anti-MDS1 and EVI1 Complex Locus (MECOM) Antibodies

Human MDS1 and EVI1 Complex Locus (MECOM) interaction partners

1. High EVI1 expression predicts poor outcome in Acute myeloid leukemia with intermediate cytogenetic risk in patients receiving chemotherapy.

2. The relationship between EVI1 and microRNAs in human malignancies. [review]

3. 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

4. Letter/Case Report: ETV6/MECOM gene fusion in therapy-related acute myeloid leukemia with t(3;12) and monosomy 7.

5. These findings highlight a novel mechanism for hepatitis B virus X-induced hepatocarcinogenesis through transcription factor EVI1 and its target lncRNAs

6. 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-like binding motif, is involved in terminal myeloid differentiation, cell cycle regulation and apoptosis

7. The expression of EVI1 and SOX9 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 inhibition and cancer metastatic potential, thus enhancing our understanding of mTOR targeting failure

8. 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.

9. oncogenic potential for EVI1 in modulating genomic stability

10. 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.

11. EVI1 overexpression alters cellular metabolism. EVI1 promotes CKMT1 expression by repressing the myeloid differentiation regulator RUNX1.

12. EVI1 transcription is directly regulated by LEF1/beta-catenin complex in myeloid blast crisis of chronic myeloid leukemia. Loss of p53 function as a key regulator for beta-catenin-EVI1 in myeloid blast crisis of chronic myeloid leukemia.

13. we demonstrated that miR-22 promoted monocyte/macrophage differentiation, and MECOM (EVI1) mRNA is a direct target of miR-22 and MECOM (EVI1) functions as a negative regulator in the differentiation.The miR-22-mediated MECOM degradation increased c-Jun but decreased GATA2 expression, which results in increased interaction between c-Jun and PU.1

14. Results establish the oncogenic contributions of EVI1 in ER- and HER2-negative subsets of breast cancer.

15. MECOM gene harbors both somatic frameshift mutations.

16. Isochromosome 3q, especially MECOM abnormality, could play a key role in Persistent polyclonal binucleated B-cell lymphocytosis.

17. MECOM deletion is associated with congenital thrombocytopenia.

18. involvement of MECOM in patients with acute myeloid leukemia and myelodysplastic syndrome with various 3q abnormalities

19. RUNX1-Evi-1 may promote proliferation and apoptosis resistance of primitive hematopoietic cell, and inhibit the differentiation of myeloid cells with the synergy of different pathways and factors.

20. EVI1 overexpression has been revealed as an important independent adverse prognostic marker in adult acute myeloid leukemia and defines distinct risk categories in 11q23-rearranged AML.

Mouse (Murine) MDS1 and EVI1 Complex Locus (MECOM) interaction partners

1. These findings highlight a novel mechanism for hepatitis B virus X-induced hepatocarcinogenesis through transcription factor EVI1 and its target lncRNAs

2. Gata2 heterozygous deletion confers selective advantage to EVI1-expressing leukemia cell expansion in recipient mice

3. 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.

4. the DNA sequences to which EVI1 binds at +35 and +37 kb and show that mutation of one of these releases Cebpa from EVI1-induced suppression.

5. Evi1(+)DA-3 cells modified to express an intracellular form of GM-CSF, acquired growth factor independence and transplantability and caused an overt leukemia in syngeneic hosts, without increasing serum GM-CSF levels.

6. Survivin partially regulates HSC function by modulating the Evi-1 transcription factor and its downstream targets

7. Thrombopoietin/MPL signaling confers growth and survival capacity to CD41-positive cells in a mouse model of Evi1 leukemia.

8. Prdm16 and Prdm3 control postnatal BAT identity and function.

9. Mice carrying a hypomorphic Evi1 allele are embryonic viable but exhibit severe congenital heart defects.

10. Lack of ME leads to a complex defect in both osseous and non-osseous musculoskeletal tissues.

11. PR-domain protein ME has an essential role in mixed-lineage leukemia (MLL) fusion protein (MFP) leukemia

12. Cotransduction of Evi1 and the shortest isoform of C/EBPbeta, liver inhibitory protein (LIP), induced acute myeloid leukemia with short latencies in a mouse bone marow transplantation model.

13. Transient Evi1 transfection inhibited TGF-beta-induced transcriptional activity and reversed the growth inhibitory effect of TGF-beta in MC-26 mouse colon cancer cells.

14. Evi1 is a key regulator of adipogenic competency

15. Data identify Prdm3 and Prdm16 as H3K9me1 methyltransferases and expose a functional framework in which anchoring to the nuclear periphery helps maintain the integrity of mammalian heterochromatin.

16. EVI1 is a critical player in tumor growth in a subset of MLL-rearranged acute myeloid leukemia.

17. our study provides important insights into the novel role for EVI1 in negatively regulating NF-kappaB-dependent inflammation

18. the results indicate that Evi-1 is expressed in a stage-specific manner during ovarian follicular development and may be involved in early follicle development.

19. Evi1 is essential for hematopoietic stem cell self-renewal, and its expression marks hematopoietic cells with long-term multilineage repopulating activity.

20. Results clearly demonstrate a critical role of PR-domain-containing Mds1-Evi1 in linking p57-kip2 regulation to long-term hematopoietic stem cell function.

Zebrafish MDS1 and EVI1 Complex Locus (MECOM) interaction partners

1. nephrogenesis in zebrafish is regulated by interactions between retinoic acid, mecom, and Notch signaling

2. Prdm3 and prdm16 are strongly expressed in the pharyngeal arches during cranioskeletal development, and their knockdown leads to defects in both the viscerocranium and the neurocranium.

Xenopus laevis MDS1 and EVI1 Complex Locus (MECOM) interaction partners

1. Evi-1 is detected by in situ hybridization in the pronephric tissue, the brain and in neural crest derivatives of the head and neck