anti-MDS1 and EVI1 Complex Locus (MECOM) Anticorps

Human MDS1 and EVI1 Complex Locus (MECOM) interaction partners

1. A novel mutation in the MECOM gene causing radioulnar synostosis with amegakaryocytic thrombocytopenia (RUSAT-2) in an infant.

2. This meta-analysis indicates EVI1(H) has an independent and significantly adverse prognostic impact on AML patients in the entire population, and this conclusion same applies to some subgroups like AML patients with ICR, NC, and young AML patients.

3. pyrrole-imidazole (PI) polyamide targeting of GPR56 using our compound is promising, useful, and safe for the treatment of EVI1(high) acute myeloid leukemia

4. Data show that MDS1-EVI1 protein (EVI1) associated with binding partner C-terminal binding protein 1 (CtBP1), suggesting a role for ataxia telangiectasia mutated protein (ATM) in regulating EVI1 protein interactions via phosphorylation.

5. Identification of an important function of the N-termini of PRDM3 and PRDM16, which bind directly to RBBP4 to facilitate an interaction with the NuRD chromatin remodeling complex.

6. neonatal bone marrow failure syndrome with multiple congenital abnormalities, including limb defects, due to a constitutional deletion of 3' MECOM

7. Creatine kinase pathway inhibition alters GSK3 and WNT signaling in EVI1-positive AML.

8. For higher-risk myelodysplastic syndrome (MDS) patients, EVI1-high patients have poorer survival rate compared with EVI1-low patients. Moreover, EVI1-high was an adverse prognostic marker for MDS with excess blasts subtype. Taken together, EVI1 overexpression is a poor prognostic marker for higher-risk MDS group and could be included in risk stratification for MDS patients.

9. These findings suggest that in colon cancer EVI1 is dispensable for epithelial-mesenchymal transition, however, is required for metastasis.

10. The evidence has been provided, that miR-9 is significantly downregulated in a subset of pediatric AML patients with high expression of EVI1, and that miR-9 has a critical role in EVI1-induced leukemogenesis in pediatric patients, thereby establishing the role of miR-9 as a tumor suppressor in the pathogenesis of EVI1-induced myeloid leukemia.

11. Our data indicated that EVI1 played an oncogenic role in nasopharyngeal carcinoma growth and metastasis

12. Furthermore, EVI1 was also likely to target the promoter region of calreticulin (CRT) in vitro. It was concluded that EVI1 can affect epithelial mesenchymal transitionassociated genes by regulating the expression of CRT in breast cancer. The results revealed that EVI1 may be a potential effective therapeutic target in breast cancer.

13. Germline mutation in MECOM is associated with congenital bone marrow failure without a radial abnormality.

14. report on the first familial germline mutation in MDS1 and EVI1 complex locus (MECOM); finding extends MECOM germline mutation associated phenotypes and proposes MECOM as a novel HMMS candidate gene.

15. Expression of ecotopic viral integration site 1 (EVI1) is positively correlated with talin1 (TLN1) in both chronic myeloid leukemia (CML)-chronic phase (CP) and CML-blast crisis (BC) cases.

16. EVI1 expression is associated with aggressive behavior in intrahepatic cholangiocarcinoma.

17. We propose the term MECOM-associated syndrome for this heterogeneous hereditary disease and inclusion of MECOM sequencing in the diagnostic workup of congenital bone marrow failure.

18. Overall, we show the importance of performing detailed molecular cytogenetic analysis of MECOM to enable appropriate management of high-risk pediatric myeloid neoplasms.

19. presence of 3q26.2/EVI1 rearrangements in MDS/MPN is associated with rapid disease progression, poor response to treatment, and a poor prognosis

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

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

1. EVI1 overexpression reprograms hematopoiesis via upregulation of Spi1 transcription.

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

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

4. 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.

5. 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.

6. 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.

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

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

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

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

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

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

13. 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.

14. 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.

15. Evi1 is a key regulator of adipogenic competency

16. 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.

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

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

19. 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.

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

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