Mouse dihydropyrimidinase-like 2,DPYSL2 ELISA Kit
- Known as:
- Mouse dihydropyrimidinase-like 2,DPYSL2 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0949Mo
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Sunlog
- Gene target:
- Mouse dihydropyrimidinase-like 2 DPYSL2 ELISA Kit
Related genes to: Mouse dihydropyrimidinase-like 2,DPYSL2 ELISA Kit
- Gene:
- DPYSL2 NIH gene
- Name:
- dihydropyrimidinase like 2
- Previous symbol:
- -
- Synonyms:
- DRP-2, DHPRP2, CRMP2, DRP2
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-27
- Date modifiied:
- 2016-10-05
Related products to: Mouse dihydropyrimidinase-like 2,DPYSL2 ELISA Kit
Related articles to: Mouse dihydropyrimidinase-like 2,DPYSL2 ELISA Kit
- Ubiquitination regulation is essential for maintaining protein homeostasis. Dysregulated ubiquitination is increasingly recognized to participate in malignant progression. Fbxw11, a substrate-recognition subunit of SCF-type E3 ligases, is involved in tumorigenesis and progression. However, its role and molecular mechanism in acute myeloid leukemia (AML) have not been elucidated. Here we demonstrat that lower levels of Fbxw11 were detected in AML patients and correlated with worse prognosis. Furthermore, overexpression of Fbxw11 delayed AML progression by reducing leukemia stem cell (LSC) frequency and inhibiting leukemia cell migration. Mechanistically, quantitative proteomics combined with co-immunoprecipitation and ubiquitination assays identified dihydropyrimidinase-like 2 (Dpysl2) as a direct substrate of Fbxw11, leading to its poly-ubiquitylation and proteasomal degradation. Moreover, overexpression of Dpysl2 reversed the effects of Fbxw11 on LSC levels and migration of AML cells as well as accelerated AML progression in vivo. In addition, inhibition of Dpysl2 with lacosamide, an FDA-approved antiepileptic drug, phenocopied Fbxw11 restoration and delayed AML progression. Lacosamide combined with cytarabine further prolonged the survival of AML mice. Our results suggest Fbxw11 as an intrinsic suppressor in AML progression by regulating the ubiquitination and degradation of Dpysl2, providing new insights into ubiquitination regulation and highlighting the potential of targeting the Fbxw11-Dpysl2 axis as a therapeutic strategy for AML. - Source: PubMed
Publication date: 2026/08/12
Wang LinaLi YifeiXie WanzhenLi RuiyunCui XiaoxiZhang SiqiRen QianZheng Guoguang - Erythromelalgia is a descriptive term for burning pain and erythema in distal extremities, often worsened by heat and improved by cold. Inherited erythromelalgia has been primarily linked to gain-of-function variants in , encoding voltage-gated sodium channel NaV1.7. However, approximately 65% to 85% of patients with erythromelalgia do not have pathogenic variants. - Source: PubMed
Publication date: 2026/08/03
Yonas Matthew COcay Don DanielGenetti Casie ALobo KimberlyFernandes MelissaGroussis NicoleHalpin MeghanWilder Robert TYu Timothy WBerde Charles BBrownstein Catherine A - Rapidly progressive Alzheimer's disease (rpAD) is a rare subtype with rapid decline, but its molecular underpinnings remain poorly defined. Here, brain-derived tau oligomers (TauO) were systematically compared across nondemented controls, slowly progressive AD (spAD), and rpAD to test whether subtype-specific TauO signatures align with clinical aggressiveness. TauO were immunoprecipitated from frontal cortex using T22 antibody and characterized by Western blotting, transmission electron microscopy, label-free quantitative proteomics, and SH-SY5Y toxicity assays, complemented by longitudinal analysis of tau phosphorylation in inoculated 3xTg AD mice. T22-positive high-molecular-weight TauO were successfully enriched from all groups, where rpAD TauO exhibited compact, densely packed oligomers under TEM and the highest phosphorylation at pS396 and pS422, exceeding both spAD and controls (p ≤ 0.0327). In 3xTg mice, pS396 showed an early increase followed by a late decline, consistent