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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. Zusätzlich bieten wir Ihnen MDS1 and EVI1 Complex Locus Proteine (8) und MDS1 and EVI1 Complex Locus Kits (2) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal MECOM Primary Antibody für ELISA, WB - ABIN4270672
Konrad, Karger, Hackl, Schwarzinger, Herbacek, Wieser: Inducible expression of EVI1 in human myeloid cells causes phenotypes consistent with its role in myelodysplastic syndromes. in Journal of leukocyte biology 2009
Letter/Case Report: ETV6 (zeige ETV6 Antikörper)/MECOM gene fusion in therapy-related acute myeloid leukemia (zeige BCL11A Antikörper) with t(3;12) and monosomy 7.
These findings highlight a novel mechanism for hepatitis B virus X-induced hepatocarcinogenesis through transcription factor EVI1 and its target lncRNAs
Findings represent the first global genome-wide study of EVI1 DNA binding associated with whole transcriptome expression analysis. Results reveal several important genes with an ETS (zeige ETS1 Antikörper)-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis
The expression of EVI1 and SOX9 (zeige SOX9 Antikörper) is associated with stem cell-like and metastasis signatures, and their depletion impairs the metastatic potential of breast cancer cells. These results establish the mechanistic link between resistance to mTOR (zeige FRAP1 Antikörper) inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR (zeige FRAP1 Antikörper) targeting failure
EVI1 contributes to PCa (zeige FLVCR1 Antikörper) progression by regulating different oncogenic functions. EVI1 regulates the PCa (zeige FLVCR1 Antikörper) stem cell compartment responsible for disease initiation and also development of CRPC.
oncogenic potential for EVI1 in modulating genomic stability
EVI1 acts as a regulator of its own expression, highlighting the complex regulation of EVI1, and open new directions to better understand the mechanisms of EVI1 overexpressing leukemias.
EVI1 overexpression alters cellular metabolism. EVI1 promotes CKMT1 (zeige CKMT1B Antikörper) expression by repressing the myeloid differentiation regulator RUNX1 (zeige RUNX1 Antikörper).
EVI1 transcription is directly regulated by LEF1 (zeige LEF1 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) complex in myeloid blast crisis of chronic myeloid leukemia (zeige BCL11A Antikörper). Loss of p53 (zeige TP53 Antikörper) function as a key regulator for beta-catenin (zeige CTNNB1 Antikörper)-EVI1 in myeloid blast crisis of chronic myeloid leukemia (zeige BCL11A Antikörper).
we demonstrated that miR (zeige MLXIP Antikörper)-22 promoted monocyte/macrophage differentiation, and MECOM (EVI1) mRNA is a direct target of miR (zeige MLXIP Antikörper)-22 and MECOM (EVI1) functions as a negative regulator in the differentiation.The miR (zeige MLXIP Antikörper)-22-mediated MECOM degradation increased c-Jun (zeige JUN Antikörper) but decreased GATA2 (zeige GATA2 Antikörper) expression, which results in increased interaction between c-Jun (zeige JUN Antikörper) and PU.1
Gata2 (zeige GATA2 Antikörper) heterozygous deletion confers selective advantage to EVI1-expressing leukemia cell expansion in recipient mice
the DNA sequences to which EVI1 binds at +35 and +37 kb and show that mutation of one of these releases Cebpa (zeige CEBPA Antikörper) from EVI1-induced suppression.
Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF (zeige CSF2 Antikörper), acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF (zeige CSF2 Antikörper) levels.
Survivin (zeige BIRC5 Antikörper) partially regulates HSC (zeige FUT1 Antikörper) function by modulating the Evi-1 transcription factor and its downstream targets
Thrombopoietin (zeige THPO Antikörper)/MPL (zeige MPL Antikörper) signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
Prdm16 (zeige PRDM16 Antikörper) and Prdm3 control postnatal BAT (zeige BAAT Antikörper) identity and function.
Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects.
PR-domain protein ME has an essential role in mixed-lineage leukemia (MLL (zeige MLL Antikörper)) fusion protein (MFP) leukemia
nephrogenesis in zebrafish is regulated by interactions between retinoic acid, mecom, and Notch (zeige NOTCH1 Antikörper) signaling
Prdm3 and prdm16 (zeige PRDM16 Antikörper) are strongly expressed in the pharyngeal arches during cranioskeletal development, and their knockdown leads to defects in both the viscerocranium and the neurocranium.
Evi-1 (zeige RUNX1 Antikörper) is detected by in situ hybridization in the pronephric tissue, the brain and in neural crest derivatives of the head and neck
The protein encoded by this gene is a transcriptional regulator and oncoprotein that may be involved in hematopoiesis, apoptosis, development, and cell differentiation and proliferation. The encoded protein can interact with CTBP1, SMAD3, CREBBP, KAT2B, MAPK8, and MAPK9. This gene can undergo translocation with the AML1 gene, resulting in overexpression of this gene and the onset of leukemia. Several transcript variants encoding a few different isoforms have been found for this gene.
AML1-EVI-1 fusion protein
, MDS1 and EVI1 complex locus protein EVI1
, MDS1 and EVI1 complex locus protein MDS1
, ecotropic virus integration site 1 protein homolog
, myelodysplasia syndrome-associated protein 1
, oncogene EVI1
, zinc finger protein Evi1
, ecotropic viral integration site 1
, ecotropic virus integration site 1 protein
, myelodysplasia syndrome 1 homolog
, myelodysplasia syndrome 1 protein homolog
, PR domain containing 3
, MDS1 and EVI1 complex locus
, MDS1 and EVI1 complex locus protein EVI1-like
, MDS1 and EVI1 complex locus protein EVI1-A
, ecotropic virus integration site 1 protein homolog-A
, myelodysplasia syndrome 1-ectopic viral integration site 1