ETV6 (i.e. translocation-Ets-leukemia virus) protein is a transcription factor that in humans is encoded by the ETV6 (previously known as TEL) gene. The ETV6 protein regulates the development and growth of diverse cell types, particularly those of hematological tissues.

Nov 19, 2020 · ETV6 thrombocytopenia and predisposition to leukemia is a nonsyndromic genetic disorder of thrombocytopenia and high risk of leukemia without any other known congenital anomalies. Formal clinical diagnostic criteria have not been published.

Mar 30, 2025 · ETV6 (ETS Variant Transcription Factor 6) is a Protein Coding gene. Diseases associated with ETV6 include Thrombocytopenia 5 and Hematologic Cancer. Among its related pathways are Signaling by PDGFR in disease and FLT3 signaling in disease.

The ETV6 (also known as TEL) gene encodes a transcriptional repressor that plays a critical role in hematopoiesis and in embryonic development. While somatic ETV6 translocations and missense mutations are frequently observed in human cancers, the ...

Etv6 is one of the few ETS proteins that functions as a transcriptional repressor. Etv6 is somewhat unusual among ETS family members because it is able to form homodimers in vivo, and its repressor activity is directly linked to its ability to self-associate [55].

Objectives: E26 transformation-specific variant 6 gene (ETV6) is one of the most consistently rearranged genes in acute leukaemia. It encodes a principal hematopoietic transcription factor.

Jan 19, 2023 · Here we describe the results of a genome-scale CRISPR–Cas9 screen revealing that the wild-type ETS TF ETS variant 6 (ETV6; also known as TEL) is a crucial Ewing-sarcoma-selective TF...

The ETV6 gene provides instructions for producing a protein that functions as a transcription factor, which means that it attaches (binds) to specific regions of DNA and controls the activity of certain genes. Learn about this gene and related health conditions.

ETV6 Regulates Hemin-Induced Erythroid Differentiation of K562 Cells through Mediating the Raf/MEK/ERK Pathway. ETV6-NCOA2 fusion induces T/myeloid mixed-phenotype leukemia through transformation of nonthymic hematopoietic progenitor cells.

ETV6/RUNX1 (E/R) is the most common fusion gene in childhood acute lymphoblastic leukemia (ALL). Multiple lines of evidence imply a “two-hit” model for the molecular pathogenesis of E/R -positive ALL, whereby E/R rearrangement is followed by a series of secondary mutations that trigger overt leukemia.