Human Tumor-Derived p53 Mutants: A Growing Family of Oncoproteins (Record no. 76491)

MARC details
000 -LEADER
fixed length control field 02668naaaa2200325uu 4500
001 - CONTROL NUMBER
control field https://directory.doabooks.org/handle/20.500.12854/49645
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20220220084009.0
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 978-2-88919-961-7
020 ## - INTERNATIONAL STANDARD BOOK NUMBER
International Standard Book Number 9782889199617
024 7# - OTHER STANDARD IDENTIFIER
Standard number or code 10.3389/978-2-88919-961-7
Terms of availability doi
041 0# - LANGUAGE CODE
Language code of text/sound track or separate title English
042 ## - AUTHENTICATION CODE
Authentication code dc
100 1# - MAIN ENTRY--PERSONAL NAME
Personal name Giovanni Blandino
Relationship auth
245 10 - TITLE STATEMENT
Title Human Tumor-Derived p53 Mutants: A Growing Family of Oncoproteins
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Name of publisher, distributor, etc. Frontiers Media SA
Date of publication, distribution, etc. 2016
300 ## - PHYSICAL DESCRIPTION
Extent 1 electronic resource (97 p.)
506 0# - RESTRICTIONS ON ACCESS NOTE
Terms governing access Open Access
Source of term star
Standardized terminology for access restriction Unrestricted online access
520 ## - SUMMARY, ETC.
Summary, etc. TP53 gene mutations are present in more than half of all human cancers. The resulting proteins are mostly full-length with a single amino acid change and are abundantly expressed in cancer cells. Some of the mutant p53 proteins gain oncogenic functions (GOF) through which it actively contribute to the aberrant cell proliferation, increased resistance to apoptotic stimuli and ability to metastasize. Gain of function mutant p53 proteins can transcriptionally regulate the expression of a large plethora of target genes. This mainly occurs through the formation of oncogenic transcriptional competent complexes that include mutant p53 protein, known transcription factors, posttranslational modifiers and scaffold proteins. Mutant p53 protein can also transcriptionally regulate the expression of microRNAs, small non-coding RNAs that regulate gene expression at the posttranscriptional level. Each microRNA can putatively target the expression of hundred mRNAs and consequently impact on many cellular functions. Thus, gain of function mutant p53 proteins can exert their oncogenic activities through the modulation of both non-coding and coding regions of human genome. Over the past 3 decades, the regulation of p53 has been extensively studied. However, the regulation of mutant p53 remained largely unexplored. This snapshot focuses on recent discovery of mutant p53 GOF and regulation.
540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE
Terms governing use and reproduction Creative Commons
Use and reproduction rights https://creativecommons.org/licenses/by/4.0/
Source of term cc
-- https://creativecommons.org/licenses/by/4.0/
546 ## - LANGUAGE NOTE
Language note English
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term mouse models
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term mutant p53
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term dominant netagive
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Uncontrolled term therapies
653 ## - INDEX TERM--UNCONTROLLED
Uncontrolled term Oncogenic addiction
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Uncontrolled term gain of function
700 1# - ADDED ENTRY--PERSONAL NAME
Personal name Ygal Haupt
Relationship auth
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="http://journal.frontiersin.org/researchtopic/3592/human-tumor-derived-p53-mutants-a-growing-family-of-oncoproteins">http://journal.frontiersin.org/researchtopic/3592/human-tumor-derived-p53-mutants-a-growing-family-of-oncoproteins</a>
Access status 0
Public note DOAB: download the publication
856 40 - ELECTRONIC LOCATION AND ACCESS
Host name www.oapen.org
Uniform Resource Identifier <a href="https://directory.doabooks.org/handle/20.500.12854/49645">https://directory.doabooks.org/handle/20.500.12854/49645</a>
Access status 0
Public note DOAB: description of the publication

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