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Core binding factor (CBF) is a heterodimeric transcription factor that binds to the core element of many enhancers and promoters. De plus, nous expédions MDS1 and EVI1 Complex Locus Anticorps (117) et MDS1 and EVI1 Complex Locus Protéines (8) et beaucoup plus de produits pour cette protéine.
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Fisher's exact SubID was used to reveal EVI1 as a transcriptional regulator of INPP4B in AML; a finding which was validated in vitro. Next, we used CoxPH SubID to conduct a pan-cancer analysis of INPP4B's prognostic significance
Letter/Case Report: ETV6 (Montrer ETV6 Kits ELISA)/MECOM gene fusion in therapy-related acute myeloid leukemia (Montrer BCL11A Kits ELISA) 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 (Montrer ETS1 Kits ELISA)-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis
The expression of EVI1 and SOX9 (Montrer SOX9 Kits ELISA) 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 (Montrer FRAP1 Kits ELISA) inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR (Montrer FRAP1 Kits ELISA) targeting failure
EVI1 contributes to PCa progression by regulating different oncogenic functions. EVI1 regulates the PCa 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 (Montrer CKMT1B Kits ELISA) expression by repressing the myeloid differentiation regulator RUNX1 (Montrer RUNX1 Kits ELISA).
EVI1 transcription is directly regulated by LEF1 (Montrer LEF1 Kits ELISA)/beta-catenin (Montrer CTNNB1 Kits ELISA) complex in myeloid blast crisis of chronic myeloid leukemia (Montrer BCL11A Kits ELISA). Loss of p53 (Montrer TP53 Kits ELISA) function as a key regulator for beta-catenin (Montrer CTNNB1 Kits ELISA)-EVI1 in myeloid blast crisis of chronic myeloid leukemia (Montrer BCL11A Kits ELISA).
Gata2 (Montrer GATA2 Kits ELISA) 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 (Montrer CEBPA Kits ELISA) from EVI1-induced suppression.
Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF (Montrer CSF2 Kits ELISA), acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF (Montrer CSF2 Kits ELISA) levels.
Survivin (Montrer BIRC5 Kits ELISA) partially regulates HSC function by modulating the Evi-1 transcription factor and its downstream targets
Thrombopoietin (Montrer THPO Kits ELISA)/MPL (Montrer MPL Kits ELISA) signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.
Prdm16 and Prdm3 control postnatal BAT 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) fusion protein (MFP) leukemia
nephrogenesis in zebrafish is regulated by interactions between retinoic acid, mecom, and Notch (Montrer NOTCH1 Kits ELISA) signaling
Prdm3 and prdm16 (Montrer PRDM16 Kits ELISA) 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 (Montrer RUNX1 Kits ELISA) 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