Human uncoupling protein 3, UCP3 ELISA Kit
- Known as:
- Human uncoupling protein 3, UCP3 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-2174
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human uncoupling protein 3 UCP3 ELISA Kit
Related genes to: Human uncoupling protein 3, UCP3 ELISA Kit
- Gene:
- UCP3 NIH gene
- Name:
- uncoupling protein 3
- Previous symbol:
- -
- Synonyms:
- SLC25A9
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-11
- Date modifiied:
- 2016-04-28
Related products to: Human uncoupling protein 3, UCP3 ELISA Kit
Related articles to: Human uncoupling protein 3, UCP3 ELISA Kit
- Per- and polyfluoroalkyl substances (PFAS), persistent environmental chemicals known as "forever chemicals," demonstrate significant neurotoxic effects across the human lifespan. This review examines the evidence linking PFAS exposure to neurodevelopmental disorders and neurological dysfunction. Epidemiological studies have shown that prenatal PFAS exposure is associated with reduced intelligence quotient in children, increased attention-deficit/hyperactivity disorder and autism spectrum disorder, and impaired motor and cognitive development, with males exhibiting greater susceptibility. Animal studies have revealed that developmental PFAS exposure disrupts neural progenitor proliferation, neuronal migration, and synaptic formation by targeting key proteins (GAP-43 and BDNF) and genes (PPARγ and UCP3), resulting in behavioral abnormalities resembling neurodevelopmental disorders. In adults, PFAS cross the blood-brain barrier (BBB) and accumulate in brain tissue, disrupting calcium homeostasis via AMPA/NMDA receptors and causing neuronal hyperexcitability. PFAS also compromise synaptic plasticity, alter neurotransmitter systems (dopamine, acetylcholine, GABA, and serotonin), and increase levels of neurodegenerative markers (tau and amyloid precursor protein). PFAS neurotoxicity operates through multiple mechanisms: (1) neuroinflammation via astrocyte activation and pro-inflammatory cytokine release (TNF-α and IL-1β); (2) oxidative stress through mitochondrial dysfunction and reactive oxygen species generation; (3) BBB disruption by reducing tight junction proteins; and (4) endocrine disruption affecting thyroid hormone regulation. PFAS are potent neurotoxicants that interfere with brain development and function through interconnected pathways. Given their environmental persistence and bioaccumulation, minimizing human exposure during critical developmental periods is essential to protect neurological health. - Source: PubMed
Publication date: 2026/06/26
Ko Moon YiMin EuijunHyun Sung-AeKa Minhan - Thyroid hormones regulate cardiovascular functions and energy homeostasis including thermogenesis through binding to nuclear thyroid hormone receptors. The thyroid hormone analogue 3,3',5-triiodothyroacetic acid (TRIAC) has recently emerged as a therapeutic candidate for thyroid hormone transporter deficiencies (Allan-Herndon-Dudley Syndrome) or thyroid hormone resistance β. Although TRIAC shows promise for these conditions, a comprehensive characterization focussing on heart and body temperature regulation has not been systematically performed in mice. - Source: PubMed
Publication date: 2026/06/24
Herrmann BeateAdam LenaOelkrug RebeccaMittag Jens - White adipose tissue (WAT) browning enhances energy expenditure and represents a promising target for metabolic disease. Growth differentiation factor 11 (GDF-11), a circulating member of the TGF-β superfamily, has been implicated in metabolic regulation, but its role in adipose tissue plasticity remains unclear. This study investigated whether GDF-11 regulates WAT browning and the underlying mechanisms. - Source: PubMed
Publication date: 2026/06/16
Sagliocchi SerenaAcampora LuciaMiro CaterinaNappi AnnaritaRestolfer FedericaDentice MonicaCicatiello Annunziata Gaetana - Mitochondrial uncoupling proteins (UCPs) play central roles in vertebrate energy metabolism, with UCP1 specializing as a thermogenic effector in placental mammals. Comparative genomics demonstrated that UCP1, UCP2, and UCP3 originated prior to the emergence of endothermy, suggesting that their ancestral functions evolved in ectothermic vertebrates. Here, we investigated the genomic organization, conserved synteny, and mRNA expression of all three UCP paralogs and homoeologs in the allotetraploid amphibian Xenopus laevis. Comparative genome analyses revealed that all three UCP paralogs and their L and S homoeologs were retained following polyploidization, although local rearrangements were evident for neighboring genes at the UCP2/UCP3 locus. Quantitative expression analyses across adult frog tissues reveal pronounced tissue specificity, with predominant expression of UCP1 and UCP2 in kidney, UCP3 in muscle, and differences in UCP2 homoeolog expression levels. Together, these findings establish a framework for UCPs in an amphibian model organism, primarily linking them to energetically demanding tissues. - Source: PubMed
Publication date: 2026/06/15
Rollwitz ErikJastroch Martin - : Exploiting the metabolic properties of postbiotics is a novel strategy for managing metabolic disorders, including diabetes. Inactivated microorganisms, a major class of postbiotics, improve glycemic control in preclinical and clinical studies. Here, we examined whether heat-killed (HK) () exerts prophylactic or therapeutic anti-hyperglycemic effects in diabetic mice. : Diabetes was induced in male BALB/c mice by streptozotocin (STZ; 150 mg/kg) injection. HK (1 mg) was given orally (three prophylactic doses before STZ) or intradermally (six weekly therapeutic doses after STZ). We assessed glycemic parameters, serum -peptide/insulin (ELISA), and tissue protein expression (Western blot). : Neither route altered body weight or glucose homeostasis in non-diabetic mice. In STZ-diabetic mice, oral prophylactic treatment significantly attenuated hyperglycemia (39-60% reduction weeks 5-8 post-STZ) and showed a trend toward improved serum -peptide, but did not affect dysregulated expression of skeletal muscle (SM), hepatic, pancreatic and renal proteins involved in glucose transport (GLUT2, GLUT4, and SGLT2), glycolysis (α-LDH), mitochondrial uncoupling (UCP2 and UCP3), and antioxidant defense (CAT). Therapeutic intradermal administration significantly decreased blood glucose (~30% at week 5, ~40% at week 6) and modestly enhanced insulin secretion. Hepatic UCP2 and α-LDH and SM UCP3 protein levels were normalized toward non-diabetic levels, whereas hepatic GLUT2 and SM GLUT4 remained largely unchanged. These correlative findings suggest effects independent of insulin-dependent glucose transport, but do not demonstrate direct functional improvement in mitochondrial or redox status. : HK exerts partial anti-hyperglycemic effects in STZ-induced diabetic mice, but the associated protein changes require functional validation before its role as a postbiotic in β-cell dysfunction can be established. - Source: PubMed
Publication date: 2026/05/22
Ali AliHakam Hanin-KhaulaEter AlaaBazzi SamerChahine AmaniAkle CharlesBahr Georges MEchtay Karim S