with dynamic shifts in tau solubility during disease evolution. Brain-derived TauO from spAD and rpAD, but not recombinant tau monomers or control-derived TauO, significantly reduced SH-SY5Y cell viability. Proteomic profiling identified 2388 TauO-associated proteins, including a shared 556-protein core and a striking expansion of rpAD-unique interactors (n = 1101). In controls and spAD, the core TauO interactome was enriched for translation, proteostasis, mitochondrial respiration, and vesicle-trafficking pathways, whereas these modules were absent in rpAD. Instead, rpAD TauO showed selective enrichment of aldehyde detoxification, amino-acid and carbon metabolism, and actin-regulatory modules, alongside increased association of SERPINA1, ALDH9A1, MAPRE3, DPYSL2, DPYSL3, and NFASC and reduced coupling to mitochondrial (MRPL17) and complement (C9) components. These convergent structural, post-translational, toxic, and interactome changes indicate that rpAD is defined by a biochemically distinct TauO species embedded in a metabolic and cytoskeleton-focused network, providing a mechanistic framework for its aggressive clinical course and a basis for subtype-specific biomarker and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/18
Saleem TayyabaMöbius WiebkeSchmitz Matthiasda Silva Correia AngelaThomas CarolinaCanaslan SezgiHermann PeterGöbel StefanZafar SaimaRoot ElisabethStadelmann ChristineAndreoletti OlivierHoppert MichaelFleming Outeiro TiagoFerrer IsidreYounas NeelamZerr Inga - Rupture of an intracranial aneurysm (IA) can result in aneurysmal subarachnoid hemorrhage (ASAH), a severe and often fatal form of stroke. The configuration of the intracranial arteries - collectively known as the circle of Willis (CoW) - influences the risk of IA development and rupture. Although CoW variation is known to be heritable, its genetic underpinnings and contribution to IA remain poorly understood. Here, we aimed to investigate the genetic architecture of CoW variation and its potential link with IA. Using a semi-automated detection tool, we characterized the diameters, bifurcation angles, and presence of arterial segments of the CoW in 1078 participants from a population-based cohort and 682 IA patients. Composite traits capturing variation in all CoW characteristics were generated through principal component analysis. We conducted a genome-wide association study (GWAS) on these composite traits and identified four loci with suggestively significant associations. Lead single-nucleotide polymorphisms (SNPs) were located in or near the genes DPYSL2, CSMD3, TRPC6, and PKD1L2. Notably, PKD1L2 is closely related to PKD1, a gene implicated in autosomal dominant polycystic kidney disease, a connective tissue disorder that increases IA susceptibility. We observed statistically significant SNP-based heritability for the second principal component of CoW variation (heritability estimate = 0.95, standard error = 0.25). All lead SNPs demonstrated nominal association (p < 0.05) with multiple CoW characteristics and other vascular traits. Our findings highlight a substantial genetic contribution to CoW morphology and offer new insights into the molecular mechanisms underlying CoW variation and its role in IA pathogenesis. - Source: PubMed
Publication date: 2026/03/13
Bakker Mark KGroenheide Phebe JVos Iris NLin Qi ChangNanninga Marloes H AGuzu AlinaPaic BarbaraVerhoeff Tessa ABekema ErwinTeumer AlexanderBülow RobinVölker UweVölzke HenryGrabe Hans JKuijf Hugo JVelthuis Birgitta KVeldink Jan HRuigrok Ynte M - The prevalence of atrial fibrillation (AF) is increasing due to the aging population. Mitophagy is crucial for maintaining cardiomyocyte function, while ion channels play a key role in cardiac electrical activity. Dysfunction of ion channels can trigger AF. However, the role of mitophagy-related ion channel genes in AF remains unclear. - Source: PubMed
Publication date: 2025/11/20
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