Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Torben Hunck"'
Autor:
Giulia Biancon, Poorval Joshi, Joshua T. Zimmer, Torben Hunck, Yimeng Gao, Mark D. Lessard, Edward Courchaine, Andrew E.S. Barentine, Martin Machyna, Valentina Botti, Ashley Qin, Rana Gbyli, Amisha Patel, Yuanbin Song, Lea Kiefer, Gabriella Viero, Nils Neuenkirchen, Haifan Lin, Joerg Bewersdorf, Matthew D. Simon, Karla M. Neugebauer, Toma Tebaldi, Stephanie Halene
Publikováno v:
Mol Cell
Splicing factor mutations are common among cancers, recently emerging as drivers of myeloid malignancies. U2AF1 carries hotspot mutations in its RNA-binding motifs; however, how they affect splicing and promote cancer remain unclear. The U2AF1/U2AF2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a9732eb1548edc00558760338c886ade
https://europepmc.org/articles/PMC8988922/
https://europepmc.org/articles/PMC8988922/
Autor:
Toma Tebaldi, Mark D. Lessard, Joshua T. Zimmer, Gabriella Viero, Poorval Joshi, Valentina Botti, Ashley Qin, Karla M. Neugebauer, Giulia Biancon, Torben Hunck, Rana Gbyli, Lea Kiefer, Andrew Es Barentine, Joerg Bewersdorf, Edward M. Courchaine, Yuanbin Song, Matthew D. Simon, Nils Neuenkirchen, Stephanie Halene, Martin Machyna, Haifan Lin, Amisha Patel, Yimeng Gao
Somatic mutations in splicing factors are of significant interest in myeloid malignancies and other cancers. U2AF1, together with U2AF2, is essential for 3’ splice site recognition. U2AF1 mutations result in aberrant splicing, but the molecular mec
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::ee3ecf3e301da6963e53d2e34aaabe26
https://doi.org/10.1101/2021.04.22.441020
https://doi.org/10.1101/2021.04.22.441020
Autor:
Giulia Biancon, Poorval Joshi, Joshua T Zimmer, Torben Hunck, Yimeng Gao, Mark D Lessard, Edward Courchaine, Andrew ES Barentine, Martin Machyna, Valentina Botti, Ashley Qin, Rana Gbyli, Amisha Patel, Yuanbin Song, Lea Kiefer, Gabriella Viero, Nils Neuenkirchen, Haifan Lin, Joerg Bewersdorf, Matthew D Simon, Karla M Neugebauer, Toma Tebaldi, Stephanie Halene
Publikováno v:
Blood. 138:321-321
Somatic mutations in splicing factor genes are drivers of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). The splicing factors U2AF1 and U2AF2 form the U2AF heterodimer that is critical in the 3' splice site (3'SS) recognition and i
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::555d27e6450c6e578e8e60c9b5020b9d
https://doi.org/10.1182/blood-2021-149618
https://doi.org/10.1182/blood-2021-149618
Autor:
Torben Hunck, Giulia Biancon, Rana Gbyli, Toma Tebaldi, Anastasia Ardasheva, Nils Neuenkirchen, Xiaoying Fu, Haifan Lin, Valentina Botti, Karla M. Neugebauer, Josh Zimmer, Matthew D. Simon, Amisha Patel, Martin Machyna, Gabriella Viero, Poorval Joshi, Stephanie Halene, Yimeng Gao, Ashley Taylor, Ashley Qin
Publikováno v:
Blood. 136:3-4
Spliceosomal gene mutations function as drivers of hematologic malignancies and other cancers with an occurrence of more than 50% in myelodysplastic syndromes and secondary acute myeloid leukemia. Hotspot mutations S34F and Q157R in the two zinc fing
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::bc70ddf09b648f11e42de46c47b39c3d
https://doi.org/10.1182/blood-2020-142854
https://doi.org/10.1182/blood-2020-142854
Autor:
Valentina Botti, Toma Tebaldi, Ashley Qin, Giulia Biancon, Anastasia Ardasheva, Stephanie Halene, Clara L. Kielkopf, Ashley Taylor, Xiaoying Fu, Karla M. Neugebauer, Gabriella Viero, Manoj M. Pillai, Mukhtar Sadykov, Poorval Joshi, Yimeng Gao, Nils Neuenkirchen, Xiaman Wang, Torben Hunck, Haifan Lin, Jane Huang
Publikováno v:
Blood. 134:1230-1230
Among genetic aberrations responsible for ineffective hematopoiesis in myelodysplastic syndromes (MDS) and acute myeloid leukemia, somatic mutations in splicing factors such as U2AF1 are of significant interest as they are recurrent, mutually exclusi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::b3658981348360e51c35e50c6dfb8891
https://doi.org/10.1182/blood-2019-130759
https://doi.org/10.1182/blood-2019-130759