PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27906185-0 2016 Anti-proliferative activity of the NPM1 interacting natural product avrainvillamide in acute myeloid leukemia. avrainvillamide 68-83 nucleophosmin 1 Homo sapiens 35-39 27906185-2 2016 Here we examined the in vitro and in vivo anti-leukemic activity of the NPM1 and chromosome region maintenance 1 homolog (CRM1) interacting natural product avrainvillamide (AVA) and a fully syntetic AVA analog. avrainvillamide 156-171 nucleophosmin 1 Homo sapiens 72-76 27906185-2 2016 Here we examined the in vitro and in vivo anti-leukemic activity of the NPM1 and chromosome region maintenance 1 homolog (CRM1) interacting natural product avrainvillamide (AVA) and a fully syntetic AVA analog. avrainvillamide 156-171 exportin 1 Homo sapiens 122-126 27906185-2 2016 Here we examined the in vitro and in vivo anti-leukemic activity of the NPM1 and chromosome region maintenance 1 homolog (CRM1) interacting natural product avrainvillamide (AVA) and a fully syntetic AVA analog. avrainvillamide 173-176 exportin 1 Homo sapiens 122-126 27906185-6 2016 AVA treatment induced nuclear retention of the NPM1 mutant protein (NPMc+) in OCI-AML3 cells and primary AML cells, caused proteasomal degradation of NPMc+ and the nuclear export factor CRM1 and downregulated wt FLT3 protein. avrainvillamide 0-3 nucleophosmin 1 Homo sapiens 47-51 27906185-6 2016 AVA treatment induced nuclear retention of the NPM1 mutant protein (NPMc+) in OCI-AML3 cells and primary AML cells, caused proteasomal degradation of NPMc+ and the nuclear export factor CRM1 and downregulated wt FLT3 protein. avrainvillamide 0-3 exportin 1 Homo sapiens 186-190 27906185-6 2016 AVA treatment induced nuclear retention of the NPM1 mutant protein (NPMc+) in OCI-AML3 cells and primary AML cells, caused proteasomal degradation of NPMc+ and the nuclear export factor CRM1 and downregulated wt FLT3 protein. avrainvillamide 0-3 fms related receptor tyrosine kinase 3 Homo sapiens 212-216