DAPK Forward PCR Primer (200bp position)
- Known as:
- DAPK Forward PCR test kit Primer (200bp position)
- Catalog number:
- MP1133
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- DAPK Forward PCR Primer (200bp position)
Related genes to: DAPK Forward PCR Primer (200bp position)
- Gene:
- DAPK1 NIH gene
- Name:
- death associated protein kinase 1
- Previous symbol:
- -
- Synonyms:
- DAPK, ROCO3
- Chromosome:
- 9q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-27
- Date modifiied:
- 2017-04-06
Related products to: DAPK Forward PCR Primer (200bp position)
Related articles to: DAPK Forward PCR Primer (200bp position)
- Vascular calcification (VC) is a life-threatening complication of chronic kidney disease (CKD) driven by vascular smooth muscle cell (VSMC) osteogenic transdifferentiation. Anoikis, a form of adhesion-dependent apoptosis, is involved in cardiovascular remodeling, yet its regulatory role in CKD-associated VC remains unexplored. - Source: PubMed
Publication date: 2026/08/24
Chen DandanDai TianzengYu WenfengXie Xi'naLi RuiWang Yan - The Alzheimer's Disease (AD) lacks effective disease-modifying therapy, even though amyloid-targeting immunotherapies have recently been applied clinically. N-methyl-D-Aspartate Receptors (NMDARs) play a central yet mechanistically complicated role in the pathophysiology of AD, where they are convergence points of amyloid-beta (Aβ) oligomer toxicity, tau-dependent excitotoxicity, and progressive synaptic failure. This critical review examines NMDAR dysfunction across the AD spectrum, with a focus on subunit-regulated signalling, subcellular localisation, and subsequent pathological cascades. The effects of Aβ oligomers on NMDAR activity involve multiple mechanisms that disrupt their function, including glutamate dysregulation mediated by GLT-1, redistribution of GluN2B to extrasynaptic areas, and inhibition of JAK2-CREB via activation of extrasynaptic receptors. Tau enhances excitotoxic injury throughdendritic mislocalization, and the tau-Fyn-GluN2B complex, which propels pro-death signalling by DAPK1. This conceptually important prevailing synaptic-extrasynaptic dichotomy is fiercely criticised here, given evidence that synaptic receptors containing GluN2A also mediate pathological signalling during sustained Aß exposure, and that tri-heteromeric receptor populations are problematic for subunit-selective targeting. Neuroinflammation, dysfunction of the blood-brain barrier, and excitotoxic amplification via GluN2C/D-enriched receptor pools in neurons, astrocytes, microglia, oligodendrocytes, and endothelial cells are underexplored therapeutic targets for neurodegenerative disease (non-neuronal NMDARs). Memantine is the only approved NMDAR-targeting agent for AD. Subunit-selective antagonists have not been translated into clinical use, and the positive allosteric modulator dalzanemdor (SAGE-718) did not pass its randomised Phase 2 trial in 2024. The most mechanistically justified approach is to advance subunit-selective, compartment-specific, or protein-complexdisrupting strategies. Although it is not established whether any single NMDAR-targeting intervention will suffice as a disease-modifying therapy, the convergence of molecular, genetic, and clinical evidence positions NMDAR dysfunction as a tractable , if therapeutically demanding , node in the AD pathogenic network, warranting continued, mechanism-informed drug discovery. - Source: PubMed
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Khan Md SirajuddinAshesh Astik ManjuMammen Mithul VAlhusaini AbdulrahmanJawaid TalhaAkhtar Md SayeedOrayj KhalidAnsari IsrarKumar DileepKumar Ajay - Integrated biomarkers for cross-sectional multidimensional assessment of Parkinson's disease (PD) remain limited. This study examined associations between serum DAPK1, a systemic molecular marker, and peripheral gastric myoelectrical activity assessed by electrogastrography (EGG) in PD. - Source: PubMed
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