Disease relevance of ETV7

• Here we report that TEL2 augments the proliferation and survival of normal mouse B cells and dramatically accelerates lymphoma development in Emu-Myc transgenic mice [1].

Psychiatry related information on ETV7

• Here we show that forced expression of TEL2 alone in mouse bone marrow causes a myeloproliferative disease with a long latency period but with high penetrance [2].

High impact information on ETV7

• Although both proteins are transcriptional inhibitors binding similar DNA recognition sequences, they have opposite biologic effects: TEL inhibits proliferation while TEL2 promotes it [2].
• TEL2 is expressed in the hematopoietic system, and its expression is up-regulated in bone marrow samples of some patients with leukemia, suggesting a role in oncogenesis [2].
• Treating mice receiving transplants with TEL2-expressing bone marrow with the chemical carcinogen N-ethyl-N-nitrosourea (ENU) resulted in significantly accelerated disease onset [2].
• Together our data identify TEL2 as a bona fide oncogene, but leukemic transformation is dependent on secondary mutations [2].
• Therefore, TEL2 and MYC also appear to cooperate in provoking a cadre of human B-cell malignancies [1].

Biological context of ETV7

• The TEL2 gene consists of 8 exons spanning approximately 21 kilobases (kb) in human chromosome 6p21 [3].
• These results suggest that TEL2 may play an important role in hematopoiesis and oncogenesis [4].
• In addition, these mutants blocked TEL2-mediated transcriptional repression of a synthetic promoter containing TEL2 binding sites [4].
• PSE1 is immunologically similar to and shares amino acid sequence with a protein (TREF) which binds the human transferrin receptor (HTFR) promoter [5].
• Given that Tel2p has been shown to bind to a variety of nucleic acid structures in vitro, we speculate that the RAD-5/CLK-2 checkpoint protein may act at sites of DNA damage, either as a sensor of DNA damage or to aid in the repair of damaged DNA [6].

Anatomical context of ETV7

• In addition, forced expression of TEL2 but not TEL blocks vitamin D3-induced differentiation of U937 and HL60 myeloid cells [2].
• Additionally, the TEL2 protein is capable of associating with itself and with TEL1 in doubly transfected Hela cells, and this interaction is mediated through the pointed (PNT) domain of TEL1 [3].
• Overexpression of TEL2 in U937 cells inhibited differentiation induced by vitamin D3 [4].
• An enhanced activity of the TEL-2 cell membrane, consisting of several thin thread-like projections either with or without an expanded termination, was involved with contacting the thymocytes [7].
• Morphological study of thymus stromal cells (TEL-2 cell) which play a role in the elimination of double positive immature thymocytes by phagocytosis [7].

Associations of ETV7 with chemical compounds

• The HD % (the percentage of high-density component, i.e., the percentage of homopolymer component) results obtained by CTREF (CRYSTAF in TREF mode) technique are used as the input data together with the respective FT-IR spectra for PLS analyses to establish a calibration curve [8].

Physical interactions of ETV7

• DNA binding assays show that TEL2 can bind the same consensus DNA binding sequence recognized by TEL1/ETV6 [3].

Other interactions of ETV7

• TEL2 is a member of the ETS family of transcription factors, which is highly similar to TEL1/ETV6 [4].
• Therefore, one of the internal primers of each translocation (ABL-2, TEL-2, AF4-2) was labeled with a characteristic fluorescent dye, and an automatic fluorescence-based DNA fragment analysis was performed [9].
• The ETS factor TEL2 is a hematopoietic oncoprotein [2].
• In the eight patients with cytogenetic or cryptic 6p gains, we identified a common overrepresented region extending for 5-6 megabases from the TNF gene to the ETV-7 gene [10].

Analytical, diagnostic and therapeutic context of ETV7

• For every session, index temperatures T90 (temperature attained at 90% of tumour related measurement points), cumulative minutes for T90 > Tref, tumour related power density (SAR: specific absorption rate, in W/kg) and the effective perfusion Weff (in ml/100 g min) were calculated [11].

References