Εξειδίκευση τύπου :	Άρθρο σε επιστημονικό περιοδικό
Τίτλος:	Functions, divergence and clinical value of TAp73 isoforms in cancer
Δημιουργός/Συγγραφέας:	Logotheti S. Pavlopoulou A. Galtsidis S. Vojtesek B. [EL] Ζουμπουρλής, Βασίλης[EN] Zoumpourlis, Vassilis
Ημερομηνία:	2013
Γλώσσα:	Αγγλικά
ISSN:	0167-7659
DOI:	10.1007/s10555-013-9424-x
Άλλο:	PubMed ID: 23592418
Περίληψη:	The p73 gene encodes the tumour suppressive full-length TAp73 and N-terminal-truncated DNp73 isoforms that act as dominant negative inhibitors of TAp73. The overall effect of p73 in oncogenesis is thought to depend on the TAp73 to DNp73 isoforms' ratio. TAp73 isoforms include a number of C-terminal variants as a result of alternative splicing in 3′-end. TAp73 isoforms protect cells from oncogenic alterations in a multifaceted way since they are implicated in the suppression of all demonstrated hallmarks and enabling characteristics of cancer. Their best established role is in apoptosis, a process which seems to be differently affected by each TAp73 C-terminal variant. Based on previous findings and our thorough bioinformatics analysis, we highlight that TAp73 variants are functionally non-equivalent, since they present major differences in their transactivation efficiencies, protein interactions, response to DNA damage and apoptotic effects that are attributable to the primary structure of their C terminus. In this review, we summarise these differences and we unveil the link between crucial C-terminal motifs/residues and the oncosuppressive potential of TAp73 isoforms, emphasising on the importance of considering C terminus during the development of p73-based anticancer biologics.
Τίτλος πηγής δημοσίευσης:	Cancer and Metastasis Reviews
Τόμος/Κεφάλαιο:	32
Τεύχος:	3-4
Σελίδες:	511-534
Θεματική Κατηγορία:	[EL] Βιολογία (Γενικά)[EN] Biology (General)
Λέξεις-Κλειδιά:	Apoptosis C terminus Cancer Cell cycle arrest DNA damage TAp73 isoforms
Αξιολόγηση από ομότιμους (peer reviewed):	Ναι
Κάτοχος πνευματικών δικαιωμάτων:	© 2013 Springer Science+Business Media New York.
Σημειώσεις:	11CZ-16-ET30; CZ.1.05/2.1.00/03.0101; Ministerstvo Školství, Mládeže a Tělovýchovy, MŠMT: CR 7AMB12GR016; European Regional Development Fund, FEDER. SL, SG and VZ were supported by ESPA grant, Czech-Greek bilateral cooperation (2012–2014): code No. 11CZ-16-ET30. BV was supported by MEYS CR 7AMB12GR016 grant and grant of the European Regional Development Fund and the State Budget of the Czech Republic (RECAMO, CZ.1.05/2.1.00/03.0101).
Εμφανίζεται στις συλλογές:	Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο