Papers on
AML1
A Rare Cytogenetic Presentation of Acute Myeloid Leukemia (AML-M2).Mir Mazloumi et al., Bengaluru, India. In Acta Med Iran, Dec 2012
Acute myeloid leukemia (AML) with t(8;21)(q22;q22) generating the AML1/ETO fusion gene on 8q22 is a distinct type of AML t(8;21) category (WHO)/AML-M2 (FAB), generally associated with a favourable prognosis.
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.Johnstone et al., Melbourne, Australia. In Cell Death Dis, Dec 2012
This notion is supported by biochemical studies demonstrating aberrant recruitment of epigenetic enzymes such as histone deacetylases (HDACs) and histone methyltransferases to promoter regions through association with oncogenic fusion proteins such as PML-RARα and AML1-ETO.
[Involvement of Wnt signaling in hippocampal plasticity].In Ross Fiziol Zh Im I M Sechenova, Dec 2012
A special attention is devoted to glycogen synthase kinase 3beta (GSK-3beta), one of most important from both plasticity and pathology perspectives component of the canonical Wnt pathway.
[Transcription factor RUNX1].Kantidze et al., In Mol Biol (mosk), Nov 2012
Transcription factor RUNX1 is one of the key regulatory proteins in vertebrates.
Epigenetic mechanisms in leukemia.Stein et al., Worcester, United States. In Adv Biol Regul, Sep 2012
For example, the oncogenic AML1-ETO protein, which results from a chromosomal translocation between chromosomes 8 and 21, is expressed in nearly 25% of all acute myelogenous leukemias, disrupts Runx1 subnuclear localization during interphase and compromises transcriptional regulation.