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Validated All-in-One™ qPCR Primer for MECOM(NM_001205194.2) Search again
Product ID:
HQP153526
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AML1-EVI-1, EVI1, KMT8E, MDS1, MDS1-EVI1, PRDM3, RUSAT2
Gene Description:
MDS1 and EVI1 complex locus
Target Gene Accession:
NM_001205194.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- Data indicate that EVI1 is involved in megakaryocytic differentiation, and the dysmegakaryocytopoiesis in 3q21q26 syndrome could be partly due to an enhanced differentiation of leukemia cells and/or megakaryocytes by constitutive expression of EVI1.
- study investigated which of the 2 gene products, AMLEVI1 or MDS1-EVI1, is involved in acute myeloid leukemia transformation and found that AMLEVI1 and not MDS1-EVI1 expression was associated with unfavorable karyotypes
- EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity
- Evi-1 acts as a general Smad corepressor to inhibit TGF-beta-, activin-, and BMP-inducible transcription
- results suggest that oligomerization may contribute to the oncogenic potential of Evi-1-containing proteins
- human AML1/EVI1/+ knock-in mouse embryos showed defective hematopoiesis in the fetal liver; fetal liver contained multilineage progenitors capable of differentiating into dysplastic myelocyte and megakaryocyte
- The general expression patterns of the EVI1 5'-end variants in a panel of 20 human tissues were similar, while pronounced differences were noted in response to all-trans retinoic acid.
- Real-time quantitative PCR analyses indicated that typically both MDS1/EVI1 and EVI1, but not MDS1, were expressed in these malignancies, with EVI1 the primary transcript.
- Murine and human forms of Evi1 with repressor domain(Rp) or Rp+9 exist, the additional 9 amino acids are encoded by a conserved 27 nucleotide exon, the overall structural organisation of the gene being preserved in the two species.
- Overexpressed in Fanconi anemia-derived acute myeloid leukemia.
- review of EVI1 expression, biochemical properties, and biological functions [review]
- ubiquitously-expressed transcript suppresses cell transformation and might mediate this function by interaction and inhibition of the biological activity of cell proliferation and survival stimulatory factors like Evi1
- High EVI1 expression is associated with acute myeloid leukemias
- In conclusion, the combined MDS-EVI1/EVI1 gene may serve as an alternative MRD marker in AML, especially in samples where other specific markers are lacking.
- Inhibition of C/EBPalpha function may be causatively related to the leukemogenic potential of RUNX1/EVI1 chimeric transcription factor.
- EVI1 and MDS1/EVI1 overexpression is associated with acute myeloid leukemia
- Genetic alterations such as aberrant expression of the EVI1 gene may contribute to the clinical heterogeneity of chronic myeloid leukemia.
- High EVI1 predicted a distinctly worse event-free survival (HR = 1.9; P = .002) and disease-free survival (HR = 2.1, P = .006) following multivariate analysis.
- Evi-1 promotes hematopoietic stem/progenitor expansion at the embryonic stage through up-regulation of GATA-2 and repression of TGF-beta signaling.
- Presence of SUV39H1 enhances Evi1 transcriptional repression in a dose dependent manner; these data establish an epigenetic role of Evi1 in cell transformation by recruiting higher order chromatin remodeling complexes.
- Presence of both EVI1 and/or BAALC in chronic myeloid patients was found to modulate the disease pattern
- The EVI1 gene locus was rearranged in all 13 myeloid malignancies patients and was associated with EVI1 overexpression. In 9 out of 13 patients, the 17q breakpoints clustered in a 250 kb region on band 17q22 encompassing the MSI2 gene
- ETV6/RUNX1 leads to EPOR up-regulation and that activation by EPO might be of relevance to the biology of ETV6/RUNX1-positive acute lymphoblastic leukemias
- EVI1 point mutant, unable to bind PU.1, restores the activation of PU.1-regulated genes and allows a normal differentiation of bone marrow progenitors in vitro.