By Leonard J. Rosenthal, Hans Wilhelm Doerr
Nearly 15 consistent with cent of human melanoma occurrence will be attributed to virus an infection, i.e. viruses signify the second one most crucial probability issue (after tobacco intake) for melanoma improvement in people. at the present time, 5 virus varieties are identified to be desirous about inflicting human melanoma: papillomaviruses, retroviruses, herpesviruses, hepadnaviruses, and flaviviruses. This quantity of "Monographs in Virology" offers a finished overview of a few DNA tumor viruses. major specialists within the box of tumor virology speak about up to date info, concentrating on the reworking genes of DNA tumor viruses, the mechanisms of transformation and the in vitro method used for his or her id and characterization. even supposing DNA tumor viruses are a various crew, in vitro stories have published numerous universal mechanisms of viral transformation. the person chapters of the e-book describe the newest examine at the id of viral oncogenes and their goals.
Read Online or Download Mechanisms of DNA tumor virus transformation PDF
Best genetics books
This e-book presents a unified number of very important, contemporary effects for the layout of sturdy controllers for doubtful platforms. many of the effects awarded are in response to H¿ regulate concept, or its stochastic counterpart, danger delicate keep watch over concept. imperative to the philosophy of the e-book is the inspiration of an doubtful approach.
Details extraction (IE) is a brand new expertise allowing correct content material to be extracted from textual details to be had electronically. IE primarily builds on traditional language processing and computational linguistics, however it can also be heavily relating to the good proven region of knowledge retrieval and contains studying.
This article offers with the genetics and molecular biology of alternative micro organism, which perform clinical, clinical, agricultural and biotechnological actions. Taking genetic variety as its topic, it illustrates phenomena resembling genetic structures controlling pathogenicity, symbiosis, chemotaxis, metabolic features, and differentiation
- NextGen Genealogy: The DNA Connection
- Journal of Researches into the Geology and Natural History of the Various Countries visited by H. M. S. Beagle
- The Molecular Biology of Neurological Disease
- Internal Medicine Review Core Curriculum, Book 5: General Internal Medicine
- How We Live and Why We Die: The Secret Lives of Cells
Extra resources for Mechanisms of DNA tumor virus transformation
J Neurovirol 1999;5: 430–435. Tornatore C, Berger JR, Houff SA, et al: Detection of JC virus DNA in peripheral lymphocytes from patients with and without progressive multifocal leukoencephalopathy. Ann Neurol 1992; 31:454 – 462. Yogo Y, Kitamura T, Sugimoto C, et al: Isolation of a possible archetypal JC virus DNA sequence from nonimmunocompromised individuals. J Virol 1990;64:3139–3143. Negrini M, Sabbioni S, Arthur RR, Castagnoli A, Barbanti-Brodano G: Prevalence of the archetypal regulatory region and sequence polymorphisms in nonpassaged BK virus variants.
DNA extracted from the insulinoma was transfected into human embryonic fibroblasts with subsequent rescue of an isolate now called BKV-IR. BKV-IR was able to transform hamster kidney cells in vitro and had a deletion and insertion in the regulatory region setting it apart from wild-type BKV. This particular study was important in that BKV was known to produce pancreatic tumors in hamsters and now had a correlate in man. In a later study, Negrini et al.  also found episomal BKV DNA in Kaposi’s sarcoma, Ewing and osteogenic sarcoma, glioma, meningioma and neuroblastoma.
Since the E143R mutant retains the ability to associate with wild-type 16K , this interaction may inhibit the activity of the pump. These genetic and biochemical findings indicate a potential role for 16K in E5 transformation. Conclusions The results described above provide strong evidence that the BPV-1 E5 oncoprotein transforms fibroblasts through specific activation of a growth factor receptor, the ␤-type PDGF-R. The mechanism by which the viral protein elicits BPV-1 E5 Oncoprotein 39 transforming ability through this PTK receptor represents a divergence from previously described mechanisms involving growth factors and their respective receptors.
Mechanisms of DNA tumor virus transformation by Leonard J. Rosenthal, Hans Wilhelm Doerr