Disease relevance of Etv6

• Tel is an Ets transcription factor that is the target of chromosome translocations in lymphoid and myeloid leukemias and in solid tumors [1].

High impact information on Etv6

• Following inactivation of Tel/Etv6, HSCs are lost in the adult bone marrow but their progeny are unaffected and transiently sustain blood formation [2].
• Tel/Etv6 is an essential and selective regulator of adult hematopoietic stem cell survival [2].
• Accordingly, absence of Tel/Etv6 after lineage commitment is ostensibly without consequence except for unexpected impairment of maturation of megakaryocytes [2].
• Tel-2 is the second mammalian member of the Tel Ets family subclass whose prototype Tel is involved in various chromosomal translocations in human cancers [3].
• The Pointed and DNA binding (DB) domains of Tel were required for all Tel-induced phenotypes [4].

Biological context of Etv6

• TEL (Translocation-ETS-Leukemia or ETV 6) is disrupted by multiple chromosomal translocations in acute leukemia [5].
• The ETS family member Tel antagonizes the Fli-1 phenotype in hematopoietic cells [6].
• In previous studies we demonstrated that Tel binds to Fli-1 and blocks transactivation of megakaryocytic promoters by Fli-1 [6].
• The Tel gene is a major target of translocations in leukemia and loss of heterozygosity is regularly observed for the non-translocated allele, thus supporting the notion that Tel is a tumor suppressor [4].
• Euryale ferox (Tel makhana(1)), Phoenix dactylifera (Chhohara(1)) and Zingiber officinale (Sonth(1)), however, stimulated humoral immunity to a greater extent than CMI [7].

Anatomical context of Etv6

• Retroviral transduction of a wild-type Tel cDNA into a clonal subline of NIH3T3 fibroblasts resulted in a striking morphologic change: at confluency, the cells reorganized into a specific "bridge-like" pattern over the entire surface of the culture dish, and started migrating, thereby leaving circular holes in the monolayer [1].
• Retroviral transduction of Tel into MS1 endothelial cells reproduced the aggregation phenotype, but not the cellular cord formation [1].

Associations of Etv6 with chemical compounds

• The t(5;12) chromosomal translocation, present in a subset of CMML patients with myeloproliferation fuses the amino terminal portion of the ets family member, Tel, with the transmembrane and tyrosine kinase domains of platelet-derived growth factor receptor beta (PDGFRbeta) gene [8].

Other interactions of Etv6

• Tel, a frequent target of leukemic translocations, induces cellular aggregation and influences expression of extracellular matrix components [1].

References