SCTR_MOUSE Sctr ELISA tesk kit
- Known as:
- SCTR_MOUSE Sctr Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen14723
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- SCTR_MOUSE Sctr ELISA tesk kit
Related genes to: SCTR_MOUSE Sctr ELISA tesk kit
- Gene:
- SCTR NIH gene
- Name:
- secretin receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-27
- Date modifiied:
- 2016-10-05
Related products to: SCTR_MOUSE Sctr ELISA tesk kit
Related articles to: SCTR_MOUSE Sctr ELISA tesk kit
- After guideline-recommended dual antiplatelet therapy (DAPT) following percutaneous coronary intervention (PCI), long-term antiplatelet monotherapy is advised, but the optimal agent in real-world practice remains uncertain. - Source: PubMed
Publication date: 2026/06/10
Cho Jun HwanChan You SengKim HoseobKim MinaJo JinhwanLee Sang-YeubKim Sang-WookSibbing DirkGorog Diana AAngiolillo Dominick JKubica JacekTantry Udaya SGurbel Paul AJeong Young-Hoon - Methamphetamine (METH) is highly addictive and causes severe public health burdens and social harm. Secretin (SCT), secreted by S cells of the duodenum and jejunum, exerts multiple biological functions in the central nervous system. Nevertheless, the role and neural mechanism of the secretin/secretin receptor (SCT/SCTR) axis in METH addiction remain largely unclear. Here, we investigated the effects of the SCT/SCTR pathway on METH-induced conditioned place preference (CPP), neuronal activity, and associated molecular alterations. Our results demonstrated that SCT expression in plasma and colon was significantly decreased in METH-addicted mice. Both intraperitoneal SCT injection and colon-specific SCT overexpression effectively alleviated METH-evoked CPP. SCTR was abundantly expressed in glutamatergic neurons of the hippocampal dentate gyrus (DG) and markedly downregulated upon METH exposure. DG-specific SCTR knockdown exacerbated addiction-like behaviors, while SCTR overexpression mitigated these deficits. METH activated DG glutamatergic neurons, and SCT/SCTR modulation substantially reversed such neuronal hyperactivity. SCTR overexpression suppressed DG neuronal excitability and glutamate levels, and SCTR knockdown abolished the protective effect of SCT. Moreover, activation of DG glutamatergic neurons abrogated the inhibitory action of SCTR overexpression on METH-induced CPP. RNA-seq further identified differentially expressed molecules associated with immune response and cytokine production following SCTR overexpression. Collectively, the SCT/SCTR pathway represents a promising novel therapeutic target for METH addiction. - Source: PubMed
Publication date: 2026/05/15
Chu ZhixiangFan XiaoshuoDu LinCao YifanLiu JingMeng FantaoZhao DiWang WentaoZhang MengdiWang DanLi ChenJiang Shujun - SARS-CoV-2 has been responsible for a worldwide public health crisis and a pandemic that began in February 2020, with approximately 679 million cases and over 6.7 million deaths to date. Despite the existence of approved COVID-19 vaccines, these vaccines are either based on mRNA technology or viral vectors. Imam Abdulrahman Bin Faisal University (IAU) has developed a thermally stable plasmid DNA (pDNA)-based vaccine candidate using a platform approach that enables the rapid development of vaccines against emerging viral diseases. The pDNA vaccine developed by IAU encodes the full-length, optimized version of the SARS-CoV-2 Spike protein. Key advantages of this pDNA vaccine are that it is cost-effective, thermally stable, and can be used to administer multiple immunizations without incurring anti-vector responses, making it a promising candidate as a vaccine booster dose. - Source: PubMed
Publication date: 2026/04/15
Almansour-Alzamil Iman - Human milk contains multiple bioactive components, many of which are influenced by the mother's nutritional status. To identify the impact of maternal vitamin D status on neuroactive compounds, we conducted a post hoc analysis of breast milk and matched infant stool samples from mothers categorized as sufficient or deficient for vitamin D. Neuroactive metabolites were quantified using both targeted and nontargeted liquid chromatography with tandem mass spectrometry (LC-MS/MS). Our findings revealed that breast milk from mothers with sufficient vitamin D levels contained significantly higher concentrations of tryptophan, phenylalanine, and tyrosine compared to milk from mothers with lower vitamin D levels. No significant differences were observed in tryptamine, kynurenine, kynurenic acid, anthranilic acid, quinolinic acid, tyramine, dopamine, epinephrine, or norepinephrine between the two groups. Among SCFAs and other acids, only hexanoic acid was significantly elevated in the breast milk of mothers with sufficient vitamin D. A nontargeted metabolomics analysis of infant stool identified distinct metabolite profiles, where oleamide, vaccenic acid, lacto-N-triaose, and N-acetyl-D-glucosamine varied according to maternal vitamin D levels, indicating that maternal nutrient status may influence the infant gut metabolome. These findings suggest that maternal vitamin D status is associated with neurotransmitter precursor levels in breast milk and a distinct metabolomic profile of infant stool. - Source: PubMed
Gutierrez Alyssa SChetta Katherine EThapa SantoshHaidacher Sigmund JHoch Kathleen MBaatz John EHaag Anthony MOezguen NumanHorvath Thomas DWagner Carol LEngevik Melinda A - Cardiac Ca release channels, type-2 ryanodine receptors (RyR2s), play a pivotal role in cardiac muscle contraction by releasing Ca from the sarcoplasmic reticulum. Over 200 missense mutations in humans have been reported to be associated with cardiac diseases. Here, we characterize three RyR2 variants, Q3925E, W4646R, and Q4937K. Q3925E and W4646R mutations are in the Ca- and caffeine-binding sites, respectively. Our molecular dynamics simulations predicted that the Q4937 residue in the carboxyl terminal domain forms a hydrogen bond with the central domain where the Ca-binding site is located. Three mutant RyR2s were expressed in heterologous cells, and activities of the recombinant mutant RyR2 channels were determined by [H]ryanodine binding methods. As expected, Q3925E greatly reduced Ca-dependent activation and W4646R abolished caffeine activation. Our novel finding is that Q3925E increased inhibitory effects by divalent cations, Ca and Mg, resulting in a strong loss-of-function phenotype. Both W4646R and Q4937K increased affinities for Ca activation, and reduced or unchanged Ca inhibitions, exhibiting typical gain-of-function phenotypes. Caffeine failed to activate the Q3925E mutant at resting Ca but restored its activation at ∼20 µM Ca, where the Q3925E mutant is in the subactivated state. Computational analysis of the mutated structures suggested that the Q3925E mutation does not reduce Ca binding to its site but rearranges domain interface between the central domain involving Ca-binding site and carboxyl terminal domain, which directly interacts with the channel pore. Thus, it is possible that the Q3925E-RyR2 mutation alters signal transmission between activating Ca binding and pore opening. Q3925E in RyR2 is a part of Ca-binding site and is known to associate with cardiac sudden death. Our functional and structural modeling data suggested that the Q3925E mutation does not reduce Ca binding but alter a domain interaction, causing an impaired Ca activation of RyR2. We also found that the Q3925E mutation increases channel inhibition by Mg and Ca, resulting in a strong loss-of-function phenotype. - Source: PubMed
Publication date: 2026/02/25
Chirasani Venkat RPatwardhan AkankshaYamaguchi Naohiro