Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Lisa H. Apken"'
Autor:
Stephanie Beel, Lina Kolloch, Lisa H. Apken, Lara Jürgens, Andrea Bolle, Nadine Sudhof, Sankar Ghosh, Eva Wardelmann, Michael Meisterernst, Konrad Steinestel, Andrea Oeckinghaus
Publikováno v:
Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
The molecular mechanisms of acinar-to-ductal metaplasia (ADM) in the course of pancreatitis and cancer development are unclear. Here, the authors show that loss of κB-Ras and consequent Ral activation promotes tumour initiation and progression throu
Externí odkaz:
https://doaj.org/article/e878ae5e8abb4a2ba7984f050a3bbfcc
Autor:
Lisa H, Apken, Andrea, Oeckinghaus
Publikováno v:
International review of cell and molecular biology. 361
The RAL proteins RALA and RALB belong to the superfamily of small RAS-like GTPases (guanosine triphosphatases). RAL GTPases function as molecular switches in cells by cycling through GDP- and GTP-bound states, a process which is regulated by several
Autor:
Andrea Oeckinghaus, Lisa H. Apken
Publikováno v:
Signal Transduction in Cancer and Immunity ISBN: 9780128237571
The RAL proteins RALA and RALB belong to the superfamily of small RAS-like GTPases (guanosine triphosphatases). RAL GTPases function as molecular switches in cells by cycling through GDP- and GTP-bound states, a process which is regulated by several
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::42f0711fc9ef19bb142b8b4cdadc1a98
https://doi.org/10.1016/bs.ircmb.2020.10.005
https://doi.org/10.1016/bs.ircmb.2020.10.005
Autor:
Lisa H. Apken, Andrea Bolle, Lara Jürgens, Stephanie Beel, Konrad Steinestel, Lina Kolloch, Nadine Sudhof, Michael Meisterernst, Sankar Ghosh, Andrea Oeckinghaus, Eva Wardelmann
Publikováno v:
Nature Communications
Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020)
Pancreatic ductal adenocarcinoma (PDAC) is associated with high mortality and therapy resistance. Here, we show that low expression of κB-Ras GTPases is frequently detected in PDAC and correlates with higher histologic grade. In a model of KRasG12D-
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a87c16063203f89f82bc09bb1d35b205
Autor:
Luisa F. Escobar-Hoyos, Peter Bailey, Karen Bai, Andrew V. Biankin, Srivatsan Raghavan, Daniel Dominguez, Daniel Kümmel, Andrew J. Aguirre, Grant A. Goda, Lisa H. Apken, Robert K. Bradley, Fong Cheng Pan, Simon J. Hogg, Cristian D. Cruz, Nicolas Lecomte, Barry S. Taylor, Joseph Saglimbeni, Paul Ogrodowski, Sruthi Babu, Kenneth R. Shroyer, Chun-Hao Pan, Hana Cho, Alex Penson, Brian M. Wolpin, Olivera Grbovic-Huezo, Scott W. Lowe, Renhe Luo, Yu-Jui Ho, Alessandro Pastore, John P. Morris, Andrea Oeckinghaus, David K. Chang, Andrea Ventura, Channing J. Der, Jerry P. Melchor, Sharon A. Lawrence, Steven D. Leach, Gokce Askan, Ram Kannan, Rohit Singh, Omar Abdel-Wahab, Direna Alonso-Curbelo, G. Aaron Hobbs, Jonathan Bermeo
Publikováno v:
Cancer Cell
Pancreatic ductal adenocarcinoma (PDAC) is driven by co-existing mutations in KRAS and TP53. However, how these mutations collaborate to promote this cancer is unknown. Here, we uncover sequence-specific changes in RNA splicing enforced by mutant p53