Search results for: PARP2 Assay Kit
#33187221 
2020/11/11
To Up
Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD.
(1) : Lung cancer (LC) is a major leading cause of death worldwide. Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 are key players in cancer. We aimed to assess PARP-1 and PARP-2 expression and activity and DNA damage in tumors and non-tumor lungs from patients with/without chronic obstructive pulmonary disease (COPD). (2) : Lung tumor and non-tumor specimens were obtained through video-assisted thoracoscopic surgery (VATS) in LC patients with/without underlying COPD (two groups of patients, = 15/group). PARP-1 and PARP-2 expression (ELISA), PARP activity (PARP colorimetric assay kit) and DNA damage (immunohistochemistry) levels were identified in all samples. (3) : Both PARP-1 and PARP-2 expression levels were significantly lower in lung tumors (irrespective of COPD)compared to non-tumor specimens, while DNA damage and PARP activity levels significantly increased in lung tumors compared to non-tumor specimens only in LC-COPD patients. PARP-2 expression was positively correlated with smoking burden in LC-COPD patients. (4) : In lung tumors of COPD patients, an overactivation of PARP enzyme was observed. A decline in PARP-1 and PARP-2 protein expression was seen in lung tumors irrespective of COPD. Other phenotypic features (airway obstruction) beyond cancer may account for the increase in PARP activity seen in the tumors of patients with underlying COPD.Jun Tang, Víctor Curull, Xuejie Wang, Coral Ampurdanés, Xavier Duran, Lara Pijuan, Alberto Rodríguez-Fuster, Rafael Aguiló, José Yélamos, Esther Barreiro
1430 related Products with: Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD.
96T96 assays 48 assays1 kit48 assays
Related Pathways
#30918653 2019/02/10
To Up
Nobiletin induces growth inhibition and apoptosis in human nasopharyngeal carcinoma C666-1 cells through regulating PARP-2/SIRT1/AMPK signaling pathway.
Nobiletin, a major polymethoxyflavones (PMFs) from citri reticulatae pericarpium (CRP), can inhibit several forms of cancer proliferation. However, the effects of nobiletin on nasopharyngeal carcinoma (NPC) C666-1 cells remain largely unknown.Guo Dong Zheng, Ping Jun Hu, Ying Xin Chao, Ying Zhou, Xiu Juan Yang, Bai Zhong Chen, Xi Yong Yu, Yi Cai
2962 related Products with: Nobiletin induces growth inhibition and apoptosis in human nasopharyngeal carcinoma C666-1 cells through regulating PARP-2/SIRT1/AMPK signaling pathway.
2 Pieces/Box2 Pieces/Box10ug2 Pieces/Box1000 1 kit(96 Wells)100ug Lyophilized1.5x10(6) cells100 μg96 wells (1 kit)1x10e7 cells2 Pieces/Box
Related Pathways
#17330260 //
To Up
Array comparative genomic hybridization analysis of chromosomal imbalances and their target genes in gastrointestinal stromal tumors.
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. The tumors characteristically harbor KIT or PDGFRA mutations, and mutant tumors respond to imatinib mesylate (Glivectrade mark). Chromosomal imbalances resulting in altered gene dosage are known to have a role in the molecular pathogenesis of these tumors, but the target genes remain to be identified. The present study aimed to identify some of these genes. In total, 35 GIST samples were screened for chromosomal imbalances by array-based comparative genomic hybridization. A cDNA array was used to define the minimal common overlapping areas of DNA copy number change. Eight confirmative, replicate hybridizations were performed using an oligonucleotide array. The most recurrent copy number losses were localized to 14q, 22q, and 1p. Gains were less common with 8q being the most recurrent. Two recurrent deleted regions of 14q were 14q11.2 harboring the PARP2, APEX1, and NDRG2 genes and 14q32.33 harboring SIVA. Additional target candidates were NF2 at chromosome 22, CDKN2A/2B at 9p, and ENO1 at 1p for copy number losses, and MYC at 8q for copy number gains. Array CGH proved to be an effective tool for the identification of chromosome regions involved in the development and progression of GISTs.Reetta Assämäki, Maarit Sarlomo-Rikala, José Antonio Lopez-Guerrero, Jerzy Lasota, Leif C Andersson, Antonio Llombart-Bosch, Markku Miettinen, Sakari Knuutila