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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Meis homeobox 1

Homeobox genes, of which the most well-characterized category is represented by the HOX genes, play a crucial role in normal development. In addition, several homeoproteins are involved in neoplasia. This gene encodes a homeobox protein belonging to the TALE ('three amino acid loop extension') family of homeodomain-containing proteins. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HOXA9, MLL, CAN, Histone, ACID
Papers on Meis1
RING1 proteins contribute to early proximal-distal specification of the forelimb bud by restricting Meis2 expression.
Koseki et al., Kawasaki, Japan. In Development, Feb 2016
We show that preferential defects in early distal specification in Ring1A/B-deficient forelimb buds accompany failures in the repression of proximal signal circuitry bound by RING1B, including Meis1/2, and the activation of distal signal circuitry in the prospective distal region.
PBX3 and MEIS1 cooperate in hematopoietic cells to drive acute myeloid leukemias characterized by a core transcriptome of the MLL-rearranged disease.
Chen et al., Chapel Hill, United States. In Cancer Res, Feb 2016
UNASSIGNED: Overexpression of HOXA/MEIS1/PBX3 homeobox genes is the hallmark of mixed lineage leukemia (MLL)-rearranged acute myeloid leukemia (AML).
Prevalence and Determinants of Periodic Limb Movements in the General Population.
Heinzer et al., Lausanne, Switzerland. In Ann Neurol, Jan 2016
Single nucleotide polymorphisms (SNP) within BTBD9 (rs3923809), TOX3 (rs3104788) and MEIS1 (rs2300478) genes were significantly associated with PLSMI>15/h.
Susceptible genes of restless legs syndrome in migraine.
Wang et al., Taipei, Taiwan. In Cephalalgia, Jan 2016
METHODS: Thirteen single-nucleotide polymorphisms (SNPs) at six RLS risk loci (MEIS1, BTBD9, MAP2K5, PTPRD, TOX3, and an intergenic region on chromosome 2p14) were genotyped in 211 migraine patients with RLS and 781 migraine patients without RLS.
DNA-dependent formation of transcription factor pairs alters their binding specificity.
Taipale et al., Seychelles. In Nature, Dec 2015
Structural analysis of the TF pairs, including a novel crystal structure of MEIS1 and DLX3 bound to their identified recognition site, revealed that the interactions between the TFs were predominantly mediated by DNA.
PU.1 affects proliferation of the human acute myeloid leukemia U937 cell line by directly regulating MEIS1.
Guan et al., Beijing, China. In Oncol Lett, Sep 2015
In the present study, PU.1 siRNA was demonstrated to efficiently inhibit the transcription level of oncogene MEIS1 in the human acute myeloid non-MLL leukemia U937 cell line.
Targeting DOT1L and HOX gene expression in MLL-rearranged leukemia and beyond.
Armstrong et al., New York City, United States. In Exp Hematol, Aug 2015
These MLL1 fusion oncoproteins drive the expression of homeobox genes such as HOXA cluster genes and myeloid ecotropic viral integration site 1 homolog (MEIS1), which are known to induce leukemic transformation of hematopoietic progenitors.
Biochemistry of the tale transcription factors PREP, MEIS, and PBX in vertebrates.
Blasi et al., Milano, Italy. In Dev Dyn, 2014
Finally, recent advances in determining the genome-wide DNA-binding sites of PREP1, MEIS1, and PBX1, and their partial correspondence with the binding sites of some HOX proteins, are reviewed.
Restless legs syndrome: update on pathogenesis.
Winkelmann et al., Palo Alto, United States. In Curr Opin Pulm Med, 2013
RECENT FINDINGS: Genome-wide association studies identified six genetic variants including MEIS1 and BTBD9 with potential relationships with iron.
MicroRNAs mark in the MLL-rearranged leukemia.
Vartholomatos et al., Préveza, Greece. In Ann Hematol, 2013
Mixed lineage leukemia (MLL) gene encodes a protein with histone methyltransferase activity, which is essential for the fine tuning of hematopoietic stem cell development and differentiation through the regulation of HOXA and MEIS1.
