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pro vyhledávání: '"R L, Redner"'
Recurrent chromosomal translocations involving the RAR alpha locus on chromosome 17 are the hallmark of acute promyelocytic leukemia (APL). The RAR alpha gene fuses to variable partners (PML, PLZF, NPM, NuMA and STAT5B: X genes) leading to the expres
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::0e9a4dd58aeb7b0d74bf3f0783f16066
http://hdl.handle.net/2318/61364
http://hdl.handle.net/2318/61364
Publikováno v:
Blood. 95(8)
The t(5;17) variant of acute promyelocytic leukemia (APL) fuses the genes for nucleophosmin (NPM) and the retinoic acid receptor alpha (RARalpha). Two NPM-RAR molecules are expressed as a result of alternative RNA splicing. Both contain RARalpha sequ
Publikováno v:
Blood. 94(2)
Publikováno v:
Blood. 94(2)
Retinoic acid receptor alpha (RARalpha) is the target of several chromosomal translocations associated with acute promyelocytic leukemias (APLs). These rearrangements fuse RARalpha to different partner genes creating the chimeric proteins: PML-RARalp
Publikováno v:
Cancer research. 59(12)
The (8;21) translocation, found in 12% of acute myeloid leukemia (AML), creates the chimeric fusion product, AML1-ETO. Previously, we demonstrated that the ETO moiety recruits a transcription repression complex that includes the histone deacetylase (
Autor:
S J, Corey, J, Locker, D R, Oliveri, S, Shekhter-Levin, R L, Redner, L, Penchansky, S M, Gollin
Publikováno v:
Leukemia. 8(8)
Acute promyelocytic leukemia (APML) almost always involves a chromosomal translocation t(15:17) that results in the fusion of the retinoic acid receptor alpha (RAR alpha) gene with a transcription factor gene called PML. Several cases of APML with t(
Publikováno v:
Oncogene. 7(1)
Jun (c-jun, jun-B and jun-D) and fos (c-fos, fos-B and fra) proteins dimerize to form the family of AP-1 transcriptional activators. If each dimer exhibits unique transactivating properties, then any phenotypic change should show a characteristic pat
Publikováno v:
Molecular and Cellular Biology. 8:963-973
To study the role of a nuclear proto-oncogene in the regulation of cell growth and differentiation, we inhibited HL-60 c-myc expression with a complementary antisense oligomer. This oligomer was stable in culture and entered cells, forming an intrace
Publikováno v:
Molecular and Cellular Biology. 8:963-973
To study the role of a nuclear proto-oncogene in the regulation of cell growth and differentiation, we inhibited HL-60 c-myc expression with a complementary antisense oligomer. This oligomer was stable in culture and entered cells, forming an intrace