Dag1 Blocking Peptide, Blocking Peptides
- Known as:
- Dag1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-7277
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- Dag1 Blocking Peptide Peptides
Related genes to: Dag1 Blocking Peptide, Blocking Peptides
- Gene:
- DAG1 NIH gene
- Name:
- dystroglycan 1
- Previous symbol:
- -
- Synonyms:
- A3a, 156DAG, AGRNR, DAG
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-22
- Date modifiied:
- 2019-04-23
Related products to: Dag1 Blocking Peptide, Blocking Peptides
Related articles to: Dag1 Blocking Peptide, Blocking Peptides
- Unexplained recurrent spontaneous abortion (URSA) accounts for approximately 50% of all recurrent spontaneous abortion cases, severely endangering the physical and mental health of women of childbearing age. Yang-Xue-An-Tai Decoction (YXAT), a traditional Chinese medicine (TCM) in-hospital preparation, has been clinically effective and safe for URSA treatment for over 30 years, but its underlying mechanism remains unclear. - Source: PubMed
Publication date: 2026/06/27
Li GuanshanHu LinlanTang JiaxinZhao XinXu ShuaiYang BinHe XianXu ZijingWang JiaboLu YawenHe Junqin - The dystrophin-glycoprotein complex (DGC) provides structural integrity to the sarcolemma, and disruption of the DGC leads to muscular dystrophy. A core member of the DGC is dystroglycan (DG), which binds to extracellular ligands via α-DG and intracellular cytoskeleton via β-DG. Mutations in or genes involved in the posttranslational processing of DG lead to a subset of neuromuscular diseases referred to as dystroglycanopathies. The importance of the α-DG extracellular interactions is well established; however, little is known about the significance of the β-DG intracellular interactions. Here, we investigate the importance of intracellular β-DG in neuromuscular health. Using a mouse that lacks a large intracellular region of β-DG (residues 777 to 893), we show that the deletion of cytoplasmic β-DG leads to skeletal muscle pathology accompanied by postsynaptic disruption. Our data show that within the specialized neuromuscular junction (NMJ), cytoplasmic β-DG is necessary for the localization of utrophin and rapsyn, and clustering of acetylcholine receptors. Moreover, we provide evidence that the postsynaptic abnormalities contribute to neuromuscular dysfunction in mice lacking the cytoplasmic region of β-DG. Further, using a mouse model that only lacks the C-terminal tail (residues 879 to 893) of β-DG, we demonstrate that skeletal muscle and NMJ health rely on β-DG residues 777 to 878. Together, our mouse models suggest that deletion of the cytodomain of β-DG surprisingly results in very severe neuromuscular pathophysiology in mice. Our results identify β-DG as a critical player in shaping and maintaining neuromuscular synapse architecture in vivo, thus further defining the molecular mechanisms underlying neuromuscular health. - Source: PubMed
Publication date: 2026/06/03
Hord Jeffrey MTurk RolfKusano HajimeRader Erik PBurns SarahGastel ZeitaProuty Sally JYu LipingBurden Steven JCampbell Kevin P - Impaired glymphatic clearance has been implicated in Alzheimer's disease (AD) through reduced clearance of amyloid-β (Aβ) and other metabolites from the brain. Mislocalisation of aquaporin-4 (AQP4), a water channel protein anchored to astrocytic endfeet by the dystrophin-associated complex (DAC), has been linked to increased Aβ accumulation, neurodegeneration and cognitive impairment. In animal models, genetic ablation of DAC subunits, leading to AQP4 mislocalisation, increases Aβ accumulation. Genetic variation in has been examined in the context of AD, but variation in key DAC genes has not been systematically investigated in humans. This study examined whether variation within glymphatic pathway genes is associated with AD-related phenotypes in individuals on the AD trajectory. - Source: PubMed
Publication date: 2026/05/06
Armstrong Ayeisha MilliganO'Brien Eleanor KFernandez Shane MDoré VincentBourgeat PierrickShishegar RositaMaruff PaulRowe Christopher CVillemagne Victor L Porter TenielleLaws Simon M - Multisite chronic pain (MCP) is a complex and increasingly prevalent health issue that significantly impairs quality of life. This study aims to identify potential therapeutic targets for MCP through a proteome-wide Mendelian randomization (MR) approach. We conducted a proteome-wide MR to explore the causal associations of plasma proteins with MCP. MCP used data from a genome-wide association study including 387,649 samples. We used protein data from UKB-PPP including 54,219 samples as the discovery analysis, and from Finngen as the replication analysis. Multiple follow-up analyses were used to investigate the potential function of the candidate proteins. Finally, druggability evaluation and phenome-wide MR analysis were used to assess the priority of these targets. We identified 11 plasma proteins significantly associated with MCP. Increased levels of LRP11, BCHE, DAG1, and SUOX exhibited protective effects, while LATS1, CEP170, SLC27A4, HEXIM1, ECM1, C8B, and MST1 increased MCP risk. After multiple validations, ECM1, C8B, LRP11, BCHE has the strongest convincing evidence. Besides, mediation analysis found 4 reliable combinations, revealed the role of plasma proteins in traits influencing MCP. Finally, druggability evaluation and phenome-wide MR indicated that C8B, and BCHE had the highest priority. - Source: PubMed
Gao JunLiu JiaHao - Environmental pollutant exposure has been associated with chronic kidney disease (CKD), yet specific chemicals related to renal function variation remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/13
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