1.

Record Nr.

UNINA9910298315403321

Autore

Inuzuka Hiroyuki

Titolo

SCF and APC E3 Ubiquitin Ligases in Tumorigenesis [[electronic resource] /] / by Hiroyuki Inuzuka, Wenyi Wei

Pubbl/distr/stampa

Cham : , : Springer International Publishing : , : Imprint : Springer, , 2014

ISBN

3-319-05026-5

Edizione

[1st ed. 2014.]

Descrizione fisica

1 online resource (119 p.)

Collana

SpringerBriefs in Cancer Research, , 2194-1173

Disciplina

616.994071

Soggetti

Cancer research

Cell cycle

Proteins 

Cancer Research

Cell Cycle Analysis

Protein Structure

Lingua di pubblicazione

Inglese

Formato

Materiale a stampa

Livello bibliografico

Monografia

Note generali

Description based upon print version of record.

Nota di bibliografia

Includes bibliographical references at the end of each chapters and index.

Nota di contenuto

1. Introduction -- 2. The Fbxw subclass of SCF E3 ubiquitin Ligases -- 3. The FbxL subclass of SCF E3 ubiquitin Ligases -- 4. The Fbxo subclass of SCF E3 ubiquitin Ligases -- 5. APC/Cdc20 and APC/Cdh1 E3 ubiquitin Ligases -- 6. Conclusions and Future Perspectives.

Sommario/riassunto

This SpringerBrief explores the physiological roles of Skp1-Cullin1-F-box Complex (SCF) and Anaphase Promoting Complex (APC) in normal cells and in tumor formation. These two related, multi-subunit E3 ubiquitin ligase enzymes, APC and SCF are thought to be the major driving forces governing proper cell cycle progression. Defective cell cycle regulation leads to genomic instability and ultimately, cancer development. Selective degradation of key cell cycle regulators by the ubiquitin-proteasome system has been proven to be a major regulatory mechanism for ensuring ordered and coordinated cell cycle progression. The SCF and APC E3 ligases have been characterized to play pivotal roles in regulating the cell cycle progression by timely degrading various critical cell cycle regulators. This Brief reviews recent



studies that have shown that deregulation of signaling pathways in which the two ubiquitin ligases are involved causes aberrant cell cycle regulation, in turn leading to tumorigenesis. The text also discusses how SCF and APC may present promising therapeutic targets to treat various cancers.