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@article{1331434,
author = {Cetkovská, Kateřina and Šustová, Hana and Kosztyu, Pavlína and Uldrijan, Stjepan},
article_location = {San Francisco},
article_number = {12},
doi = {http://dx.doi.org/10.1371/journal.pone.0144753},
keywords = {IMMUNODEFICIENCY-VIRUS TYPE-1; WILLIAMS-BEUREN-SYNDROME; P53 TUMOR-SUPPRESSOR; LONG TERMINAL REPEAT; HISTONE DEACETYLASE-3; HUMAN CYTOMEGALOVIRUS; P53-INDEPENDENT ROLE; HIV-1 TRANSCRIPTION; ACIDIC DOMAIN; CELL-CYCLE},
language = {eng},
issn = {1932-6203},
journal = {Plos one},
title = {A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity},
volume = {10},
year = {2015}
}
TY - JOUR
ID - 1331434
AU - Cetkovská, Kateřina - Šustová, Hana - Kosztyu, Pavlína - Uldrijan, Stjepan
PY - 2015
TI - A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity
JF - Plos one
VL - 10
IS - 12
SP - 1-19
EP - 1-19
PB - Public Library of Science
SN - 19326203
KW - IMMUNODEFICIENCY-VIRUS TYPE-1
KW - WILLIAMS-BEUREN-SYNDROME
KW - P53 TUMOR-SUPPRESSOR
KW - LONG TERMINAL REPEAT
KW - HISTONE DEACETYLASE-3
KW - HUMAN CYTOMEGALOVIRUS
KW - P53-INDEPENDENT ROLE
KW - HIV-1 TRANSCRIPTION
KW - ACIDIC DOMAIN
KW - CELL-CYCLE
N2 - Williams-Beuren syndrome-associated transcription factor TFII-I plays a critical regulatory role in bone and neural tissue development and in immunity, in part by regulating cell proliferation in response to mitogens. Mdm2, a cellular oncogene responsible for the loss of p53 tumor suppressor activity in a significant proportion of human cancers, was identified in this study as a new binding partner for TFII-I and a negative regulator of TFII-I-mediated transcription. These findings suggest a new p53-independent mechanism by which increased Mdm2 levels found in human tumors could influence cancer cells. In addition to that, we present data indicating that TFII-I is an important cellular regulator of transcription from the immediate-early promoter of human cytomegalovirus, a promoter sequence frequently used in mammalian expression vectors, including vectors for gene therapy. Our observation that Mdm2 over-expression can decrease the ability of TFII-I to activate the CMV promoter might have implications for the efficiency of experimental gene therapy based on CMV promoter-derived vectors in cancers with Mdm2 gene amplification.
ER -
CETKOVSKÁ, Kateřina, Hana ŠUSTOVÁ, Pavlína KOSZTYU a Stjepan ULDRIJAN. A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity. \textit{Plos one}. San Francisco: Public Library of Science, 2015, roč.~10, č.~12, s.~1-19. ISSN~1932-6203. Dostupné z: https://dx.doi.org/10.1371/journal.pone.0144753.
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