Ask about this productRelated genes to: Nptx1 Blocking Peptide
- Gene:
- NPTX1 NIH gene
- Name:
- neuronal pentraxin 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-12
- Date modifiied:
- 2019-04-16
Related products to: Nptx1 Blocking Peptide
Related articles to: Nptx1 Blocking Peptide
- Recent studies have shown that UFMylation plays an important role in cancer, but its specific function in gastric cancer (GC) remains to be fully elucidated. This study aimed to develop a prognostic signature based on UFMylation-related genes (URGs) for survival prediction in GC. - Source: PubMed
Publication date: 2026/07/27
Chen GuohaoGao XianDai LingchenDeng ShukangWang HaoyangHuang XinkunFeng Ying - Parkinson's disease (PD) is characterized by progressive degeneration of nigrostriatal dopamine neurons and synucleinopathy, which is the accumulation of aggregated α-synuclein (α-syn). Increasing evidence implicates α-syn-associated neuroinflammation as a contributor to PD pathogenesis, yet immune mechanisms linking synucleinopathy to neurodegeneration remain incompletely defined. Activation of the complement cascade occurs in PD and other synucleinopathies, but most studies report complement activation after overt neurodegeneration, making it difficult to conclude if complement is directly activated by pathological α-syn or secondarily following neurodegeneration. We used the rat α-syn preformed fibril (PFF) model, in vitro complement assays and postmortem human PD tissue to investigate whether pathological α-syn directly activates complement prior to overt neurodegeneration. The α-syn PFF model exhibits a protracted pathological time course and distinct temporal separation between peak α-syn aggregation and nigrostriatal degeneration. Thus, we quantified complement expression, activation, and regulation during the aggregation phase. Synucleinopathy caused complement activation prior to nigrostriatal degeneration, including upregulation of components of both the classical (C1qa, C1r, C4b) and alternative (Cfd, Cfb) pathways, the anaphylatoxin (C3aR, C5aR) and phagocytic (CR3) complement receptors, and activation of complement C3. During early synucleinopathy microglia upregulated C3, which significantly correlated with synucleinopathy burden across several brain regions, including the substantia nigra pars compacta (SNc) and cortex. Concurrently, complement regulators, including Cd55, Cd59, neuronal pentraxin-1 (Nptx1), and the neuronal pentraxin receptor were downregulated in the synucleinopathy-affected SNc. Importantly, increased levels of C1q and iC3b along with downregulation of CD55 and NPTX1 protein were also observed in human postmortem PD SNc tissue, supporting the translational relevance of our findings. Mechanistically, we demonstrate that aggregated, but not monomeric, α-syn directly binds C1q and activates the complement cascade in a C1q-dependent manner. These data provide the first in vivo evidence that synucleinopathy triggers complement activation and dysregulation prior to neurodegeneration. - Source: PubMed
Publication date: 2026/07/20
Khan HinaGifford MaryKordbacheh ArashBury AsherPanoushek SpencerCole-Strauss AllysonKemp Christopher JLuk Kelvin CSteece-Collier KathyKuhn Nathan CKanaan Nicholas MSortwell Caryl EPatterson Joseph RBenskey Matthew J - Alzheimer's disease (AD) is characterized by progressive cognitive decline accompanied by synaptic dysfunction and neuronal loss. Dysregulation of specific microRNAs (miRNAs) has been increasingly implicated in AD pathogenesis, suggesting that miRNA-mediated regulatory pathways may represent important mechanisms underlying neuronal vulnerability. Here, we identified mmu-microRNA-204-5p (miR-204) as a critical regulator of neuronal survival that is markedly downregulated in the hippocampus of 5xFAD mice. Through integrated bioinformatics analysis and experimental validation, we established neuronal pentraxin-1 (NPTX1) as a direct post-transcriptional target of miR-204. In primary cultured neurons, exposure to Aβ₁₋₄₂ oligomer (oAβ) drove marked upregulation of NPTX1 and precipitated neuronal injury, manifested by aberrant reactive oxygen species (ROS) accumulation, collapse of mitochondrial membrane potential, diminished cell viability, and dendritic degeneration. Inhibition of miR-204 further exacerbated these pathological changes and engaged mitochondrial apoptotic signaling, as evidenced by Bax upregulation, cytochrome c release, and caspase-3 cleavage. Conversely, restoration of miR-204 expression or genetic knockdown of NPTX1 attenuated oxidative stress, preserved mitochondrial integrity, and restored neuronal survival. Collectively, our findings uncover a previously unrecognized miR-204-NPTX1 regulatory axis that governs mitochondrial integrity and apoptotic susceptibility in AD, highlighting miR-204 as a potential therapeutic target for AD and related oxidative stress-associated neurodegenerative disorders. - Source: PubMed
Publication date: 2026/06/23
Ha Tae-YoungLim Seung MinPark HyunjunChang Keun-A - Spinocerebellar ataxia (SCA)-50 is a recently reported rare subtype. We describe the first case of SCA-50 from the Indian subcontinent. A 22-year-old man presented with progressive cerebellar ataxia over 2 years, along with oculomotor abnormalities and imaging findings indicating mild cerebellar atrophy. Genetic testing revealed an NPTX1 gene mutation, which correlates with SCA-50. Its unique pathogenesis distinguishes it from other SCA subtypes. - Source: PubMed
Publication date: 2026/05/29
Taparia VijyetaChawla TanushreeGoyal ChanchalGoyal Vinay - The synaptic transmission of memory engrams is important for their roles in memory storage and retrieval, and can be regulated by multiple neuronal adhesion molecules. This study focuses on the roles of neuronal pentraxin (NPTX) family members (NPTX1 and NPTX2), which are biomarkers for cognitive decline, in the synaptic transmission of Fos-(F-RAM) and Npas4-(N-RAM)-dependent engrams formed during contextual fear conditioning in the dentate gyrus. - Source: PubMed
Publication date: 2026/05/13
Mao FeihuangYang YangJiang ZhuyingLe QiuminJin Tao