Disease relevance of Nptx1

• In primary cortical neurons, NP1 protein was induced >2.5-fold (p < 0.001) after their exposure to hypoxia that caused approximately 30-40% neuronal death [1].
• Pregnancy increased (p < 0.01) food intake, body weight, weight gain, and food efficiency ratio (P2 vs NP2 and P1 vs NP1, respectively), but the treatment of oil included in the diets did not alter these parameters [2].

High impact information on Nptx1

• We have named this protein neuronal pentraxin (NP), as Northern analysis and in situ hybridization demonstrate high message levels in neurons of cerebellum, hippocampus, and cerebral cortex [3].
• Neuronal pentraxin, a secreted protein with homology to acute phase proteins of the immune system [3].
• These results indicate that NP1 is part of the gene expression program of apoptotic cell death activated by nondepolarizing culture conditions in cerebellar granule cells [4].
• This cDNA was homologous to the 3' mRNA end of neuronal pentraxin 1 (NP1), a gene encoding a secreted glycoprotein whose expression is restricted to the nervous system [4].
• Furthermore, acute treatment with lithium significantly inhibited both overexpression of NP1 and cell death evoked by low potassium [4].

Biological context of Nptx1

• Time-course studies indicated that overexpression of NP1 protein reaches a maximum after 4 h of exposure to potassium deprivation and 4 h before significant cell death [4].
• Our hypothesis is that an incomplete DNA hydrolysis to nucleosides by the conventional nuclease P1 (NP1) and alkaline phosphatase (AP) digestion system plays an important role in contributing to the variability of measurements using HPLC coupled with UV and electrochemical (EC) detection [5].
• Inhibiting the phosphorylation of the p38 mitogen-activated protein kinase without modifying JNK, neither diminishes cell death nor inhibits NP1 overexpression in nondepolarizing conditions [6].
• This novel protein, NPCD (Neuronal Pentraxin with Chromo Domain), has multiple cytoplasmic isoforms generated by alternative splicing that are selectively expressed in neurons [7].
• These cytoplasmic NPCD isoforms are composed of a neuronal pentraxin domain (formerly thought exclusively extracellular) linked to a chromo domain (formerly thought exclusively nuclear); this protein motif organization is unprecedented [7].

Anatomical context of Nptx1

• Immunofluorescence analyses revealed elevated neuronal expression of NP1 in the ipsilateral cerebral cortex from 6 hr to 7 d and in the hippocampal CA1 and CA3 regions from 24 hr to 7 d after HI [1].
• RT-PCR, western and immunocytochemical analyses revealed that oligodendrocytes expressed NP1, several alternatively spliced isoforms of NP2, and a broad spectrum of both soluble (Class 3), membrane-spanning (Class 4-6), and membrane-tethered (Class 7) semaphorin ligands [8].

Associations of Nptx1 with chemical compounds

• Our results show that NP1 induction mediates hypoxic-ischemic injury probably by interacting with and modulating GluR1 and potentially other excitatory glutamate receptors [1].
• Subsequently, DNA was analysed by nuclease P1 (NP1) or butanol-enriched 32P-postlabeling [9].
• DNA obtained from the liver of rats fed IQ was 32P-labeled by the standard method and the 32P-labeled nucleotides obtained were incubated with PNK and NP1 to remove 3'-phosphate groups and then digested with PDEI [10].

Other interactions of Nptx1

• Transfecting cortical neurons with antisense oligodeoxyribonucleotides directed against NP1 mRNA (NP1AS) significantly inhibited (p < 0.01) hypoxia-induced NP1 protein induction and neuronal death (p < 0.001), demonstrating a specific requirement of NP1 in hypoxic neuronal injury [1].
• Selective expression of Narp, a secreted neuronal pentraxin, in orexin neurons [11].
• Neuronal pentraxin receptor, a novel putative integral membrane pentraxin that interacts with neuronal pentraxin 1 and 2 and taipoxin-associated calcium-binding protein 49 [12].
• In this study, we demonstrate that orexin neurons display robust expression of neuronal activity-regulated pentraxin (Narp), a secreted neuronal pentraxin, implicated in regulating clustering of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors [11].

Analytical, diagnostic and therapeutic context of Nptx1

• Reverse-Northern and Northern blot analyses confirmed that treatment with low potassium induces overexpression of NP1 mRNA, with a subsequent increase in NP1 protein levels [4].

References