4.4 Article

Tissue-specific transplantation antigen P35B immune response-mediated metabolism coupling cell cycle to postreplication repair network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) by biocomputation

期刊

IMMUNOLOGIC RESEARCH
卷 52, 期 3, 页码 258-268

出版社

HUMANA PRESS INC
DOI: 10.1007/s12026-012-8337-z

关键词

Tissue-specific transplantation antigen P35B (TSTA3); No-tumor hepatitis/cirrhotic tissues (HBV or HCV infection); Immune response-mediated metabolism coupling cell cycle to postreplication repair network; Biocomputation

资金

  1. National Natural Science Foundation in China [60871100, 61171114]
  2. Returned Overseas Chinese Scholars for Scientific research Foundation of State Education Ministry, Significant Science and Technology Project for New Transgenic Biological Species [2009ZX08012-001B]
  3. Tsinghua University [20111081023, 20111081010]
  4. State Key Lab of Pattern Recognition Open Foundation

向作者/读者索取更多资源

We constructed the low-expression tissue-specific transplantation antigen P35B immune response-mediated metabolism coupling cell cycle to postreplication repair network in no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection) compared with high-expression (fold change a parts per thousand yen 2) human hepatocellular carcinoma in GEO data set, by using integration of gene regulatory network inference method with gene ontology analysis of activated up- and downstream networks. Our results showed upstream-activated etc and downstream-activated etc in no-tumor hepatitis/cirrhotic tissues. -activated network enhanced the regulation of apoptosis, cyclin-dependent protein kinase activity, cell migration, insulin secretion, transcription, cell division, cell proliferation, DNA replication, postreplication repair, cell differentiation, T-cell homeostasis, neutrophil-mediated immunity, neutrophil chemotaxis, interleukin-8 production, inflammatory response, immune response, B-cell activation, humoral immune response, actin filament organization, xenobiotic metabolism, lipid metabolism, phospholipid metabolism, leukotriene biosynthesis, organismal lipid catabolism, phosphatidylcholine metabolism, arachidonic acid secretion, activation of phospholipase A2, deoxyribonucleotide biosynthesis, heterophilic cell adhesion, activation of MAPK activity, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, G-protein-coupled receptor protein signaling pathway, response to toxin, acute-phase response, DNA damage response, intercellular junction assembly, cell communication, and cell recognition, as a result of inducing immune response-mediated metabolism coupling cell cycle to postreplication repair in no-tumor hepatitis/cirrhotic tissues.

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