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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 29 Mar 2014.

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, CAN, HAD, ETV6, Akt
Papers on AML1
The enhancer and promoter landscape of human regulatory and conventional T-cell subpopulations.
Rehli et al., Regensburg, Germany. In Blood, 26 Apr 2014
For all in vitro expanded subsets, we additionally generated global maps of poised and active enhancer elements marked by histone H3 lysine 4 monomethylation and histone H3 lysine 27 acetylation, describe their cell type-specific motif signatures, and evaluate the role of candidate transcription factors STAT5, FOXP3, RUNX1, and ETS1 in both Treg- and Tconv-specific enhancer architectures.
Cis-regulatory elements are harbored in Intron5 of the RUNX1 gene.
Gutierrez et al., In Bmc Genomics, 24 Apr 2014
BACKGROUND: Human RUNX1 gene is one of the most frequent target for chromosomal translocations associated with acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL).
Targeting Epstein-Barr virus oncoprotein LMP1-mediated glycolysis sensitizes nasopharyngeal carcinoma to radiation therapy.
Cao et al., Changsha, China. In Oncogene, 24 Apr 2014
The LMP1-mediated attenuation of the PI3-K/Akt-GSK3beta-FBW7 signaling axis resulted in the stabilization of c-Myc.
A RAG driver on the road to pediatric ALL.
Waanders et al., Nijmegen, Netherlands. In Nat Genet, 28 Feb 2014
A new whole-genome sequencing study of ETV6-RUNX1-positive ALL has now identified RAG-mediated recombination, which specifically targets genes and regulatory elements active during B cell differentiation, as the underlying mechanism.
RAG-mediated recombination is the predominant driver of oncogenic rearrangement in ETV6-RUNX1 acute lymphoblastic leukemia.
Campbell et al., Madrid, Spain. In Nat Genet, 28 Feb 2014
The ETV6-RUNX1 fusion gene, found in 25% of childhood acute lymphoblastic leukemia (ALL) cases, is acquired in utero but requires additional somatic mutations for overt leukemia.
[Effect of Bushen Huatan Recipe on the Akt signal pathway in polycystic ovarian syndrome model rats with insulin resistance: an experimental research].
Wu et al., In Zhongguo Zhong Xi Yi Jie He Za Zhi, 28 Feb 2014
The expression of insulin receptor substrate 1 (IRS-1), glycogen synthetase kinase-3beta (GSK-3beta), glucose transporter 4 (GLUT-4), and peroxisome proliferator activated receptor (PPAR-gamma) mRNA were detected by RT-PCR.
Clinical impact of gene mutations and lesions detected by SNP-array karyotyping in acute myeloid leukemia patients in the context of gemtuzumab ozogamicin treatment: Results of the ALFA-0701 trial.
Preudhomme et al., Lille, France. In Oncotarget, 20 Feb 2014
In the present study, we performed mutational analysis of 11 genes (FLT3, NPM1, CEBPA, MLL, WT1, IDH1/2, RUNX1, ASXL1, TET2, DNMT3A), EVI1 overexpression screening, and 6.0 single-nucleotide polymorphism array (SNP-A) analysis in diagnostic samples of the 278 AML patients enrolled in the ALFA-0701 trial.
Structural basis for hijacking CBF-β and CUL5 E3 ligase complex by HIV-1 Vif.
Huang et al., Harbin, China. In Nature, 09 Feb 2014
The larger domain (α/β domain) of Vif binds to the same side of CBF-β as RUNX1, indicating that Vif and RUNX1 are exclusive for CBF-β binding.
How I treat ALL in Down's syndrome: pathobiology and management.
Whitlock et al., Tel Aviv-Yafo, Israel. In Blood, 02 Feb 2014
Although relapse is the major determinant of poor outcomes in this population, de-escalation of chemotherapy intensity might be feasible in the 10% to 15% DS-ALL patients with ETV6-RUNX1 or high hyperdipoidy in whom TRM is the major limiting event.
The genetic basis of myelodysplasia and its clinical relevance.
Malcovati et al., Pavia, Italy. In Blood, Jan 2014
About 90% of MDS patients carry ≥1 oncogenic mutations, and two thirds of them are found in individuals with a normal karyotype.
Global chromatin profiling reveals NSD2 mutations in pediatric acute lymphoblastic leukemia.
Stegmeier et al., Cambridge, United States. In Nat Genet, Nov 2013
Sequencing analysis of >1,000 pediatric cancer genomes identified the NSD2 p.E1099K alteration in 14% of t(12;21) ETV6-RUNX1-containing ALLs.
Intrachromosomal amplification of chromosome 21 is associated with inferior outcomes in children with acute lymphoblastic leukemia treated in contemporary standard-risk children's oncology group studies: a report from the children's oncology group.
Raetz et al., Birmingham, United States. In J Clin Oncol, Oct 2013
Intrachromosomal amplification of a region of chromosome 21 (iAMP21; three or more extra copies of RUNX1 on an abnormal chromosome 21) is a recently identified recurrent genomic lesion associated with inferior outcome in some studies.
RUNX1 meets MLL: epigenetic regulation of hematopoiesis by two leukemia genes.
Osato et al., Singapore, Singapore. In Leukemia, Sep 2013
A broad range of human leukemias carries RUNX1 and MLL genetic alterations.
RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response.
Nagase et al., Chiba, Japan. In Int J Genomics, 2012
RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis.
Contributions of the histone arginine methyltransferase PRMT6 to the epigenetic function of RUNX1.
Lausen, Frankfurt am Main, Germany. In Crit Rev Eukaryot Gene Expr, 2012
Hematopoietic differentiation is directed by transcription factors such as RUNX1.
Hypothalamic glycogen synthase kinase 3β has a central role in the regulation of food intake and glucose metabolism.
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.
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?
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.
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.
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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