ArticleExperimental hematology2011
Mad2 haploinsufficiency protects hematopoietic progenitor cells subjected to cell-cycle stress in vivo and to inhibition of redox function of Ape1/Ref-1 in vitro.
Article in Experimental hematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- APEX1 Nuclease and Redox Functions are Both Essential for Adult Mouse Hematopoietic Stem and Progenitor Cells.Stem cell reviews and reports · 2023Article
- Prion protein deficiency impairs hematopoietic stem cell determination and sensitizes myeloid progenitors to irradiation.Haematologica · 2020Article
- Human adipose-derived stem cells ameliorate cigarette smoke-induced murine myelosuppression via secretion of TSG-6.Stem cells (Dayton, Ohio) · 2015Article
- Haploinsufficiency of SGO1 results in deregulated centrosome dynamics, enhanced chromosomal instability and colon tumorigenesis.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveCell-cycle checkpoints guarantee movement through the cell cycle. Mitotic arrest deficiency 2 (Mad2), a mitotic checkpoint protein, appears crucial for generating the wait anaphase signal to prevent onset of anaphase. We evaluated effects of Mad2 haploinsufficiency on hematopoietic stem (HSC) and progenitor (HPC) function in response to stress. MATERIALS AND
methodsWe studied effects of Mad2(+/-) on in vivo recovery of bone marrow HPC from cytotoxic effects and also effects of cytostatic agents on HPC growth in vitro using Mad2(+/-) mice.
resultsMad2(+/-) HPCs were protected from cytotoxic effects in vivo of a cell-cycle-specific agent, Ara-C, events consistent with Mad2(+/-) HPCs being in a slow or noncycling state, but not from recovery of functional HPC after treatment with non-cycle-specific cyclophosphamide or sublethal irradiation. There were no differences in phenotyped HSCs in Mad2(+/-) &Mad2(+/+) mice, information confirmed by no changes in short- or long-term repopulating HSC assay. To better understand Mad2(+/-) HPC function, E3330, a cytostatic agent, was used to assess redox function of Ape1/Ref-1; colony growth was examined under 5% and 20% O(2) tension. Mad2(+/-) HPCs were less responsive to E3330 than Mad2(+/+) HPCs, and E3330 was more effective under lowered O(2) tension. Mad2(+/-) HPCs were not enhanced at lowered oxygen, as were Mad2(+/+) HPCs.
conclusionsOur studies have unexpectedly found that Mad2 haploinsufficiency is protective in the presence of a cycle-specific DNA synthesis agent in vivo, and Ape1/Ref-1 inhibitor in vitro.
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