Abstract
| Original language | English |
|---|---|
| Title of host publication | Marek's Disease |
| Subtitle of host publication | An Evolving Problem |
| Pages | 32-48 |
| ISBN (Electronic) | 9780080479187 |
| Publication status | Published - Jun 30 2004 |
| Externally published | Yes |
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Marek's disease virus oncogenicity: Molecular mechanisms. / Nair, Venugopal K.; Kung, Hsing-Jien.
Marek's Disease : An Evolving Problem. 2004. p. 32-48.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Marek's disease virus oncogenicity: Molecular mechanisms
AU - Nair, Venugopal K.
AU - Kung, Hsing-Jien
PY - 2004/6/30
Y1 - 2004/6/30
N2 - This chapter discusses the oncogenicity of Marek's disease virus (MDV). It provides an overview of the roles of MDV genes that are potentially associated with latency/transformation. The onset of MDV-induced tumors is very rapid. The ability to induce rapid-onset tumors resembling those caused by some of the acutely transforming retroviruses suggests the direct involvement of virus-encoded transforming gene(s) in oncogenesis. Biochemical and genetic studies carried out in recent years suggest that Meq is the principal oncogene of MDV. Meq is a versatile protein that binds DNA, RNA, and a variety of other proteins. It also plays a potential role in the virulence replication and latency of MDV. Various investigations aimed at unravelling the oncogenic determinants of MDV have led to the identification of a number of other genes that have potential roles in the pathogenesis of MDV. Some of these MDV genes with a potential role in Marek's disease pathogenicity include the BamH1–H family of transcripts, the pp38/pp24 group of cytoplasmic phosphoproteins, the MDV-encoded CXC chemokine (vIL-8), the MDV-encoded telomerase RNA (vTR) subunit, and the MDV ICP4 homologue-related transcripts. The application of rapid, targeted, or random mutagenesis techniques enables rapid delineation of the molecular mechanisms and determinants for MDV-induced oncogenesis.
AB - This chapter discusses the oncogenicity of Marek's disease virus (MDV). It provides an overview of the roles of MDV genes that are potentially associated with latency/transformation. The onset of MDV-induced tumors is very rapid. The ability to induce rapid-onset tumors resembling those caused by some of the acutely transforming retroviruses suggests the direct involvement of virus-encoded transforming gene(s) in oncogenesis. Biochemical and genetic studies carried out in recent years suggest that Meq is the principal oncogene of MDV. Meq is a versatile protein that binds DNA, RNA, and a variety of other proteins. It also plays a potential role in the virulence replication and latency of MDV. Various investigations aimed at unravelling the oncogenic determinants of MDV have led to the identification of a number of other genes that have potential roles in the pathogenesis of MDV. Some of these MDV genes with a potential role in Marek's disease pathogenicity include the BamH1–H family of transcripts, the pp38/pp24 group of cytoplasmic phosphoproteins, the MDV-encoded CXC chemokine (vIL-8), the MDV-encoded telomerase RNA (vTR) subunit, and the MDV ICP4 homologue-related transcripts. The application of rapid, targeted, or random mutagenesis techniques enables rapid delineation of the molecular mechanisms and determinants for MDV-induced oncogenesis.
M3 - Chapter
SN - 9780120883790
SP - 32
EP - 48
BT - Marek's Disease
ER -