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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 16 Apr 2015.

Runt-related transcription factor 1

AML1, GSK-3beta, RUNX1, glycogen synthase kinase 3beta
Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. The protein encoded by this gene represents the alpha subunit of CBF and is thought to be involved in the development of normal hematopoiesis. Chromosomal translocations involving this gene are well-documented and have been associated with several types of leukemia. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ETO, HAD, CAN, ETV6, MLL
Papers on AML1
Myeloid and Lymphoid Neoplasm With Abnormalities of FGFR1 Presenting With Trilineage Blasts and RUNX1 Rearrangement: A Case Report and Review of Literature.
New
Luu et al., Dallas, United States. In Am J Clin Pathol, 31 May 2015
We report a case of a patient with a novel t(17;21)(p13;q22) with RUNX1 rearrangement and trilineage blasts.
Adenosine signaling promotes hematopoietic stem and progenitor cell emergence.
New
Zon et al., Cambridge, United States. In J Exp Med, 13 May 2015
Elevated adenosine levels increased runx1(+)/cmyb(+) HSPCs in the dorsal aorta, whereas blocking the adenosine pathway decreased HSPCs.
PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.
Review
New
Badie et al., Oxford, United Kingdom. In Carcinogenesis, 06 Apr 2015
Other mechanisms linked to PU.1 downregulation in human AML include TP53 deletion, Flt3-ITD mutation and the recurrent AML1-ETO [t(8;21)] and PML-RARA [t(15;17)] translocations.
Genetic predisposition syndromes: when should they be considered in the work-up of MDS?
Review
New
Bessler et al., Philadelphia, United States. In Best Pract Res Clin Haematol, 31 Mar 2015
In addition to the classic hereditary bone marrow failure syndromes (BMFS) such as Fanconi Anemia and Dyskeratosis Congenita, in recent years there has been an increased awareness of non-syndromic familial MDS/AML predisposition syndromes such as those caused by mutations in GATA2, RUNX1, CEBPA, and SRP72 genes.
Chemical biology. A small-molecule inhibitor of the aberrant transcription factor CBFβ-SMMHC delays leukemia in mice.
New
Impact
Bushweller et al., Charlottesville, United States. In Science, 13 Mar 2015
The transcription factor fusion CBFβ-SMMHC (core binding factor β and the smooth-muscle myosin heavy chain), expressed in AML with the chromosome inversion inv(16)(p13q22), outcompetes wild-type CBFβ for binding to the transcription factor RUNX1, deregulates RUNX1 activity in hematopoiesis, and induces AML.
Oncogene regulation. An oncogenic super-enhancer formed through somatic mutation of a noncoding intergenic element.
New
Impact
Look et al., Boston, United States. In Science, Jan 2015
MYB binds to this new site and recruits its H3K27 acetylase-binding partner CBP, as well as core components of a major leukemogenic transcriptional complex that contains RUNX1, GATA-3, and TAL1 itself.
Esculetin Downregulates the Expression of AML1-ETO and C-Kit in Kasumi-1 Cell Line by Decreasing Half-Life of mRNA.
New
Saluja et al., New Delhi, India. In J Oncol, Dec 2014
One of the most frequent genetic aberrations in acute myeloid leukemia (AML) is chromosomal translocation between AML1/RUNX1 on chromosome 21 and ETO gene on chromosome 8 resulting in the expression of chimeric oncogene AML1-ETO.
Molecular cytogenetics in childhood acute lymphoblastic leukemia: a hospital-based observational study.
New
Koul et al., Jammu, India. In Clin Med Insights Oncol, Dec 2014
Among the remaining 22 cases, 8 had TEL-AML1 (20%), 6 had BCR-ABL (15%), 4 had MLL-AF4 (10%), 2 had E2A-PBX1 (5%) fusion genes, and 2 had hyperdiploidy.
RUNX1/ETO blocks selectin-mediated adhesion via epigenetic silencing of PSGL-1.
New
Wichmann et al., München, Germany. In Oncogenesis, Dec 2014
RUNX1/ETO (RE), the t(8;21)-derived leukemic transcription factor associated with acute myeloid leukemia (AML) development, deregulates genes involved in differentiation, self-renewal and proliferation.
