Ets Variant 6 (ETV6) ELISA Kits

Mouse (Murine) Ets Variant 6 (ETV6) interaction partners

1. Etv6 optimizes the resolution of cDC1 and pDC expression programs and the functional fitness of cDC1, thereby facilitating T cell cross-priming and tumor-specific responses.

2. Study reveals a previously unrecognized synergism between ETV6/RUNX1 and BCL2 impacting on malignant disease and autoimmunity.

3. Together with similar observations made in human PAX5-ETV6(+) B-ALLs, these data identified PAX5-ETV6 fusion as a potent oncoprotein that drives B-cell leukemia development.

4. ETV6 DNA binding inhibition is established by the stability of its inhibitory helix

5. Studied the combination of Etv6-RUNX1 and Pax5(+/-) alleles, they generated a transplantable B220 + CD19+ B-ALL with a significant disease incidence; RNA-seq analysis showed a gene expression pattern consistent with arrest at the pre-B stage.

6. In murine models of B-cell progenitors, evidence found that ETV6- RUNX1 alters the expression of cytoskeletal regulatory genes, resulting in a block of the CDC42 signaling pathway, and compromises the chemotactic response to CXCL12.

7. ETV6-SAM domain interface mutations block ETV6-NTRK3-induced cellular transformation

8. the autoinhibition of ETV6 DNA binding by sequences C-terminal to its ETS domain

9. find that both IRS1 and kinase active IGF1R are required for ETV6-NTRK3 transformation, that tyrosine phosphorylated IRS1 is present in high molecular weight complexes with EN and IGF1R, and that EN colocalizes with IGF1R at the plasma membrane

10. Cytogenetic study of 33 children with ETV6-RUNX1 positive acute lymphoblastic leukemia predict long term survival.

11. TEL binding to IRF-8 for recruitment of HDAC3 is regulated by gamma-interferon

12. role in accelerating differentiation of Friend erythroleukemia cells

13. the ability of TEL to repress transcription and suppress growth is regulated by sumoylation and nuclear export

14. nucleo-cytoplasmic delocalization of the major isoform of TEL-ETV6 is regulated by V-src

15. TEL-mediated repression of Bcl-XL likely affects cell survival via regulation of the apoptotic pathway.

16. ETV6-NTRK3.IRS-1 complex formation through the NTRK3 C terminus is essential for ETV6-NTRK3 transformation

17. establish Tel/Etv6 as a selective and essential regulator of postembryonic hematopoietic stem cells

18. leukemogenic effect of meningioma 1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome

19. Data suggest that TEL exerts a tumor suppressive function through augmenting the p53 pathway.

20. These results suggest that several Ets factors, including Fli1 itself, are involved in the transcriptional regulation of Fli1 in lymphocytes.

Zebrafish Ets Variant 6 (ETV6) interaction partners

1. Dominant-negative truncated ETV6 with deletions of the ETS domain or the PNT domain interfered with repression by full-length ETV6 and affected expression of early hematopoietic and erythroid markers in embryos.

2. the transcriptional repressor Tel plays an evolutionarily conserved role in angiogenesis: it is indispensable for the sprouting of human endothelial cells and for normal development of the Danio rerio blood circulatory system

Human Ets Variant 6 (ETV6) interaction partners

1. results suggest that age-associated dysregulation of splicing factor expression and cellular senescence may derive in part from altered activity of ERK and AKT signaling and may act in part through the ETV6 and FOXO1 transcription factors

2. Case Report: high-grade salivary secretory carcinoma with ETV6-MET gene fusion.

3. STAT1 as a significant ETV6-NTRK3 (EN) fusion-regulated transcription factor and a crucial mediator of EN-induced tumorigenesis.

4. Report molecular analysis of a group of mammary analog secretory carcinomas harboring a novel ETV6-RET translocation.

5. In this study, the presence of clonal heterogeneity and impaired FCM-MRD clearance among ETV6/RUNX1-positive patients, ultimately influenced prognosis.

6. Authors have shown that the stability of ETV6/FLT3 is regulated by the Hsp90 chaperone. ETV6/FLT3 fusion protein forms a complex with Hsp90 by coimmunoprecipitation analyses using an Hsp90 antibody.

7. None of the genitourinary pseudosarcomatous myofibroblastic proliferations was found to harbour USP6 (0/12), ROS1 (0/8) or ETV6 (0/7) rearrangements

8. ETV6 rearrangements often accompany other molecular mutations. Thirty-three distinct partner bands of ETV6 that contain various fusion genes were detected which plays a vital role in obtaining information about leukaemia genesis. RXDX-101 and PKC412 were reported to be inhibitors of ETV6-NTRK3.

9. We did not find the AIF1L-ETV6 and ABL1-AIF1L fusions in other ETV6-ABL1-positive ALL. Nevertheless, functional studies would be needed to establish the biological role of AIF1L-ETV6 and ABL1-AIF1L and to determine whether they contribute to leukemogenesis and/or to the final leukemia phenotype.

10. Data indicate that single nucleotide polymorphism rs2238126 in ETS variant 6 transcription factor (ETV6) associated with colorectal cancer risk.

11. ETV6/NTRK3 fusion oncogene is associated with papillary thyroid carcinoma.

12. Nasopharyngeal carcinoma (NPC) super-enhancers with extraordinarily broad and high H3K27ac signals were identified, and they were linked to genes important for oncogenesis including ETV6. ETV6 was also highly expressed in NPC biopsies by immunohistochemistry

13. ETV6-RUNX1 mutation is associated with childhood acute B-lymphoblastic leukemia.

14. Several studies addressed the mechanism by which ETV6/RUNX1 (E/R) contributes to leukemogenesis, including the necessary secondary genetic lesions, the cellular framework in which E/R initially arises and the maintenance of a pre-leukemic condition. [review]

15. Patients with t(12;22)/MN1-EVT6 oncogene, are frequently associated with myeloid neoplasms, poor response to chemotherapy, and inferior outcome.

16. Presence of fusion the genes BCR/ABL1, ETV6/RUNX1, and MLL/AF4 does not have any impact on the clinical and laboratory features of ALL at presentation.

17. ETV6/RUNX1 (+) ALL may be heterogeneous in terms of prognosis, and variables such as MRD at end ofremission induction or additional structural abnormalities of 12p could define a subset of patients who are likely to have poor outcome.

18. Case Reports: mammary analog secretory carcinoma of the thyroid gland with ETV6 rearrangement and ETV6-NTRK3 gene fusion.

19. The prevalence of ETV6-NTRK3 kinase fusions were determined in papillary thyroid cancer ofan adult population

20. We report the case of a patient with an initial diagnosis of salivary acinic cell carcinoma later reclassified as Mammary analogue secretory carcinoma after next-generation sequencing revealed an ETV6-NTRK3 fusion.