Anticancer Genes by Stefan Grimm (eds.)

By Stefan Grimm (eds.)

This ebook discusses the emergence of a brand new classification of genes with a selected anticancer task. those genes, lately outlined as “Anticancer Genes”, are reviewed in person chapters on their mode of motion, the categorical telephone demise signs they set off, and the prestige of makes an attempt to translate them into scientific application.

Anticancer Genes presents an summary of this nascent box, its genesis, present nation, and prospect. It discusses how Anticancer Genes may well bring about the identity of a repertoire of signaling pathways directed opposed to mobile adjustments which are particular for tumor cells.

With contributions from specialists all over the world, Anticancer Genes is an important consultant to this dynamic subject for researchers and scholars in melanoma learn, molecular drugs, pharmacology and toxicology and genetics in addition to clinicians and medical researchers drawn to the healing capability of this intriguing new field.

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Chen K et al (2011) Gallus Heat shock cognate protein 70, a novel binding partner of Apoptin. Virol J 8:324 52. Teodoro JG et al (2004) The viral protein Apoptin associates with the anaphase-promoting complex to induce G2/M arrest and apoptosis in the absence of p53. Genes Dev 18(16):1952–1957 53. Cheng CM et al (2003) The viral death protein Apoptin interacts with Hippi, the protein interactor of Huntingtin-interacting protein 1. Biochem Biophys Res Commun 305(2):359–364 54. Zheng L et al (2001) The death effector domain-associated factor plays distinct regulatory roles in the nucleus and cytoplasm.

In the same cells Apoptin expression triggered translocation of Hsc70 from the cytoplasm to the nucleus and Hsc70 was required for Apoptin-induced downregulation of p65, a member of the NF-κB transcription factor family. However, whether this holds true for human cells and is a general molecular mechanism for Apoptin function remains to be established. In a concurrently published study they confirmed the interaction of Apoptin and Hsc70 as well as Hsc70 nuclear translocation in transformed human embryonic kidney (HEK293T) cells [50].

7 Conclusive Remarks A major goal of cancer treatment is the eradication of malignant cells while minimizing damage to normal cells. A number of proteins such as TRAIL and HAMLET have been reported to selectively kill tumor cells by sensing essential molecular and cellular changes during carcinogenic transformation and redirecting these pathways towards cell death. Since its identification in the early 1990s as the apoptosis-inducing component of CAV, Apoptin has become of interest due to its ability to induce p53-independent cell death specifically in transformed cells.

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