Genetic and epigenetic pathways in myelodysplastic syndromes: A brief overview.
Review
New
Jhanwar, New York City, United States. In Adv Biol Regul, Dec 2014
The most common driver gene mutations detected in patients with MDS include RNA splicing (SF3B1,SRSF2,U2F1,ZRSR2), DNA methylation (TET2,DNMT3A,IDH1/IDH2), chromatin modification (ASXL1,EZH2), transcription regulation (RUNX1,BCOR) and DNA repair control p53.
Posttranslational modifications of RUNX1 as potential anticancer targets.
Review
New
Mulloy et al., Cincinnati, United States. In Oncogene, Oct 2014
The transcription factor RUNX1 is a master regulator of hematopoiesis.
Somatic mutations predict poor outcome in patients with myelodysplastic syndrome after hematopoietic stem-cell transplantation.
New
Impact
Ebert et al., San Diego, United States. In J Clin Oncol, Oct 2014
PURPOSE: Recurrently mutated genes in myelodysplastic syndrome (MDS) are pathogenic drivers and powerfully associated with clinical phenotype and prognosis.
Targeting transcription regulation in cancer with a covalent CDK7 inhibitor.
New
Impact
Gray et al., Boston, United States. In Nature, Aug 2014
Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects transcription of RUNX1 and suggests that sensitivity to THZ1 may be due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core transcriptional regulatory circuitry of these tumour cells.
Reprogramming human endothelial cells to haematopoietic cells requires vascular induction.
New
Impact
Rafii et al., New York City, United States. In Nature, Aug 2014
Highly purified non-haemogenic human umbilical vein endothelial cells or adult dermal microvascular endothelial cells were transduced with the transcription factors FOSB, GFI1, RUNX1 and SPI1 (hereafter referred to as FGRS), and then propagated on serum-free instructive vascular niche monolayers to induce outgrowth of haematopoietic colonies containing cells with functional and immunophenotypic features of multipotent progenitor cells (MPPs).
Systems biology of megakaryocytes.
Review
Kaushansky et al., Seattle, United States. In Adv Exp Med Biol, 2013
Several transcription factors critical for generating megakaryocytes were identified by promoter analysis of megakaryocyte-specific genes, and their biological roles then verified by gene knockout studies; for example, GATA-1, NF-E2, and RUNX1 were identified in this way.
Hypothalamic glycogen synthase kinase 3β has a central role in the regulation of food intake and glucose metabolism.
GeneRIF
Tups et al., Marburg an der Lahn, Germany. In Biochem J, 2012
increased hypothalamic GSK3beta signalling contributes to deleterious effects of leptin deficiency and exacerbates high-fat diet-induced weight gain and glucose intolerance
Prdm3 and Prdm16 are H3K9me1 methyltransferases required for mammalian heterochromatin integrity.
Impact
GeneRIF
Jenuwein et al., Freiburg, Germany. In Cell, 2012
Data identify Prdm3 and Prdm16 as H3K9me1 methyltransferases and expose a functional framework in which anchoring to the nuclear periphery helps maintain the integrity of mammalian heterochromatin.
Epithelial cell adhesion molecules and epithelial mesenchymal transition (EMT) markers in Ewing's sarcoma family of tumors (ESFTs). Do they offer any prognostic significance?
GeneRIF
Llombart-Bosch et al., Valencia, Spain. In Virchows Arch, 2012
Desmoplakin and pGSK3beta constitute independent good prognostic factors for progression free survival in Ewing Sarcoma patients.
GSK3β/axin-1/β-catenin complex is involved in semaphorin3A signaling.
GeneRIF
Goshima et al., Yokohama, Japan. In J Neurosci, 2012
Semaphorin (Sema)3A induces formation of the GSK3beta/axin-1/beta-catenin complex, which regulates the signaling cascade of Sema3A via an endocytotic mechanism in dorsal root ganglion neurons.
Regulation of postnatal forebrain amoeboid microglial cell proliferation and development by the transcription factor Runx1.
GeneRIF
Stifani et al., Montréal, Canada. In J Neurosci, 2012
This study demonistrated that Runx1 regulate postnatal forebrain amoeboid microglial cell proliferation and development in mice.
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