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

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
High-resolution antibody array analysis of childhood acute leukemia cells.
Kalina et al., Praha, Czech Republic. In Mol Cell Proteomics, Feb 2016
In addition, OPAL1 overexpression corresponded to ETV6-RUNX1 chromosomal translocation.
Myelodysplastic syndromes: Contemporary review and how we treat.
Tefferi et al., Rochester, United States. In Am J Hematol, Jan 2016
With the advent of next generation sequencing, recurrent somatic mutations in genes involved in epigenetic regulation (TET2, ASXL1, EZH2, DNMT3A, IDH1/2), RNA splicing (SF3B1, SRSF2, U2AF1, ZRSR2), DNA damage response (TP53), transcriptional regulation (RUNX1, BCOR, ETV6) and signal transduction (CBL, NRAS, JAK2) have been identified in MDS.
[Detection of copy number variations in pediatric ETV6/RUNX1-positive acute lymphoblastic leukemia with multiplex ligation-dependent probe amplification].
Zhu et al., Tianjin, China. In Zhongguo Dang Dai Er Ke Za Zhi, Jan 2016
OBJECTIVE: To investigate the application of multiplex ligation-dependent probe amplification (MLPA) in the detection of copy number variations (CNVs) in pediatric ETV6/RUNX1-positive acute lymphoblastic leukemia (ALL), to compare this method with conventional karyotype analysis and fluorescence in situ hybridization (FISH), and to evaluate the value of MLPA.
RUNX1 and FOXP3 interplay regulates expression of breast cancer related genes.
Rubinstein et al., Buenos Aires, Argentina. In Oncotarget, Jan 2016
UNASSIGNED: Runx1 participation in epithelial mammary cells is still under review.
Germline Mutations in Predisposition Genes in Pediatric Cancer.
Downing et al., Memphis, United States. In N Engl J Med, Jan 2016
The most commonly mutated genes in the affected patients were TP53 (in 50 patients), APC (in 6), BRCA2 (in 6), NF1 (in 4), PMS2 (in 4), RB1 (in 3), and RUNX1 (in 3).
Do somatic mutations in de novo MDS predict for response to treatment?
DeZern et al., Saint Louis, United States. In Hematology Am Soc Hematol Educ Program, Jan 2016
No abnormalities in other epigenetic regulators (DNMT3A, ASXL1), RNA splicing (SF3B1, SRSF2, URAF1, ZRSR2), transcription factors (RUNX1 or ETV6), or signaling (CBL, NRAS, KIT, JAK2, MPL) were detected.
Leukemia-Associated Cohesin Mutants Dominantly Enforce Stem Cell Programs and Impair Human Hematopoietic Progenitor Differentiation.
Majeti et al., Stanford, United States. In Cell Stem Cell, Jan 2016
These effects are restricted to immature HSPC populations, where cohesin mutants show increased chromatin accessibility and likelihood of transcription factor binding site occupancy by HSPC regulators including ERG, GATA2, and RUNX1, as measured by ATAC-seq and ChIP-seq.
Messenger RNA delivery of a cartilage-anabolic transcription factor as a disease-modifying strategy for osteoarthritis treatment.
Ohba et al., Tokyo, Japan. In Sci Rep, Dec 2015
When polyplex nanomicelles carrying the cartilage-anabolic, runt-related transcription factor (RUNX) 1 mRNA were injected into mouse OA knee joints, OA progression was significantly suppressed compared with the non-treatment control.
Synthetic lethal targeting of oncogenic transcription factors in acute leukemia by PARP inhibitors.
So et al., Hong Kong, Hong Kong. In Nat Med, Dec 2015
Here we demonstrate that AML driven by repressive transcription factors, including AML1-ETO (encoded by the fusion oncogene RUNX1-RUNX1T1) and PML-RARα fusion oncoproteins (encoded by PML-RARA) are extremely sensitive to poly (ADP-ribose) polymerase (PARP) inhibition, in part owing to their suppressed expression of key homologous recombination (HR)-associated genes and their compromised DNA-damage response (DDR).
RUNX1 haploinsufficiency results in granulocyte colony-stimulating factor hypersensitivity.
Osato et al., Singapore, Singapore. In Blood Cancer J, Dec 2015
RUNX1/AML1 is among the most commonly mutated genes in human leukemia.
Myeloproliferative neoplasms: Current molecular biology and genetics.
Saeidi, Kermān, Iran. In Crit Rev Oncol Hematol, Dec 2015
Some other genes' location such as TET oncogene family member 2 (TET2), additional sex combs-like 1 (ASXL1), casitas B-lineage lymphoma proto-oncogene (CBL), isocitrate dehydrogenase 1/2 (IDH1/IDH2), IKAROS family zinc finger 1 (IKZF1), DNA methyltransferase 3A (DNMT3A), suppressor of cytokine signaling (SOCS), enhancer of zeste homolog 2 (EZH2), tumor protein p53 (TP53), runt-related transcription factor 1 (RUNX1) and high mobility group AT-hook 2 (HMGA2) have also identified to be involved in MPNs phenotypes.
Resistance in the Ribosome: RUNX1, pre-LSCs, and HSPCs.
Ito et al., United States. In Cell Stem Cell, Sep 2015
Now in Cell Stem Cell, Cai et al. (2015) show that loss-of-function mutations in RUNX1 reduce ribosome biogenesis and provide pre-LSCs a selective advantage over normal hematopoietic cells through increased stress resistance.
Epoxyeicosatrienoic acids enhance embryonic haematopoiesis and adult marrow engraftment.
Zon et al., Boston, United States. In Nature, 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.
Coexistent t(8;21)(q22;q22) Translocation and 5q Deletion in Acute Myeloid Leukemia.
Minami et al., In J Clin Exp Hematop, 2014
These results indicated a diagnosis of AML with t(8;21)(q22;q22)/RUNX1/RUNX1T1 rather than MDS, even though the percentage of bone marrow myeloblasts was less than 20%.
Goryainova, In Lik Sprava, 2014
In addition to the conventional risk factors molecular genetic alterations, such as mutations of NPM1, CEBPA, c-KIT, AML1/RUNX1, WT1, FLT3 and others, are also important prognostic factors in AML patients.
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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