The effect of mutations that truncate the WT1 protein on in vitro hematopoietic differentiation from embryonal stem cells has been examined by CFU-A assay, o-dianisidine staining for heme, and RT-PCR analysis of the expression of fetal and adult globins. In two independently isolated ES cell lines the mutations delay but do not abolish hematopoiesis. Analysis of replated CFU-A colonies indicates that the delay occurs prior to the formation of hematopoietic stem cells. The results demonstrate a role for WT1 at the onset of hematopoiesis.
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http://dx.doi.org/10.1006/bcmd.2002.0529 | DOI Listing |
J Biol Chem
November 2024
Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA. Electronic address:
Nature
October 2024
Paris Cardiovascular Research Center, Université Paris Cité, INSERM U970, Paris, France.
Stem Cell Reports
April 2024
The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Melbourne, VIC 3052, Australia. Electronic address:
The histone lysine acetyltransferase KAT6B (MYST4, MORF, QKF) is the target of recurrent chromosomal translocations causing hematological malignancies with poor prognosis. Using Kat6b germline deletion and overexpression in mice, we determined the role of KAT6B in the hematopoietic system. We found that KAT6B sustained the fetal hematopoietic stem cell pool but did not affect viability or differentiation.
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May 2024
Department of Pathology, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Mail Stop 342, Memphis, TN, 38105, USA.
MGA (Max-gene associated) is a dual-specificity transcription factor that negatively regulates MYC-target genes to inhibit proliferation and promote differentiation. Loss-of-function mutations in MGA have been commonly identified in several hematological neoplasms, including acute myeloid leukemia (AML) with RUNX1::RUNX1T1, however, very little is known about the impact of these MGA alterations on normal hematopoiesis or disease progression. We show that representative MGA mutations identified in patient samples abolish protein-protein interactions and transcriptional activity.
View Article and Find Full Text PDFBlood
April 2024
Molecular Medicine, Columbia University Medical Center, New York, NY.
Increased eosinophil counts are associated with cardiovascular disease and may be an independent predictor of major cardiovascular events. However, the causality and underlying mechanisms are poorly understood. Genome-wide association studies have shown an association of a common LNK variant (R262W, T allele) with eosinophilia and atherothrombotic disorders.
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