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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters.
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Human Polyclonal MECOM Primary Antibody for 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
Fisher's exact SubID was used to reveal EVI1 as a transcriptional regulator of INPP4B (show INPP4B Antibodies) in AML (show RUNX1 Antibodies); a finding which was validated in vitro. Next, we used CoxPH SubID to conduct a pan (show SUPT6H Antibodies)-cancer analysis of INPP4B's prognostic significance
Letter/Case Report: ETV6 (show ETV6 Antibodies)/MECOM gene fusion in therapy-related acute myeloid leukemia (show BCL11A Antibodies) 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 Antibodies)-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis
The expression of EVI1 and SOX9 (show SOX9 Antibodies) 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 Antibodies) inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR (show FRAP1 Antibodies) targeting failure
EVI1 contributes to PCa (show FLVCR1 Antibodies) progression by regulating different oncogenic functions. EVI1 regulates the PCa (show FLVCR1 Antibodies) 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 Antibodies) expression by repressing the myeloid differentiation regulator RUNX1 (show RUNX1 Antibodies).
EVI1 transcription is directly regulated by LEF1 (show LEF1 Antibodies)/beta-catenin (show CTNNB1 Antibodies) complex in myeloid blast crisis of chronic myeloid leukemia (show BCL11A Antibodies). Loss of p53 (show TP53 Antibodies) function as a key regulator for beta-catenin (show CTNNB1 Antibodies)-EVI1 in myeloid blast crisis of chronic myeloid leukemia (show BCL11A Antibodies).
Gata2 (show GATA2 Antibodies) 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 Antibodies) from EVI1-induced suppression.
Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF (show CSF2 Antibodies), acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF (show CSF2 Antibodies) levels.
Survivin (show BIRC5 Antibodies) partially regulates HSC (show FUT1 Antibodies) function by modulating the Evi-1 transcription factor and its downstream targets
Thrombopoietin (show THPO Antibodies)/MPL (show MPL Antibodies) signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
Prdm16 (show PRDM16 Antibodies) and Prdm3 control postnatal BAT (show BAAT Antibodies) 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 Antibodies)) fusion protein (MFP) leukemia
nephrogenesis in zebrafish is regulated by interactions between retinoic acid, mecom, and Notch (show NOTCH1 Antibodies) signaling
Prdm3 and prdm16 (show PRDM16 Antibodies) 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 Antibodies) 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