The findings, published in the Proceedings of the National Academy of Sciences, describe how
myeloid differentiation factor (MyD88), a protein that plays a major role in mediating host defense response against invading pathogens, is tightly regulated to prevent uncontrolled inflammation.
Not exact matches
Using mice deficient in Del - 1, they found that the protein promotes proliferation and
differentiation of hematopoetic stem cells, sending more of these progenitor cells down a path toward becoming
myeloid cells, such as macrophages and neutrophils, rather than lymphocytes, such as T cells and B cells.
He uses the paradigm of nuclear hormone receptor activation / signaling and the contribution of this process to
myeloid cell
differentiation, function, and to diseases, involving these cells, such as atherosclerosis, tissue regeneration, metabolic, and various inflammatory disorders, as his model systems.
Induction of
Differentiation and Cellular Manipulation of Human
Myeloid HL - 60 Leukemia Cells.
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.
My recent studies have demonstrated that during tumor progression, TGFβ signaling controls
differentiation of CD39 + CD73 +
myeloid cells (MC).
Adequate zinc status is essential for T - cell division, maturation and
differentiation; lymphocyte response to mitogens; programmed cell death of lymphoid and
myeloid origins; gene transcription; and biomembrane function.