Neuronal pentraxin with chromo domain (NPCD) is a novel class of protein expressed in multiple neuronal domains

2004 ◽  
Vol 481 (4) ◽  
pp. 391-402 ◽  
Author(s):  
Bo Chen ◽  
John L. Bixby
Keyword(s):  
Chromo Domain ◽  
Neuronal Pentraxin

scholarly journals Endothelial cells derived from patients with diabetic macular edema recapitulate clinical evaluations of anti-VEGF responsiveness through the Neuronal Pentraxin 2 pathway

2020 ◽  
Author(s):  
Ada Admin ◽  
Marta Vila Gonzalez ◽  
Magdalini Eleftheriadou ◽  
Sophia Kelaini ◽  
Hojjat Naderi-Meshkin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Vision Loss ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
First Year ◽  
Differential Outcomes ◽  
Anti Vegf ◽  
Neuronal Pentraxin

Diabetic macular edema (DME) remains a leading cause of vision loss worldwide. DME is commonly treated with intravitreal injections of vascular endothelial growth factor (VEGF) neutralising antibodies. Anti-VEGFs are effective but not all patients fully respond to them. Given their potential side effects, inconvenience and high cost, identifying who may not respond appropriately to anti-VEGFs and why is essential. <p>Herein, we determine first the response to anti-VEGFs in a cohort of DME patients using spectral-domain optical coherence tomography scans obtained throughout the first year of treatment. We found that in 28% of eyes full clearance of fluid occurred at any time during the first year (“full responders”); in 66% fluid cleared only partly (“partial responders”); in 6% fluid remained unchanged (“non-responders”). To understand this differential response, we generated induced pluripotent stem cells (iPS) from “full responders” and “non-responders” and from diabetic subjects with no DME and age-matched non-diabetic volunteers and differentiated them into endothelial cells (iPS-ECs). Monolayers of iPS-ECs derived from diabetics showed marked and prolonged increased permeability upon exposure to VEGF when compared with non-diabetic controls; the response was significantly exaggerated in iPS-ECs from “non-responders” when compared with “full responders”. Moreover, phosphorylation of key cellular proteins in response to VEGF, including VEGFR2, and gene expression profiles, such as Neuronal Pentraxin 2 (NPTX2) expression, differed between “full responders” and “non-responders”. </p> <p>In the current study, iPS were used to predict patient response to anti-VEGF and identify key mechanisms underpinning the differential outcomes observed in the clinic. This approach has identified NPTX2 as playing a significant role in patient-linked responses and has potential as a new therapeutic target for DME. </p>

scholarly journals Neuronal pentraxin II is highly upregulated in Parkinson’s disease and a novel component of Lewy bodies

2007 ◽  
Vol 115 (4) ◽  
pp. 471-478 ◽  
Author(s):  
Linda B. Moran ◽  
Lorraine Hickey ◽  
Gregory J. Michael ◽  
Maria Derkacs ◽  
Lynne M. Christian ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Lewy Bodies ◽  
Neuronal Pentraxin

scholarly journals As a downstream target of the AKT pathway, NPTX1 inhibits proliferation and promotes apoptosis in hepatocellular carcinoma

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Yue Zhao ◽  
Yaqi Yu ◽  
Wenxiu Zhao ◽  
Song You ◽  
Min Feng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Akt Pathway ◽  
Serine Threonine Kinase ◽  
Signaling Mechanism ◽  
Downstream Target ◽  
Clinicopathological Significance ◽  
Neuronal Pentraxin ◽  
Underlying Mechanisms ◽  
And Function ◽  
Hcc Cells

Abstract Hepatocellular carcinoma (HCC) is correlated with a poor prognosis and high mortality worldwide. Neuronal pentraxin 1 (NPTX1) has been reported to play an oncogenic role in several types of tumors. However, its expression and function in HCC is not yet fully understood. In the present study, we aimed to investigate the clinicopathological significance of NPTX1 in HCC and the underlying mechanisms. We observed that the expression of NPTX1 was decreased significantly in HCC and was associated with tumor size and metastasis in patients. Gain-of-function approaches revealed that NPTX1 suppressed the growth ability of HCC cells and contributed to mitochondria- related apoptosis. Furthermore, mechanistic investigations showed that the AKT (AKT serine/threonine kinase) pathway can regulate the effects of NPTX1 in HCC cells. After blocking the AKT pathway, the action of NPTX1 was greatly increased. In summary, we demonstrated that NPTX1 inhibited growth and promoted apoptosis in HCC via an AKT-mediated signaling mechanism. These findings indicate that NPTX1 is a potential clinical therapeutic target.

