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Your search keyword '"Holland-Letz, Tim"' showing total 6 results
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6 results on '"Holland-Letz, Tim"'

1. No Evidence for Hematopoietic Stem Cell Self-Renewal in-Vivo Following Inflammatory Challenge

Author

Bogeska, Ruzhica, primary, Kaschutnig, Paul, primary, Paffenholz, Stella V, primary, Knoch, Julia, primary, Mallm, Jan-Philipp, primary, Fawaz, Malak, primary, Buettner, Florian, primary, Walter, Dagmar, primary, Frauhammer, Felix, primary, Holland-Letz, Tim, primary, Asada, Noboru, primary, Mikecin Drazic, Ana-Matea, primary, Buechler-Schaff, Marleen, primary, Correno-Gonzalez, Martha, primary, Ball, Melanie, primary, Staeble, Sina, primary, Gräsel, Julius, primary, Haas, Simon, primary, Lipka, Daniel B., primary, Rippe, Karsten, primary, Brors, Benedikt, primary, Frenette, Paul S., primary, Rieger, Michael A., primary, Essers, Marieke A. G., primary, and Milsom, Michael D., primary

Published
2019
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2. Hematopoietic Stem Cells Fail to Regenerate In Vivo Following Inflammatory Stress

Author

Bogeska, Ruzhica, primary, Kaschutnig, Paul, additional, Paffenholz, Stella, additional, Maassen, Julia, additional, Mallm, Jan-Philipp, additional, Wertek, Felix, additional, Walter, Dagmar, additional, Sandra, Blaszkiewicz, additional, Holland-Letz, Tim, additional, Asada, Noboru, additional, Gräsel, Julius, additional, Stäble, Sina, additional, Block, Milena, additional, Gizlenci, Özge, additional, Prendergast, Áine M., additional, Haas, Simon, additional, Lipka, Daniel B, additional, Rippe, Karsten, additional, Brors, Benedikt, additional, Frenette, Paul S., additional, Essers, Marieke A. G., additional, and Milsom, Michael D., additional

Published
2016
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3. Altered HSC Metabolism in Response to Stress Leads to De Novo dna Damage and Cellular Attrition

Author

Geiselhart, Anja, primary, Walter, Dagmar, additional, Lier, Amelie, additional, Thalheimer, Frederic B., additional, Huntscha, Sina, additional, Brocks, David, additional, Bayindir, Irem, additional, Kaschutnig, Paul, additional, Müdder, Katja, additional, Sobotta, Mirko, additional, Dick, Tobias, additional, Holland-Letz, Tim, additional, Schmezer, Peter, additional, Schröder, Timm, additional, Lane, Steven W, additional, Essers, Marieke, additional, Rieger, Michael A., additional, Williams, David A., additional, Trumpp, Andreas, additional, and Milsom, Michael D., additional

Published
2014
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4. No Evidence for Hematopoietic Stem Cell Self-Renewal in-VivoFollowing Inflammatory Challenge

Author

Bogeska, Ruzhica, Kaschutnig, Paul, Paffenholz, Stella V, Knoch, Julia, Mallm, Jan-Philipp, Fawaz, Malak, Buettner, Florian, Walter, Dagmar, Frauhammer, Felix, Holland-Letz, Tim, Asada, Noboru, Mikecin Drazic, Ana-Matea, Buechler-Schaff, Marleen, Correno-Gonzalez, Martha, Ball, Melanie, Staeble, Sina, Gräsel, Julius, Haas, Simon, Lipka, Daniel B., Rippe, Karsten, Brors, Benedikt, Frenette, Paul S., Rieger, Michael A., Essers, Marieke A.G., and Milsom, Michael D.

Abstract

Elevated levels of inflammation have been previously linked to both inherited and acquired bone marrow failure (BMF) syndromes, as well as to normal aging, suggesting a role in the etiology of these conditions. One potential explanation for this phenomenon is that repeated inflammation can promote the suppression of hematopoietic stem cell (HSC) function.We have previously demonstrated that interferon-α can accelerate HSC attrition by driving HSCs out of quiescence, leading to the development of BMF in a mouse model of Fanconi anemia (Walter et al. