Mortalin and DJ-1 coordinately regulate hematopoietic stem cell function through the control of oxidative stress

Blood ◽  
2014 ◽  
Vol 123 (1) ◽  
pp. 41-50 ◽  
Author(s):  
Ikue Tai-Nagara ◽  
Sahoko Matsuoka ◽  
Hiroyoshi Ariga ◽  
Toshio Suda

Key Points Mitochondrial heat shock protein, mortalin, is essential for the maintenance of HSCs via the control of oxidative stress. Mortalin directly interact with DJ-1 to regulate ROS levels in the mitochondria of HSCs.

Blood ◽  
2013 ◽  
Vol 121 (25) ◽  
pp. 5015-5024 ◽  
Author(s):  
Sarah J. Stein ◽  
Albert S. Baldwin

Key Points p65 is an important factor in hematopoiesis through the regulation of hematopoietic stem cell function and lineage commitment. p65 controls the expression of genes encoding key factors that promote hematopoietic stem cell homeostasis.


Blood ◽  
2015 ◽  
Vol 125 (12) ◽  
pp. 1890-1900 ◽  
Author(s):  
Sarah A. Kinkel ◽  
Roman Galeev ◽  
Christoffer Flensburg ◽  
Andrew Keniry ◽  
Kelsey Breslin ◽  
...  

Key Points Depletion of Jarid2 in mouse and human hematopoietic stem cells enhances their activity. Jarid2 acts as part of PRC2 in hematopoietic stem and progenitor cells.


Blood ◽  
2017 ◽  
Vol 130 (5) ◽  
pp. 619-624 ◽  
Author(s):  
Brian S. Garrison ◽  
Adrian P. Rybak ◽  
Isabel Beerman ◽  
Balthasar Heesters ◽  
Francois E. Mercier ◽  
...  

Key Points ZFP521 regulates HSC self-renewal and differentiation. ZFP521 facilitates leukemogenesis in an MLL-AF9–mediated leukemia model.


Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2903-2910 ◽  
Author(s):  
John C. H. Byon ◽  
Jing Chen ◽  
Raymond T. Doty ◽  
Janis L. Abkowitz

Key Points FLVCR deletion causes proerythroblast apoptosis and lethal anemia but leads to increased megakaryocyte ploidy and platelet counts. Loss of FLVCR is dispensable for hematopoietic stem cell function during steady-state and stress conditions.


2017 ◽  
Vol 1 (26) ◽  
pp. 2520-2528 ◽  
Author(s):  
Safa F. Mohamad ◽  
Linlin Xu ◽  
Joydeep Ghosh ◽  
Paul J. Childress ◽  
Irushi Abeysekera ◽  
...  

Key Points OM, osteoblast, and megakaryocyte interactions regulate HSC function in the niche. OMs differ functionally and phenotypically from BM-derived macrophages.


Blood ◽  
2016 ◽  
Vol 127 (15) ◽  
pp. 1881-1885 ◽  
Author(s):  
Christelle Vincent-Fabert ◽  
Nadine Platet ◽  
Amelle Vandevelde ◽  
Mathilde Poplineau ◽  
Myriam Koubi ◽  
...  

Key Points Inactivation of PLZF promotes phenotype of HSC aging. PLZF controls HSC cell cycle.


Blood ◽  
2013 ◽  
Vol 122 (11) ◽  
pp. 1914-1922 ◽  
Author(s):  
Andrew G. Muntean ◽  
Wei Chen ◽  
Morgan Jones ◽  
Eric M. Granowicz ◽  
Ivan Maillard ◽  
...  

Key Points The PAFc subunit, Cdc73, is required for the proliferation and proper epigenetic regulation of proleukemic oncogenes in AML cells. Disrupting the MLL-PAFc interaction selectively inhibits the growth of MLL-associated leukemic cells without altering normal hematopoietic stem cell function.


Blood ◽  
2015 ◽  
Vol 126 (2) ◽  
pp. 167-175 ◽  
Author(s):  
Stanley C. W. Lee ◽  
Sarah Miller ◽  
Craig Hyland ◽  
Maria Kauppi ◽  
Marion Lebois ◽  
...  

Key Points Inactivation of Suz12 results in a rapid and marked exhaustion of the HSC pool. Lymphoid development is completely dependent on PRC2, but numerous myeloid lineages develop in the absence of PRC2.


Blood ◽  
2019 ◽  
Vol 134 (20) ◽  
pp. 1712-1716 ◽  
Author(s):  
Jill M. Goldstein ◽  
Hilal Sengul ◽  
Kathleen A. Messemer ◽  
Marcos Fernández-Alfara ◽  
Jessica C. Garbern ◽  
...  

Key Points Genetic deletion of Gdf11 does not affect red blood cell formation during homeostasis or after transplant. Hematopoietic stem cell function is preserved in mice lacking Gdf11 expression within the blood lineage.


Blood ◽  
2015 ◽  
Vol 125 (15) ◽  
pp. 2344-2348 ◽  
Author(s):  
Jad I. Belle ◽  
David Langlais ◽  
Jessica C. Petrov ◽  
Mercedes Pardo ◽  
Russell G. Jones ◽  
...  

Key Points Developmental defects and impairment in lymphopoiesis in Mysm1-knockout mice are the result of p53 activation. Loss of hematopoietic stem cell function and bone marrow failure in Mysm1-knockout mice are the result of p53 activation.


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