A gene signature of response to radiotherapy in patients with grade II-III oligodendrogliomas.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 2041-2041
Author(s):  
Elizabeth Moyal ◽  
Julia Gilhodes ◽  
Guillaume Peyraga ◽  
Emmanuelle Uro-Coste ◽  
Damien Pouessel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Risk Score ◽  
Metabotropic Glutamate Receptor ◽  
Expression Profiles ◽  
Progression Free Survival ◽  
Penalized Regression ◽  
Age At Diagnosis ◽  
Linear Predictor ◽  
Grade Ii ◽  
Neuronal Pentraxin

2041 Background: Grade II and III Oligodendroglioma associate mutations of isocitrate deshydrogenase 1 or 2 genes and the whole-arm chromosomal loss of 1p and 19q and have a better prognosis than other gliomas. However, even if the preferred treatment consists of a combination of radiotherapy (RT) and chemotherapy, some patients will less respond to this treatment and will relapse faster , in part because of an heterogeneity in the response to RT. In the aim to identify factors of response to RT, we analyzed clinical and molecular data of patients with grade II-III oligodendroglioma exclusively treated with RT in the POLA cohort. Methods: Gene expression profiles on Affymetrix expression arrays of patients from the POLA cohort with co-deleted 1p/19q grade II/II gliomas treated by exclusive RT were used to identify a gene expression set predictive of radiation sensitivity. The primary endpoint was the progression free survival (PFS), defined as the time from treatment start until progression or death. A supervised approach with penalized regression was applied to select most informative predictors, and then a risk score was created based on the linear predictor given by the multivariable model. Results: Forty-five patients corresponded to the study criteria, with a median age at diagnosis of 45 (range 23- 64). The supervised approach allowed identifying a three-gene prognostic set including Semaphorin -3C (SEMA3C), Neuronal Pentraxin 2 (NPTX2 ) and the Metabotropic Glutamate Receptor 5 (GRM5), involved in proliferation, migration and inflammation. The risk score associated to these three genes was statistically associated to PFS (HR = 2.72, p = 0.00005) and remains significant when adjusted on clinical covariates age at diagnosis, necrosis, endothelial proliferation and type of surgery (complete, partial or subtotal surgery) (HRadj = 2.36, p = 0.001). Conclusions: We report an independent three genes SEMA3C-NPTX2-GRM5 risk score signature of response to radiotherapy in patients with oligodendroglioma, which highlights the heterogeneous response in this reputed good prognosis population. This signature could help in determining the adapted treatment as well as potential new targets to address.

scholarly journals Neuronal Pentraxin 2 Supports Clear Cell Renal Cell Carcinoma by Activating the AMPA-Selective Glutamate Receptor-4

2014 ◽  
Vol 74 (17) ◽  
pp. 4796-4810 ◽  
Author(s):  
Christina A. von Roemeling ◽  
Derek C. Radisky ◽  
Laura A. Marlow ◽  
Simon J. Cooper ◽  
Stefan K. Grebe ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Glutamate Receptor ◽  
Renal Cell ◽  
Clear Cell ◽  
Cell Renal Cell Carcinoma ◽  
Neuronal Pentraxin

scholarly journals Novel candidate colorectal cancer biomarkers identified by methylation microarray-based scanning

2011 ◽  
Vol 18 (4) ◽  
pp. 465-478 ◽  
Author(s):  
Yuriko Mori ◽  
Alexandru V Olaru ◽  
Yulan Cheng ◽  
Rachana Agarwal ◽  
Jian Yang ◽  
...  
Keyword(s):  
Zinc Finger Protein ◽  
Characteristic Curve ◽  
Receiver Operator Characteristic Curve ◽  
Dna Hypermethylation ◽  
Specific Pcr ◽  
A Genome ◽  
Junction Protein ◽  
Genome Wide Search ◽  
Glucagon Like Peptide 1 ◽  
Neuronal Pentraxin

DNA hypermethylation is a common epigenetic abnormality in colorectal cancers (CRCs) and a promising class of CRC screening biomarkers. We conducted a genome-wide search for novel neoplasia-specific hypermethylation events in the colon. We applied methylation microarray analysis to identify loci hypermethylated in 17 primary CRCs relative to eight non-neoplastic colonic mucosae (NCs) from neoplasia-free subjects. These CRC-associated hypermethylation events were then individually evaluated for their ability to discriminate neoplastic from non-neoplastic cases, based on real-time quantitative methylation-specific PCR (qMSP) assays in 113 colonic tissues: 51 CRCs, nine adenomas, 19 NCs from CRC patients (CRC–NCs), and 34 NCs from neoplasia-free subjects (control NCs). A strict microarray data filtering identified 169 candidate CRC-associated hypermethylation events. Fourteen of these 169 loci were evaluated using qMSP assays. Ten of these 14 methylation events significantly distinguished CRCs from age-matched control NCs (P<0.05 by receiver operator characteristic curve analysis); methylation of visual system homeobox 2 (VSX2) achieved the highest discriminative accuracy (83.3% sensitivity and 92.3% specificity, P<1×10−6), followed by BEN domain containing 4 (BEND4), neuronal pentraxin I (NPTX1), ALX homeobox 3 (ALX3), miR-34b, glucagon-like peptide 1 receptor (GLP1R), BTG4, homer homolog 2 (HOMER2), zinc finger protein 583 (ZNF583), and gap junction protein, gamma 1 (GJC1). Adenomas were significantly discriminated from control NCs by hypermethylation of VSX2, BEND4, NPTX1, miR-34b, GLP1R, and HOMER2 (P<0.05). CRC–NCs were significantly distinguished from control NCs by methylation of ALX3 (P<1×10−4). In conclusion, systematic methylome-wide analysis has identified ten novel methylation events in neoplastic and non-neoplastic colonic mucosae from CRC patients. These potential biomarkers significantly discriminate CRC patients from controls. Thus, they merit further evaluation in stool- and circulating DNA-based CRC detection studies.

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