Not exact matches
The protein is now known to interact
with and
control dozens of different genes and proteins, and it helps regulate the
cycle of molecular events by which
cells grow and reproduce.
It is therefore essential that there be
control mechanisms capable of detecting errors in this process and halting the
cell cycle with the aim of allowing the
cell to repair the breakages or, if not possible, to eliminate the damaged
cell.
Significantly, treatment
with 6AN specifically decreased the activity of genes
with malignant, cancer - spreading functions, like
cell cycle control and DNA repair.
How the vital processes of
cell cycle control (
with the final event of cytokinesis) and signalling for
cell wall biosynthesis are exactly coordinated remains to be determined.
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.
This diverse «toolkit» of genes correlates
with critical aspects of all metazoan body plans, and comprises
cell cycle control and growth, development, somatic - and germ -
cell specification,
cell adhesion, innate immunity and allorecognition.
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