Zobrazeno 1 - 10
of 37
pro vyhledávání: '"Mizuki Azuma"'
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 11 (2023)
EWSR1 (Ewing sarcoma breakpoint region 1) was originally identified as a part of an aberrant EWSR1/FLI1 fusion gene in Ewing sarcoma, the second most common pediatric bone cancer. Due to formation of the EWSR1/FLI1 fusion gene in the tumor genome, th
Externí odkaz:
https://doaj.org/article/0ddbbfbf64d24010b6277a5cbd7aab86
Autor:
Chris Merkes, Timothy K Turkalo, Nicole Wilder, Hyewon Park, Luke W Wenger, Seth J Lewin, Mizuki Azuma
Publikováno v:
PLoS ONE, Vol 10, Iss 1, p e0116627 (2015)
Ewing sarcoma is the second most common skeletal (bone and cartilage) cancer in adolescents, and it is characterized by the expression of the aberrant chimeric fusion gene EWS/FLI1. Wild-type EWS has been proposed to play a role in mitosis, splicing
Externí odkaz:
https://doaj.org/article/ea167aecbf3a4fd097855d0e478e839b
Publikováno v:
PLoS ONE, Vol 2, Iss 10, p e979 (2007)
BACKGROUND:The Ewing sarcoma breakpoint region 1 gene (EWSR1), also known as EWS, is fused to a number of different partner genes as a result of chromosomal translocation in diverse sarcomas. Despite the involvement of EWSR1 in these diverse sarcomas
Externí odkaz:
https://doaj.org/article/fdf7b61619934eb695911bf6a8a03895
Supplementary Figure 2 from Ewing Sarcoma Fusion Protein EWSR1/FLI1 Interacts with EWSR1 Leading to Mitotic Defects in Zebrafish Embryos and Human Cell Lines
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::837d88ed76e3d715b80375b83f2d9fd1
https://doi.org/10.1158/0008-5472.22377480
https://doi.org/10.1158/0008-5472.22377480
Supplementary Figure 1 from Ewing Sarcoma Fusion Protein EWSR1/FLI1 Interacts with EWSR1 Leading to Mitotic Defects in Zebrafish Embryos and Human Cell Lines
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11fd327ddd3a3e742701ce7bc8fe3a3b
https://doi.org/10.1158/0008-5472.22377483.v1
https://doi.org/10.1158/0008-5472.22377483.v1
Supplementary Figure 4 from Ewing Sarcoma Fusion Protein EWSR1/FLI1 Interacts with EWSR1 Leading to Mitotic Defects in Zebrafish Embryos and Human Cell Lines
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2d5bbd29a878a61998bfda302901053a
https://doi.org/10.1158/0008-5472.22377474
https://doi.org/10.1158/0008-5472.22377474
Supplementary Figure 5 from Ewing Sarcoma Fusion Protein EWSR1/FLI1 Interacts with EWSR1 Leading to Mitotic Defects in Zebrafish Embryos and Human Cell Lines
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3dd5ef95d776c8d6b00156ee89d3d0d8
https://doi.org/10.1158/0008-5472.22377471.v1
https://doi.org/10.1158/0008-5472.22377471.v1
Supplementary Figure 3 from Ewing Sarcoma Fusion Protein EWSR1/FLI1 Interacts with EWSR1 Leading to Mitotic Defects in Zebrafish Embryos and Human Cell Lines
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0662941c914a073fd2b59ba960871424
https://doi.org/10.1158/0008-5472.22377477.v1
https://doi.org/10.1158/0008-5472.22377477.v1
Autor:
Chengjian Zhao, Jonathan Matalonga, Joseph J. Lancman, Lu Liu, Chaoxin Xiao, Shiv Kumar, Keith P. Gates, Jiaye He, Alyssa Graves, Jan Huisken, Mizuki Azuma, Zhenghao Lu, Chong Chen, Bi-Sen Ding, P. Duc Si Dong
Publikováno v:
Proceedings of the National Academy of Sciences. 119
Despite the robust healing capacity of the liver, regenerative failure underlies numerous hepatic diseases, including the JAG1 haploinsufficient disorder, Alagille syndrome (ALGS). Cholestasis due to intrahepatic duct (IHD) paucity resolves in certai
EWSR1 (Ewing sarcoma breakpoint region 1) was originally identified as a part of an aberrant EWSR1/FLI1 fusion gene in Ewing sarcoma, the second most common pediatric bone cancer. Due to formation of the EWSR1/FLI1 fusion gene in the tumor genome, th
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d1d21f4b91c8a470a2c1136aa2096eec
https://doi.org/10.1101/2022.06.17.496636
https://doi.org/10.1101/2022.06.17.496636