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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Jul 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
Prognostification of ALL by Cytogenetics.
Review
New
Lone et al., Srīnagar, India. In Indian J Hematol Blood Transfus, 30 Sep 2015
Some chromosomal abnormalities are associated with more favorable outcomes, such as high hyperdiploidy (51-65 chromosomes) and the ETV6-RUNX1 fusion.
The immunogenetics of Psoriasis: A comprehensive review.
New
Bowcock et al., New York City, United States. In J Autoimmun, 24 Aug 2015
These genes span an array of functions that involve antigen presentation (HLA-Cw6, ERAP1, ERAP2, MICA), the IL-23 axis (IL12Bp40, IL23Ap19, IL23R, JAK2, TYK2), T-cell development and T-cells polarization (RUNX1, RUNX3, STAT3, TAGAP, IL4, IL13), innate immunity (CARD14, c-REL, TRAF3IP2, DDX58, IFIH1), and negative regulators of immune responses (TNIP1, TNFAIP3, NFKBIA, ZC3H12C, IL36RN, SOCS1).
Epoxyeicosatrienoic acids enhance embryonic haematopoiesis and adult marrow engraftment.
New
Impact
Zon et al., Boston, United States. In Nature, 23 Aug 2015
The pro-haematopoietic effects of EETs were conserved in the developing zebrafish embryo, where 11,12-EET promoted HSPC specification by activating a unique activator protein 1 (AP-1) and runx1 transcription program autonomous to the haemogenic endothelium.
Chronic FLT3-ITD Signaling in Acute Myeloid Leukemia Is Connected to a Specific Chromatin Signature.
New
Cockerill et al., Birmingham, United Kingdom. In Cell Rep, 22 Aug 2015
This strategy revealed cooperation between the MAP kinase (MAPK) inducible transcription factor AP-1 and RUNX1 as a major driver of a common, FLT3-ITD-specific gene expression and chromatin signature, demonstrating a major impact of MAPK signaling pathways in shaping the epigenome of FLT3-ITD AML.
Runx1 Deficiency Decreases Ribosome Biogenesis and Confers Stress Resistance to Hematopoietic Stem and Progenitor Cells.
New
Impact
Speck et al., Philadelphia, United States. In Cell Stem Cell, 07 Aug 2015
UNASSIGNED: The transcription factor RUNX1 is frequently mutated in myelodysplastic syndrome and leukemia.
Next-generation-sequencing of recurrent childhood high hyperdiploid acute lymphoblastic leukemia reveals mutations typically associated with high risk patients.
New
Fischer et al., Düsseldorf, Germany. In Leuk Res, 14 Jul 2015
Structural genomic alterations affected genes regulating B-cell development (IKZF1, PBX1, RUNX1).
Targeted gene correction of RUNX1 in induced pluripotent stem cells derived from familial platelet disorder with propensity to myeloid malignancy restores normal megakaryopoiesis.
Review
New
Kurokawa et al., Tokyo, Japan. In Exp Hematol, 25 Jun 2015
UNASSIGNED: Familial platelet disorder with propensity to myeloid malignancy (FPD/AML) is an autosomal dominant disease associated with germline mutation in RUNX1 gene and characterized by thrombocytopenia and an increased risk for developing myeloid malignancies.
Myeloid and lymphoid neoplasm with abnormalities of FGFR1 presenting with trilineage blasts and RUNX1 rearrangement: a case report and review of literature.
Review
New
Luu et al., Dallas, United States. In Am J Clin Pathol, May 2015
We report a case of a patient with a novel t(17;21)(p13;q22) with RUNX1 rearrangement and trilineage blasts.
IS THE AMPLIFICATION OF c-MYC, MLL AND RUNX1 GENES IN AML AND MDS PATIENTS WITH TRISOMY 8, 11 AND 21 A FACTOR FOR A CLONAL EVOLUTION IN THEIR KARYOTYPE?
New
Simeonova et al., In Tsitol Genet, May 2015
The aim of our study was 1) to define if the amplification of c-MYC, MLL and RUNX1 genes is related to the progressive changes of the karyotype in patients with AML and MDS with trisomy 8, 11 and 21 (+8, +11 and +21) in bone marrow and 2) can that amplification be accepted as part of the clonal evolution (CE).
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, 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.
Hematopoietic transcription factor mutations and inherited platelet dysfunction.
Review
New
Rao et al., Philadelphia, United States. In F1000prime Rep, Dec 2014
These hematopoietic transcription factors include RUNX1, FLI1, GATA-1, and GFI1B.
Harnessing the Therapeutic Potential of Th17 Cells.
Review
New
Mageed et al., Arbīl, Iraq. In Mediators Inflamm, Dec 2014
For development, Th17 cells require activation of the transcription factors STAT3 and RORγt while RUNX1, c-Maf, and Aiolos are involved in changes of phenotype/functions.
Expression differences in TEL-AML1 fusion gene in leukemia glucocorticoid-sensitive and -resistant cell lines.
New
Xu et al., Chongqing, China. In Genet Mol Res, Dec 2014
We investigated the expression differences of the TEL-AML1 fusion gene in a leukemia glucocorticoid (GC)-sensitive cell line (CEM) and a GC-resistant cell line (Jurkat).
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.
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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