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All ETS (Erythroblast Transformation Specific) family members are identified through a highly conserved DNA binding domain, the ETS domain, which is a winged helix-turn-helix structure that binds to DNA sites with a central GGA(A/T) DNA sequence.
ETS domain-containing protein Elk-3 is a protein that in humans is encoded by the ELK3 gene. [ 5 ] [ 6 ] The protein encoded by this gene is a member of the ETS-domain transcription factor family and the ternary complex factor (TCF) subfamily.
The protein encoded by this gene is a member of an epithelium-specific subclass of the ETS transcription factor family.In addition to its role in regulating the later stages of terminal differentiation of keratinocytes, it appears to regulate a number of epithelium-specific genes found in tissues containing glandular epithelium such as salivary gland and prostate.
Protein C-ets-1 is a protein that in humans is encoded by the ETS1 gene. [5] The protein encoded by this gene belongs to the ETS family of transcription factors . [ 6 ]
ETS Like-1 protein Elk-1 is a protein that in humans is encoded by the ELK1. [5] Elk-1 functions as a transcription activator.It is classified as a ternary complex factor (TCF), a subclass of the ETS family, which is characterized by a common protein domain that regulates DNA binding to target sequences.
ERG (ETS-related gene) is an oncogene. [ 5 ] [ 6 ] [ 7 ] ERG is a member of the ETS (erythroblast transformation-specific) family of transcription factors. [ 8 ] The ERG gene encodes for a protein, also called ERG, that functions as a transcriptional regulator.
This gene is a member of the Ets family of transcription factors and of the ternary complex factor (TCF) subfamily. Proteins of the TCF subfamily form a ternary complex by binding to the serum response factor and the serum response element in the promoter of the c-fos proto-oncogene.
Fli-1 is a member of the ETS transcription factor family that was first identified in erythroleukemias induced by Friend Murine Leukemia Virus ().Fli-1 is activated through retroviral insertional mutagenesis in 90% of F-MuLV-induced erythroleukemias.