gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 07 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 oncofusion protein FUS-ERG targets key hematopoietic regulators and modulates the all-trans retinoic acid signaling pathway in t(16;21) acute myeloid leukemia.
New
Martens et al., Nijmegen, Netherlands. In Oncogene, 06 Aug 2015
Here, we show that FUS-ERG acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype.
CD200/BTLA deletions in pediatric precursor-B cell acute lymphoblastic leukemia treated according to the EORTC-CLG 58951 protocol.
New
De Moerloose et al., Caen, France. In Haematologica, 02 Aug 2015
Genetically, CD200/BTLA deletions were strongly associated with ETV6-RUNX1 positive leukemias (p<0.0001),
Genome-scale definition of the transcriptional programme associated with compromised PU.1 activity in acute myeloid leukaemia.
New
Göttgens et al., Cambridge, United Kingdom. In Leukemia, 01 Aug 2015
Although mutations of the key haematopoietic transcription factor PU.1 are rare in human acute myeloid leukemia (AML), they are common in murine models of radiation-induced AML, and PU.1 downregulation and/or dysfunction has been described in human AML patients carrying the fusion oncogenes RUNX1-ETO and PML-RARA.
Transient myeloproliferative disorder with partial trisomy 21.
New
Shimada et al., Okayama, Japan. In Pediatr Blood Cancer, 01 Aug 2015
which included DYRK1A, ERG, and ETS but not the RUNX1 gene.
Integrative Analysis Reveals Regulatory Programs in Endometriosis.
New
Taylor et al., Beijing, China. In Reprod Sci, 30 Jul 2015
The IRN has shown that the most regulated gene in endometriosis is RUNX1, which is targeted by 14 of 26 TFs also involved in endometriosis.
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.
PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML.
Review
New
Badie et al., Melbourne, Australia. In Carcinogenesis, 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.
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.
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).
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.
share on facebooktweetadd +1mail to friends