Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Meiqiongzi Zhang"'
Autor:
Angelos Heldin, Matko Cancer, Mireia Palomar-Siles, Susanne Öhlin, Meiqiongzi Zhang, Alexander Sun-Zhang, Anna Mariani, Jianping Liu, Vladimir J.N. Bykov, Klas G. Wiman
Publikováno v:
RNA Biology, Vol 20, Iss 1, Pp 368-383 (2023)
The TP53 and PTEN tumour suppressor genes are inactivated by nonsense mutations in a significant fraction of human tumours. TP53 nonsense mutant tumours account for approximately one million new cancer cases per year worldwide. We have screened chemi
Externí odkaz:
https://doaj.org/article/daccee69e3db47eebcd34fa7604e554b
Autor:
Mireia Palomar-Siles, Angelos Heldin, Meiqiongzi Zhang, Charlotte Strandgren, Viktor Yurevych, Jip T. van Dinter, Sem A. G. Engels, Damon A. Hofman, Susanne Öhlin, Birthe Meineke, Vladimir J. N. Bykov, Sebastiaan van Heesch, Klas G. Wiman
Publikováno v:
Cell Death and Disease, Vol 13, Iss 11, Pp 1-17 (2022)
Abstract TP53 nonsense mutations in cancer produce truncated inactive p53 protein. We show that 5-FU metabolite 5-Fluorouridine (FUr) induces full-length p53 in human tumor cells carrying R213X nonsense mutant TP53. Ribosome profiling visualized tran
Externí odkaz:
https://doaj.org/article/d20df1692ffe43d69b4b2923e7b6b3b8
Autor:
Meiqiongzi Zhang, Angelos Heldin, Mireia Palomar-Siles, Susanne Öhlin, Vladimir J. N. Bykov, Klas G. Wiman
Publikováno v:
Frontiers in Oncology, Vol 7 (2018)
The tumor suppressor gene TP53 is inactivated by mutation in a large fraction of human tumors. Around 10% of TP53 mutations are nonsense mutations that lead to premature termination of translation and expression of truncated unstable and non-function
Externí odkaz:
https://doaj.org/article/c9f326e71b9542559f7bd6d0988eefe1
Autor:
Mireia Palomar-Siles, Angelos Heldin, Vladimir J.N. Bykov, Meiqiongzi Zhang, Susanne Öhlin, Klas G. Wiman
Publikováno v:
Frontiers in Oncology, Vol 7 (2018)
Frontiers in Oncology
Frontiers in Oncology
The tumor suppressor gene TP53 is inactivated by mutation in a large fraction of human tumors. Around 10% of TP53 mutations are nonsense mutations that lead to premature termination of translation and expression of truncated unstable and non-function
Autor:
Meiqiongzi Zhang, Sophia Ceder, Klas G. Wiman, Lars Abrahmsen, Qiang Zhang, Vladimir J.N. Bykov
Publikováno v:
Frontiers in Oncology
Frontiers in Oncology, Vol 6 (2016)
Frontiers in Oncology, Vol 6 (2016)
TP53 is the most frequently mutated gene in cancer. The p53 protein activates transcription of genes that promote cell cycle arrest or apoptosis, or regulate cell metabolism and other processes . Missense mutations in TP53 abolish specific DNA bindin
Autor:
Bykov, Vladimir J. N., Qiang Zhang, Meiqiongzi Zhang, Ceder, Sophia, Abrahmsen, Lars, Wiman, Klas G.
Publikováno v:
Frontiers in Oncology; 2/3/2016, p1-7, 7p
Autor:
Klas G. Wiman, Meiqiongzi Zhang, Elias S.J. Arnér, Francesca Conserva, Gihan Hosny, Vladimir J.N. Bykov, Galina Selivanova, Xiaoxiao Peng
Publikováno v:
Cell Death & Disease
The low-molecular-weight compound APR-246 (PRIMA-1(MET)) restores wild-type conformation and function to mutant p53, and triggers apoptosis in tumor cells. We show here that APR-246 also targets the selenoprotein thioredoxin reductase 1 (TrxR1), a ke