Ask about this productRelated genes to: DPYSL3 Blocking Peptide
- Gene:
- DPYSL3 NIH gene
- Name:
- dihydropyrimidinase like 3
- Previous symbol:
- -
- Synonyms:
- DRP-3, ULIP, CRMP4
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-27
- Date modifiied:
- 2015-11-25
Related products to: DPYSL3 Blocking Peptide
Related articles to: DPYSL3 Blocking Peptide
- Focused ultrasound (FUS) and microbubbles can transiently increase blood brain barrier (BBB) permeability, yet BBB opening (BBBO) verification relies mainly on contrast-enhanced MRI, offering limited insight into the molecular consequences of barrier modulation. Sonobiopsy, which uses FUS induced BBBO to release brain derived molecules into the bloodstream, provides a molecular readout from blood samples. Nanobubbles (NBs) are smaller agents that circulate more effectively in the brain microvasculature and have shown enhanced BBBO in capillaries. Here, we establish NB-based sonobiopsy as a platform for enhanced biomarker efflux and molecular sensitivity, and apply it to define the proteomic signature of BBBO in healthy and glioblastoma (GBM) models. Plasma collected before and after NB-mediated FUS underwent data-independent acquisition-based mass spectrometry, revealing post-BBBO changes in healthy and tumor bearing mice. In healthy cohorts, 77 proteins were reproducibly altered after BBBO. Six proteins (Dpysl3, Myl1, Mybpc1, Vsig4, Krt33a, Krtap6-5) were detectable only after BBBO in healthy mice. In 005 glioma bearing mice, the BBBO signature identified in healthy animals was preserved with clear pre- vs post-BBBO separation. Candidate BBBO-associated proteins identified in the NB cohort were subsequently evaluated in an MB cohort, where the pre-to-post BBBO changes observed with NBs were not reproduced. These findings establish NB-mediated proteomic sonobiopsy as a promising method for BBBO verification across healthy and disease-relevant conditions and support the development of scalable molecular readouts for BBBO confirmation. This platform may also complement disease-focused sonobiopsy approaches, including protein-based biomarker studies in neuro-oncology. - Source: PubMed
Publication date: 2026/05/02
Gattegno RoniSher DivshaBismuth MikeZohar OrMoskov KerenKabaha SinaFriedmann-Morvinski DinorahIlovitsh Tali - Bladder cancer (BC) is a prevalent malignant tumor worldwide, posing a significant public health burden and challenge to human society. Current therapeutic modalities for BC include surgical treatment, radiotherapy, chemotherapy, targeted therapy, and immunosuppressive therapy. However, almost all patients experience disease progression and ultimately succumb to BC. Our study demonstrated that elevated expression of Heat Shock Protein Beta-6 (HSPB6) correlated with higher clinical grades and stages, establishing it as an independent prognostic risk factor for BC. Enrichment analysis indicated that HSPB6 is associated with the extracellular matrix in BC. Experimental validation revealed that HSPB6 overexpression inhibits the proliferation of BC cell line T24. This effect may be achieved by inhibiting the PI3K/Akt signaling pathway, which in turn leads to inhibition of epithelial-mesenchymal transition (EMT). Furthermore, we developed a prognostic risk model that incorporated DDR2, DPYSL3, MFAP5, PDGFRB, and SPOCD1, allowing accurate prediction of patient outcomes based on immunological status. In conclusion, this study highlights that HSPB6 overexpression can restrain the proliferation of BC cells and inhibit EMT, underscoring its potential as a diagnostic marker and therapeutic target in BC. - Source: PubMed
Publication date: 2026/04/20
Wang Jian-SheQiu Yi-FanZhang LuJi BoLiang SenWang Ya-XuanZhu Hai-Xia - 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 - Neurons in the central nervous system (CNS) display a high capacity for axon growth during early development but lose this ability at a pivotal differentiation stage marked by synaptic maturation, circuit integration, and a profound shift in gene transcription. Once mature, most CNS neurons fail to reverse this transcriptional switch after axon injury, fundamentally constraining their intrinsic capacity for axon regeneration. Here, we show with single-nucleus RNA sequencing that forced expression of the transcription factor Sox11 in mature corticospinal tract (CST) neurons produces large-scale and stable changes in gene expression that are highly enriched for growth-relevant processes, and which strongly resemble those of pre-synaptic embryonic stages. Moreover, Sox11 is equally effective when delivered to chronically injured CST neurons. These data reveal Sox11's ability to reverse a critical step of neuronal maturation even in otherwise unperturbed neurons, clarifying the transcriptional underpinnings and highlighting Sox11 as a potent regulator of pro-regenerative gene networks. - Source: PubMed
Publication date: 2025/12/23
Batsel ElizabethWang ZimeiOtten ElizabethRoshan SyedMohammad RabiaPascual PaulaO'Shea DarbyRosas JoseTsoulfas PantelisBlackmore Murray G - Neurons in the central nervous system (CNS) display a high capacity for axon growth during early development but lose this ability at a pivotal differentiation stage marked by synaptic maturation, circuit integration, and a profound shift in gene transcription. Once mature, most CNS neurons fail to reverse this transcriptional switch after axon injury, fundamentally constraining their intrinsic capacity for axon regeneration. Here, we show with single-nucleus RNA sequencing that forced expression of the transcription factor Sox11 in mature corticospinal tract (CST) neurons produces large-scale and stable changes in gene expression that are highly enriched for growth-relevant processes, and which strongly resemble those of pre-synaptic embryonic stages. Moreover, Sox11 is equally effective when delivered to chronically injured CST neurons. These data reveal the ability of Sox11 to reverse a critical step of neuronal maturation even in otherwise unperturbed neurons, clarifying the transcriptional underpinnings and highlighting the potential of Sox11 to act as a pro-regenerative stimulus. - Source: PubMed
Publication date: 2025/09/30
Batsel ElizabethWang ZimeiOtten ElizabethMohammad RabiaPascual PaulaO'Shea DarbyRosas JoseTsoulfas PantelisBlackmore Murray G