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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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