings demonstrate that testosterone supports mitochondrial-lysosomal homeostasis and autophagy during toxic liver injury, whereas androgen deprivation favors defective autophagy and maladaptive apoptosis, underscoring hormone-dependent regulation of hepatocellular stress responses. - Source: PubMed
Publication date: 2026/07/16
Verma ShobhitVaishnav SomyaYadav ManishaVerma SmritiWashimkar Kaveri RKumar AkhileshMugale Madhav Nilakhanth - Septic cardiomyopathy is cardiac dysfunction caused by sepsis and is a common consequence of sepsis. Clinical studies have found patients with sepsis syndrome commonly have low serum selenium (Se) levels, and Se supplementation at doses higher than the daily requirement may reduce mortality; however, the underlying mechanism remains unclear. We found that downregulation of thioredoxin-2 (TXN2)-induced mitochondrial reactive oxygen species (mtROS), which increased inflammatory and oxidative injury in cardiomyocytes, might be a major contributor to septic cardiomyopathy. Mitoquinone mesylate (MitoQ), an antioxidant specifically targeted to mitochondria, increased TXN2 expression and decreased mtROS, thioredoxin-interacting protein (TXNIP, a negative regulator of TXN), nucleotide-binding oligomerization domain (NOD)-like receptor protein-3 (NLRP3) inflammasome activation, and ferroptosis. The results suggest that the TXN2-ferroptosis-NLRP3 pathway may represent a therapeutic target for sepsis-induced cardiac injury. In addition, we found that Se supplementation improved cardiac function and relieved mtROS accumulation and ferroptosis in sepsis-associated cardiac injury by regulating TXN2 and TXNIP/NLRP3 expression. - Source: PubMed
Publication date: 2026/07/01
Zhang LeiZhu DandanYu Jian