Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Deborah Shan‐Krauer"'
Autor:
Nina Orfali, Deborah Shan‐Krauer, Tracey R. O’Donovan, Nigel P. Mongan, Lorraine J. Gudas, Mary R. Cahill, Mario P. Tschan, Sharon L. McKenna
Publikováno v:
Molecular Oncology, Vol 14, Iss 6, Pp 1297-1309 (2020)
Ubiquitin/ISG15‐conjugating enzyme E2L6 (UBE2L6) is a critical enzyme in ISGylation, a post‐translational protein modification that conjugates the ubiquitin‐like modifier, interferon‐stimulated gene 15 (ISG15), to target substrates. Previous
Externí odkaz:
https://doaj.org/article/d6f2dd270c9a47d8aa678254a9db298c
Autor:
Elena A. Federzoni, Severin Gloor, Jing Jin, Deborah Shan-Krauer, Martin F. Fey, Bruce E. Torbett, Mario P. Tschan
Publikováno v:
Leukemia Research Reports, Vol 4, Iss 1, Pp 32-35 (2015)
In an mRNA profiling screen performed to unveil novel mechanisms of leukemogenesis, we found that the sentrin-specific protease 5 (SENP5) was significantly repressed in clinical acute myeloid leukemia when compared to healthy neutrophil samples. SENP
Externí odkaz:
https://doaj.org/article/69215a012400486e927be1cc503d2cad
Autor:
Sharon L. McKenna, Deborah Shan-Krauer, Mario P. Tschan, Nina Orfali, Mary R. Cahill, Tracey R. O’Donovan, Lorraine J. Gudas, Nigel P. Mongan
Publikováno v:
Orfali, Nina; Shan-Krauer, Deborah; O'Donovan, Tracey R; Mongan, Nigel P; Gudas, Lorraine J; Cahill, Mary R; Tschan, Mario P.; McKenna, Sharon L (2020). Inhibition of UBE2L6 attenuates ISGylation and impedes ATRA-induced differentiation of leukemic cells. Molecular oncology, 14(6), pp. 1297-1309. Wiley 10.1002/1878-0261.12614
Molecular Oncology
Molecular Oncology, Vol 14, Iss 6, Pp 1297-1309 (2020)
Molecular Oncology
Molecular Oncology, Vol 14, Iss 6, Pp 1297-1309 (2020)
Ubiquitin/ISG15‐conjugating enzyme E2L6 (UBE2L6) is a critical enzyme in ISGylation, a post‐translational protein modification that conjugates the ubiquitin‐like modifier, interferon‐stimulated gene 15 (ISG15), to target substrates. Previous
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::10006782c9d47cbf5decb8a44761b933
https://boris.unibe.ch/138110/1/Orfali_et_al-2019-Molecular_Oncology.pdf
https://boris.unibe.ch/138110/1/Orfali_et_al-2019-Molecular_Oncology.pdf
Autor:
Deborah Shan-Krauer, Thomas Kaufmann, Elena A. Federzoni, Magali Humbert, Steffen Frese, Aladin Haimovici, Thomas Brunner, Bruce E. Torbett, Mario P. Tschan
Publikováno v:
Cell Death Differ
The hematopoietic Ets-domain transcription factor PU.1/SPI1 orchestrates myeloid, B- and T-cell development, and also supports hematopoietic stem cell maintenance. Although PU.1 is a renowned tumor suppressor in acute myeloid leukemia (AML), a diseas
Autor:
Shida Yousefi, Jing Jin, Anna M. Schläfli, Hans-Uwe Simon, Jasmin Batliner, Deborah Shan-Krauer, Mario P. Tschan, Magali Humbert, Marion Ernst, Bruce E. Torbett, Adrian Britschgi, Elena A. Federzoni
Publikováno v:
Oxidative Medicine and Cellular Longevity
Oxidative Medicine and Cellular Longevity, Vol 2018 (2018)
Jin, Jing; Britschgi, Adrian; Schläfli, Anna M.; Humbert, Magali; Shan-Krauer, Deborah; Batliner, Jasmin; Federzoni, Elena A.; Ernst, Marion; Torbett, Bruce E.; Yousefi, Shida; Simon, Hans-Uwe; Tschan, Mario (2018). Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy. Oxidative medicine and cellular longevity, 2018, p. 1482795. Hindawi 10.1155/2018/1482795
Oxidative Medicine and Cellular Longevity, Vol 2018 (2018)
Jin, Jing; Britschgi, Adrian; Schläfli, Anna M.; Humbert, Magali; Shan-Krauer, Deborah; Batliner, Jasmin; Federzoni, Elena A.; Ernst, Marion; Torbett, Bruce E.; Yousefi, Shida; Simon, Hans-Uwe; Tschan, Mario (2018). Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy. Oxidative medicine and cellular longevity, 2018, p. 1482795. Hindawi 10.1155/2018/1482795
Autophagy is an intracellular degradation system that ensures a dynamic recycling of a variety of building blocks required for self-renewal, homeostasis, and cell survival under stress. We used primary acute myeloid leukemia (AML) samples and human A
Autor:
Severin Gloor, Jing Jin, Deborah Shan-Krauer, Mario P. Tschan, Elena A. Federzoni, Martin F. Fey, Bruce E. Torbett
Publikováno v:
Federzoni, Elena; Gloor, Severin; Jin, Jing; Krauer, Deborah; Fey, Martin; Torbett, Bruce E; Tschan, Mario (2015). Linking the SUMO protease SENP5 to neutrophil differentiation of AML cells. Leukemia research reports, 4(1), pp. 32-35. Elsevier 10.1016/j.lrr.2015.04.002
Leukemia Research Reports
Leukemia research reports
Leukemia Research Reports, Vol 4, Iss 1, Pp 32-35 (2015)
Leukemia Research Reports
Leukemia research reports
Leukemia Research Reports, Vol 4, Iss 1, Pp 32-35 (2015)
In an mRNA profiling screen performed to unveil novel mechanisms of leukemogenesis, we found that the sentrin-specific protease 5 (SENP5) was significantly repressed in clinical acute myeloid leukemia when compared to healthy neutrophil samples. SENP
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a7ad490668c7f691874ddba046413c5f
https://boris.unibe.ch/70313/1/1-s2.0-S2213048914200112-main.pdf
https://boris.unibe.ch/70313/1/1-s2.0-S2213048914200112-main.pdf