Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Nadja Bitomsky"'
Autor:
M. Liebl, Thomas G. Hofmann, M. Meister, S. Schumacher, Christoph Herbel, Sonja Matt, Eva Krieghoff-Henning, V. Greiner, Nadja Bitomsky, E. Conrad, B. Kriznik, Tilman Polonio-Vallon
Publikováno v:
Cell Death and Differentiation
Upon severe DNA damage a cellular signalling network initiates a cell death response through activating tumour suppressor p53 in association with promyelocytic leukaemia (PML) nuclear bodies. The deacetylase Sirtuin 1 (SIRT1) suppresses cell death af
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1fb63bafb4af070b088b353ec8866d95
https://doi.org/10.1038/cdd.2015.75
https://doi.org/10.1038/cdd.2015.75
Publikováno v:
BioEssays. 35:55-64
In response to DNA-damage, cells have to decide between different cell fate programmes. Activation of the tumour suppressor HIPK2 specifies the DNA damage response (DDR) and tips the cell fate balance towards an apoptotic response. HIPK2 is activated
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c93224b0b229eb5a1437a859331ec8f0
https://doi.org/10.1002/bies.201200060
https://doi.org/10.1002/bies.201200060
Autor:
Thomas G. Hofmann, Nadja Bitomsky
Publikováno v:
FEBS Journal. 276:6074-6083
Genomic stability is constantly threatened by DNA damage, caused by numerous environmental and intrinsic sources, including radiation, chemicals and oncogene expression. Consequently, cells have evolved a sophisticated signal transduction network to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5595872e252a98543d10c27fe8eef39b
https://doi.org/10.1111/j.1742-4658.2009.07331.x
https://doi.org/10.1111/j.1742-4658.2009.07331.x
Publikováno v:
Oncogene. 23:7484-7493
The transformation suppressor gene Pdcd4 (programmed cell death gene 4) inhibits the tumor-promoter mediated transformation of mouse keratinocytes and has recently been implicated as a potential tumor suppressor gene in the development of human lung
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7b4e4a2cb00cf4b615f27da1159ab897
https://doi.org/10.1038/sj.onc.1208064
https://doi.org/10.1038/sj.onc.1208064
Autor:
Vera Greiner, Thomas G. Hofmann, Carolina Glas, Elisa Conrad, Francesca Peri, Kathrin Schultheiss, Christoph Herbel, Dirk Sombroek, Nadja Bitomsky, Christian Moritz, Fiamma Mantovani, Tilman Polonio-Vallon, Giannino Del Sal
Publikováno v:
Proceedings of the National Academy of Sciences
Excessive genome damage activates the apoptosis response. Protein kinase HIPK2 is a key regulator of DNA damage-induced apoptosis. Here, we deciphered the molecular mechanism of HIPK2 activation and show its relevance for DNA damage-induced apoptosis
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1c5ea1d50ca2efa391d6caca5bd88909
https://doi.org/10.5167/uzh-183597
https://doi.org/10.5167/uzh-183597
Autor:
Nadja, Bitomsky, Thomas G, Hofmann
Publikováno v:
The FEBS journal. 276(21)
Genomic stability is constantly threatened by DNA damage, caused by numerous environmental and intrinsic sources, including radiation, chemicals and oncogene expression. Consequently, cells have evolved a sophisticated signal transduction network to
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::cd7649888cc62c99cccc47bcc3bfa277
https://pubmed.ncbi.nlm.nih.gov/19788416
https://pubmed.ncbi.nlm.nih.gov/19788416
Publikováno v:
Cancer letters. 292(1)
The molecular mechanisms by which hypoxic tumor cells escape radio- and chemotherapy are largely unclear. Homeodomain-interacting protein kinase 2 (HIPK2) drives the apoptotic program in response to DNA-damaging chemotherapeutic drug treatment by pho
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::578c51140a726d338df9d2a114ed1f19
https://pubmed.ncbi.nlm.nih.gov/20018442
https://pubmed.ncbi.nlm.nih.gov/20018442
Publikováno v:
Oncogene. 27(35)
The transformation suppressor gene, programmed cell death gene 4 (Pdcd4), inhibits tumor-promoter-mediated transformation of mouse keratinocytes and has been implicated as a tumor suppressor gene in the development of human cancer. The Pdcd4 protein
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c8031d86c0b441dc3ac7b32b87d44cad
https://pubmed.ncbi.nlm.nih.gov/18427550
https://pubmed.ncbi.nlm.nih.gov/18427550