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  • oncogene
  • It is closely related to FMS PROTO-ONCOGENE PROTEIN and is commonly mutated in acute MYELOID LEUKEMIA. (curehunter.com)
  • PI3K activity is probably regulated through various interactions between FLT3, SH2 -containing sequence proteins (SHCs) and one or more other proteins, such as SH2 -domain-containing inositol phosphatase (SHIP), SH2 -domain containing protein tyrosine phosphatase 2 (SHP2), CBL (a proto-oncogene) and GRB2 -binding protein (GAB2). (diff.org)
  • binds
  • sFlt-1 (soluble fms-like tyrosine kinase-1 - also known as soluble VEGF receptor-1) binds and reduces free circulating levels of the proangiogenic factors VEGF (vascular endothelial growth factor) and PlGF (placental growth factor). (wikipedia.org)
  • and c) the C-terminal DNA-binding domain, ETS, which binds to the consensus DNA sequence, 5-GGAA/T-3 within a 9-to-10 bp sequence, in the target genes it regulates. (wikipedia.org)
  • Its two SH3 domains direct complex formation with proline-rich regions of other proteins, and its SH2 domain binds tyrosine phosphorylated sequences. (wikipedia.org)
  • FLT3-ITD
  • Ama : Bu al mada, ran l normal sitogenetikli akut miyeloid l semi (NS-AML) hastalar nda FMS-benzeri tirozin kinaz 3 (FLT3-ITD ve FLT3-TKD) ile n kleofosmin 1 (NPM1) mutasyonlar n n s kl n de erlendirdik. (tjh.com.tr)
  • Recently, ponatinib was shown to be active against AC220-resistant kinase domain mutants of AML-expressing FLT3-ITD ( 6 , 11 ). (aacrjournals.org)
  • regulates
  • Tamura T. An ataxia-teleaniectasia-mutated (ATM) kinase mediated response to DNA damage down-regulates the mRNA-binding potential of THOC5. (wikipedia.org)
  • Genes
  • THOC5, thereby contributes to the 3′ processing and/or export of immediate-early genes induced by extracellular stimuli. (wikipedia.org)
  • PI3K
  • Activated FLT3 transduces progrowth and prosurvival signaling through STAT5, PI3K/AKT, and RAS/RAF/ERK1/2 pathways ( 2, 3 ). (aacrjournals.org)
  • vivo
  • We show that macaque-specific CCR5 ZFNs efficiently induce CCR5 disruption at levels of up to 64% ex vivo, 40% in vivo early posttransplant, and 3% to 5% in long-term repopulating cells over 6 months following HSPC transplant. (nih.gov)