T-cell receptor α enhancer is inactivated in αβ T lymphocytes.
Armilla, Spain. In Proc Natl Acad Sci U S A, 07 May 2015
Eα inactivation resulted in the disruption of functional long-range enhancer-promoter interactions and was associated with loss of Eα-dependent histone modifications at promoter and enhancer regions, and reduced expression and recruitment of E2A to the Eα enhanceosome in T cells.
Inhibitor of differentiation 4 (ID4): From development to cancer.
Atlanta, United States. In Biochim Biophys Acta, Jan 2015
Apart from some degree of functional redundancy such as HLH dependent interactions with bHLH protein E2A, many of the functions of ID4 are distinct from ID1, ID2 and ID3: ID4 proteins a) regulate distinct developmental processes and tissue expression in the adult, b) promote stem cell survival, differentiation and/or timing of differentiation, c) epigenetic inactivation/loss of expression in several advanced stage cancers and d) increased expression in some cancers such as those arising in the breast and ovary.
The establishment of B versus T cell identity.
San Diego, United States. In Trends Immunol, May 2014
In B cell progenitors, E-proteins E2A and HEB (HeLa E-box binding protein) are crucial for the induction of a B lineage-specific program of gene expression and for orchestrating the assembly of the immunoglobulin loci.
Transcriptional control of pre-B cell development and leukemia prevention.
Australia. In Curr Top Microbiol Immunol, 2013
The triad of DNA-binding proteins, E2A, EBF1, and PAX5 is critical for both the early specification and commitment of B cell progenitors, while a larger number of secondary determinants, such as members of the Ikaros, ETS, Runx, and IRF families have more direct roles in promoting stage-specific pre-B gene-expression program.
Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.
Dundee, United Kingdom. In Cancer Manag Res, 2013
Recurrent mutations in ID3 or TCF3 (E2A) that promote signaling through PI3-kinase have recently been identified in human BL samples, and new therapeutic strategies based on coordinately targeting both the prosurvival factor, B-cell lymphoma-XL, and the PI3-kinase/AKT/mammalian target of rapamycin (mTOR) signaling pathway to synergistically induced BL apoptosis have been proposed.