SALL4 as a transcriptional and epigenetic regulator in normal and leukemic hematopoiesis

Abstract

In recent years, there has been substantial progress in our knowledge of the molecular pathways by which stem cell factor SALL4 regulates the embryonic stem cell (ESC) properties, developmental events, and human cancers. This review summarizes recent advances in the biology of SALL4 with a focus on its regulatory functions in normal and leukemic hematopoiesis. In the normal hematopoietic system, expression of SALL4 is mainly enriched in the bone marrow hematopoietic stem/progenitor cells (HSCs/HPCs), but is rapidly silenced following lineage differentiation. In hematopoietic malignancies, however, SALL4 expression is abnormally re-activated and linked with deteriorated disease status in patients. Further, SALL4 activation participates in the pathogenesis of tumor initiation and disease progression. Thus, a better understanding of SALL4’s biologic functions and mechanisms will facilitate development of advanced targeted anti-leukemia approaches in future.

A transcriptomics resource reveals a transcriptional transition during ordered sarcomere morphogenesis in flight muscle

“…Here we demonstrated that Salm is continuously required for correct sarcomere morphogenesis, as late salm knock-down leads to defects in sarcomere growth during the late sarcomere maturation phase, causing severe muscle atrophy in adults. It might do so by modifying the cooperation between Mef2 and E2F or by changing chromatin states, as vertebrate spalt homologs are recently discussed as epigenetic regulators ( Yang, 2018 ; Zhang et al, 2015 ). However, Salm cannot be solely responsible for the transcriptional transition after 30 hr APF, as the transition still partially occurs in its absence.…”

Gilteritinib: a novel FLT3 inhibitor for acute myeloid leukemia

“…Recurrent and novel genetic mutations are increasingly discovered through FISH, PCR and next-generation sequencing studies of leukemia specimens [1][2][3][4][5]. These findings led to new classifications of leukemia [2,6].…”

Tissue microenvironment initiates an immune response to structural components of Staphylococcus aureus

“…We first analysed the surface expression of CD68 and HLA-DR, markers expressed by macrophages. [23] Fibroblast-conditioned medium HKSA decreased the level of These results were correlated with the number of cells expressing macrophage marker CD68 ( Figure 3B-C). Under both treatments, we observed two populations that were discriminated by their level of CD14 expression: CD14 high CD68 + and CD14 low CD68 + .…”