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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. Additionally we are shipping MDS1 and EVI1 Complex Locus Antibodies (118) and MDS1 and EVI1 Complex Locus Kits (2) and many more products for this protein.
Showing 4 out of 8 products:
Letter/Case Report: ETV6 (show ETV6 Proteins)/MECOM gene fusion in therapy-related acute myeloid leukemia (show BCL11A Proteins) 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 (show ETS1 Proteins)-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis
The expression of EVI1 and SOX9 (show SOX9 Proteins) 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 (show FRAP1 Proteins) inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR (show FRAP1 Proteins) targeting failure
EVI1 contributes to PCa (show FLVCR1 Proteins) progression by regulating different oncogenic functions. EVI1 regulates the PCa (show FLVCR1 Proteins) 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 (show CKMT1B Proteins) expression by repressing the myeloid differentiation regulator RUNX1 (show RUNX1 Proteins).
EVI1 transcription is directly regulated by LEF1 (show LEF1 Proteins)/beta-catenin (show CTNNB1 Proteins) complex in myeloid blast crisis of chronic myeloid leukemia (show BCL11A Proteins). Loss of p53 (show TP53 Proteins) function as a key regulator for beta-catenin (show CTNNB1 Proteins)-EVI1 in myeloid blast crisis of chronic myeloid leukemia (show BCL11A Proteins).
we demonstrated that miR (show MLXIP Proteins)-22 promoted monocyte/macrophage differentiation, and MECOM (EVI1) mRNA is a direct target of miR (show MLXIP Proteins)-22 and MECOM (EVI1) functions as a negative regulator in the differentiation.The miR (show MLXIP Proteins)-22-mediated MECOM degradation increased c-Jun (show JUN Proteins) but decreased GATA2 (show GATA2 Proteins) expression, which results in increased interaction between c-Jun (show JUN Proteins) and PU.1
Gata2 (show GATA2 Proteins) 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 (show CEBPA Proteins) from EVI1-induced suppression.
Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF (show CSF2 Proteins), acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF (show CSF2 Proteins) levels.
Survivin (show BIRC5 Proteins) partially regulates HSC (show FUT1 Proteins) function by modulating the Evi-1 transcription factor and its downstream targets
Thrombopoietin (show THPO Proteins)/MPL (show MPL Proteins) signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
Prdm16 (show PRDM16 Proteins) and Prdm3 control postnatal BAT (show BAAT Proteins) 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 (show MLL Proteins)) fusion protein (MFP) leukemia
nephrogenesis in zebrafish is regulated by interactions between retinoic acid, mecom, and Notch (show NOTCH1 Proteins) signaling
Prdm3 and prdm16 (show PRDM16 Proteins) 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 (show RUNX1 Proteins) 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