Blockade of miR-150 maturation by MLL-fusion/MYC/LIN-28 is required for MLL-associated leukemia.
Chen et al., Chicago, United States. In Cancer Cell, 2012
Forced expression of miR-150 dramatically inhibited leukemic cell growth and delayed MLL-fusion-mediated leukemogenesis, likely through targeting FLT3 and MYB and thereby interfering with the HOXA9/MEIS1/FLT3/MYB signaling network, which in turn caused downregulation of MYC/LIN28.
Segregation of eye and antenna fates maintained by mutual antagonism in Drosophila.
Sun et al., Taipei, Taiwan. In Development, 2012
Loss of Ct and Hth in the antenna disc resulted in ectopic eye development in the antenna.
Dual actions of Meis1 inhibit erythroid progenitor development and sustain general hematopoietic cell proliferation.
Murphy et al., Saint Louis, United States. In Blood, 2012
overexpression of Meis1 repressed the development of early erythroid progenitors, acting in vivo at the megakaryocyte-erythroid progenitor stage to skew development away from erythroid generation and toward megakaryocyte development
Selective treatment of mixed-lineage leukemia leukemic stem cells through targeting glycogen synthase kinase 3 and the canonical Wnt/β-catenin pathway.
So et al., London, United Kingdom. In Curr Opin Hematol, 2012
RECENT FINDINGS: Glycogen synthase kinase 3 (GSK3) plays a critical role in mediating Hox/MEIS1 transcriptional program and its inhibition shows promise in suppressing leukemia carrying MLL fusions or aberrant Hox expression.
Downregulation of MEIS1 impairs long-term expansion of CD34+ NPM1-mutated acute myeloid leukemia cells.
Huls et al., In Leukemia, 2012
the cellular context in which HOX/MEIS1 is overexpressed appears to be very important, and other relevant genes are most likely required as well to maintain the expanding capacity of the CD34thorn NPMcthorn acute myeloid leukemia cells
miR-196b directly targets both HOXA9/MEIS1 oncogenes and FAS tumour suppressor in MLL-rearranged leukaemia.
Chen et al., Chicago, United States. In Nat Commun, 2011
findings show that HOXA9 and MEIS1 are direct targets of miRNA-196b, a microRNA located adjacent to and co-expressed with HOXA9, in MLL-rearranged leukaemic cells
Cell of origin in AML: susceptibility to MN1-induced transformation is regulated by the MEIS1/AbdB-like HOX protein complex.
Humphries et al., Vancouver, Canada. In Cancer Cell, 2011
Complementation studies of CMP-signature genes in GMPs demonstrated that MN1-leukemogenicity required the MEIS1/AbdB-like HOX-protein complex.
MEIS1, PREP1, and PBX4 are differentially expressed in acute lymphoblastic leukemia: association of MEIS1 expression with higher proliferation and chemotherapy resistance.
Jave-Suárez et al., Guadalajara, Mexico. In J Exp Clin Cancer Res, 2010
up-regulation of MEIS1 is important for sustaining proliferation of leukemic cells and that down-regulation of MEIS1
Combinatorial transcriptional control in blood stem/progenitor cells: genome-wide analysis of ten major transcriptional regulators.
Göttgens et al., Cambridge, United Kingdom. In Cell Stem Cell, 2010
Here, we report the genome-wide binding patterns and combinatorial interactions for ten key regulators of blood stem/progenitor cells (SCL/TAL1, LYL1, LMO2, GATA2, RUNX1, MEIS1, PU.1, ERG, FLI-1, and GFI1B), thus providing the most comprehensive TF data set for any adult stem/progenitor cell type to date.
GSK-3 promotes conditional association of CREB and its coactivators with MEIS1 to facilitate HOX-mediated transcription and oncogenesis.
Cleary et al., Stanford, United States. In Cancer Cell, 2010
GSK-3 maintains the MLL leukemia stem cell transcriptional program by promoting the conditional association of CREB and its coactivators TORC and CBP with homedomain protein MEIS1, which in turn facilitates HOX-mediated transcription and transformation.
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