• Title/Summary/Keyword: Protein Network

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GSnet: An Integrated Tool for Gene Set Analysis and Visualization

  • Choi, Yoon-Jeong;Woo, Hyun-Goo;Yu, Ung-Sik
    • Genomics & Informatics
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    • v.5 no.3
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    • pp.133-136
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    • 2007
  • The Gene Set network viewer (GSnet) visualizes the functional enrichment of a given gene set with a protein interaction network and is implemented as a plug-in for the Cytoscape platform. The functional enrichment of a given gene set is calculated using a hypergeometric test based on the Gene Ontology annotation. The protein interaction network is estimated using public data. Set operations allow a complex protein interaction network to be decomposed into a functionally-enriched module of interest. GSnet provides a new framework for gene set analysis by integrating a priori knowledge of a biological network with functional enrichment analysis.

Identification of a Variant Form of Cellular Inhibitor of Apoptosis Protein (c-IAP2) That Contains a Disrupted Ring Domain

  • Park, Sun-Mi;Kim, Ji-Su;Park, Ji-Hyun;Kang, Seung-Goo;Lee, Tae Ho
    • IMMUNE NETWORK
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    • v.2 no.3
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    • pp.137-141
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    • 2002
  • Among the members of the inhibitor of apoptosis (IAP) protein family, only Livin and survivin have been reported to have variant forms. We have found a variant form of c-IAP2 through the interaction with the X protein of HBV using the yeast two-hybrid system. In contrast to the wild-type c-IAP2, the variant form has two stretches of sequence in the RING domain that are repeated in the C-terminus that would disrupt the RING domain. We demonstrate that the variant form has an inhibitory effect on TNF-mediated $NF-{\kappa}B$ activation unlike the wild-type c-IAP2, which increases TNFmediated $NF-{\kappa}B$ activation. These results suggest that this variant form has different activities from the wild-type and the RING domain may be involved in the regulation of TNF-induced $NF-{\kappa}B$ activation.

Identification of Diseasomal Proteins from Atopy-Related Disease Network (아토피관련 질병 네트워크로부터 질병단백체 발굴)

  • Lee, Yoon-Kyeong;Yeo, Myeong-Ho;Kang, Tae-Ho;Yoo, Jae-Soo;Kim, Hak-Yong
    • The Journal of the Korea Contents Association
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    • v.9 no.4
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    • pp.114-120
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    • 2009
  • In this study, we employed the idea that disease-related proteins tend to be work as an important factor for architecture of the disease network. We initially obtained 43 atopy-related proteins from the Online Mendelian Inheritance in Man (OMIM) and then constructed atopy-related protein interaction network. The protein network can be derived the map of the relationship between different disease proteins, denoted disease interaction network. We demonstrate that the associations between diseases are directly correlated to their underlying protein-protein interaction networks. From constructed the disease-protein bipartite network, we derived three diseasomal proteins, CCR5, CCL11, and IL/4R. Although we use the relatively small subnetwork, an atopy-related disease network, it is sufficient that the discovery of protein interaction networks assigned by diseases will provide insight into the underlying molecular mechanisms and biological processes in complex human disease system.

Analysis of Essential Proteins in Protein-Protein Interaction Networks (단백질 상호작용 네트워크에서 필수 단백질의 견고성 분석)

  • Ryu, Jae-Woon;Kang, Tae-Ho;Yoo, Jae-Soo;Kim, Hak-Yong
    • The Journal of the Korea Contents Association
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    • v.8 no.6
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    • pp.74-81
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    • 2008
  • Protein interaction network contains a small number of highly connected protein, denoted hub and many destitutely connected proteins. Recently, several studies described that a hub protein is more likely to be essential than a non-hub protein. This phenomenon called as a centrality-lethality rule. This nile is widely credited to exhibit the importance of hub proteins in the complex network and the significance of network architecture as well. To confirm whether the rule is accurate, we Investigated all protein interaction DBs of yeast in the public sites such as Uetz, Ito, MIPS, DIP, SGB, and BioGRID. Interestingly, the protein network shows that the rule is correct in lower scale DBs (e.g., Uetz, Ito, and DIP) but is not correct in higher scale DBs (e.g., SGD and BioGRID). We are now analyzing the features of networks obtained from the SGD and BioGRD and comparing those of network from the DIP.

Construction of a Protein-Protein Interaction Network for Chronic Myelocytic Leukemia and Pathway Prediction of Molecular Complexes

  • Zhou, Chao;Teng, Wen-Jing;Yang, Jing;Hu, Zhen-Bo;Wang, Cong-Cong;Qin, Bao-Ning;Lv, Qing-Liang;Liu, Ze-Wang;Sun, Chang-Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.13
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    • pp.5325-5330
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    • 2014
  • Background: Chronic myelocytic leukemia is a disease that threatens both adults and children. Great progress has been achieved in treatment but protein-protein interaction networks underlining chronic myelocytic leukemia are less known. Objective: To develop a protein-protein interaction network for chronic myelocytic leukemia based on gene expression and to predict biological pathways underlying molecular complexes in the network. Materials and Methods: Genes involved in chronic myelocytic leukemia were selected from OMIM database. Literature mining was performed by Agilent Literature Search plugin and a protein-protein interaction network of chronic myelocytic leukemia was established by Cytoscape. The molecular complexes in the network were detected by Clusterviz plugin and pathway enrichment of molecular complexes were performed by DAVID online. Results and Discussion: There are seventy-nine chronic myelocytic leukemia genes in the Mendelian Inheritance In Man Database. The protein-protein interaction network of chronic myelocytic leukemia contained 638 nodes, 1830 edges and perhaps 5 molecular complexes. Among them, complex 1 is involved in pathways that are related to cytokine secretion, cytokine-receptor binding, cytokine receptor signaling, while complex 3 is related to biological behavior of tumors which can provide the bioinformatic foundation for further understanding the mechanisms of chronic myelocytic leukemia.