JANČÁLEK, Radim. The role of the TP73 gene and its transcripts in neuro-oncology. British journal of neurosurgery. London: Informa Healthcare, 2014, vol. 28, No 5, p. 598-605. ISSN 0268-8697. Available from: https://dx.doi.org/10.3109/02688697.2014.908162.
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Basic information
Original name The role of the TP73 gene and its transcripts in neuro-oncology
Authors JANČÁLEK, Radim (203 Czech Republic, guarantor, belonging to the institution).
Edition British journal of neurosurgery, London, Informa Healthcare, 2014, 0268-8697.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30000 3. Medical and Health Sciences
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 0.960
RIV identification code RIV/00216224:14110/14:00077492
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.3109/02688697.2014.908162
UT WoS 000341753500004
Keywords in English gliomagenesis; isoforms; TP73 gene; p73 protein
Tags EL OK
Tags International impact, Reviewed
Changed by Changed by: Soňa Böhmová, učo 232884. Changed: 27/11/2014 14:52.
Abstract
Protein p73 is a member of the p53 protein family that can induce cell cycle arrest or apoptosis by the activation of p53-responsive genes as well as p53-independent pathways. Alternative promoter usage, together with differential splicing of the C-terminal exons, forms several distinct mRNAs that are translated into corresponding protein isoforms containing different domains. While TAp73 isoforms respond to genotoxic stress in a manner similar to tumor suppressor p53, Delta TAp73 isoforms inhibit apoptosis during normal development and in cancer cell lines. Thus, the impact of p73 on tumorigenesis depends on a subtle balance between tumor-promoting and-suppressing isoforms. Due to the structural homology between p53 and p73, a subtle balance among p53 family members and their isoforms could influence glioma cell evolution toward malignancy. Thus, the p73 status has to be considered when studying the regulatory role of p53 protein in gliomagenesis. The presented review summarizes recent knowledge about the issue of p73 and its isoforms with respect to neuro-oncology research.
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