Sentences with phrase «factor pu»

Mechanistically, decitabine acted synergistically with chidamide to enhance the interaction of KMT2D with transcription factor PU.1, regulated H3K4me - associated signaling pathways, and sensitized T - lymphoma cells to chidamide.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

Interferon - regulatory factor 4 (IRF4) or IRF8 binds this motif following interaction with the transcription factor PU.1.

Not exact matches

A few years ago, Singh and colleagues identified a transcription factor called PU.1 that acts as the primary signal, a central genetic switch to initiate development of myeloid progenitor cells.

The group of promoters, whose H3K4me3 levels were affected by combined chidamide and decitabine treatment, but not by either chidamide or decitabine treatment alone, was enriched with binding site motifs for PU.1, a transcription factor that activates gene expression during myeloid and B - cell lymphoid cell development15, 16 (Figure 5C).

Besides, some other potential cis - acting elements for transcription factors [such as CAAT / enhancer binding protein (C / EBP) and PU.1] have been also noted in the RIG - G gene promoter.

Their system was based on earlier studies in which Singh and his colleagues identified a transcription factor called PU.1 as a central genetic switch that triggers development of myeloid progenitor cells.