A Novel Interaction between TFII-I and Mdm2 with a Negative
Effect on TFII-I Transcriptional Activity

J 2015

A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity

CETKOVSKÁ, Kateřina, Hana ŠUSTOVÁ, Pavlína KOSZTYU a Stjepan ULDRIJAN

Základní údaje

Originální název

A Novel Interaction between TFII-I and Mdm2 with a Negative Effect on TFII-I Transcriptional Activity

Autoři

CETKOVSKÁ, Kateřina (203 Česká republika, domácí), Hana ŠUSTOVÁ (203 Česká republika, domácí), Pavlína KOSZTYU (203 Česká republika, domácí) a Stjepan ULDRIJAN (203 Česká republika, garant, domácí)

Vydání

Plos one, San Francisco, Public Library of Science, 2015, 1932-6203

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 3.057

Kód RIV

RIV/00216224:14110/15:00081495

Organizační jednotka

Lékařská fakulta

DOI

http://dx.doi.org/10.1371/journal.pone.0144753

UT WoS

000366903600085

Klíčová slova anglicky

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

Štítky

EL OK

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 20. 1. 2016 13:28, Ing. Mgr. Věra Pospíšilíková

Anotace

V originále

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.

Návaznosti

GA301/09/1324, projekt VaV

Název: Funkce centrální domény onkoproteinu Mdm2 a jejích nových vazebných partnerů při regulaci nádorového supresoru p53

Investor: Grantová agentura ČR, Funkce centrální domény onkoproteinu Mdm2 a jejich nových vazebných partnerů při regulaci nádorového supresoru p53

MUNI/A/1123/2014, interní kód MU

Název: Molekulární a buněčná biomedicína (Akronym: MBB)

Investor: Masarykova univerzita, Molekulární a buněčná biomedicína, DO R. 2020_Kategorie A - Specifický výzkum - Studentské výzkumné projekty

Citovat

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. 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.

@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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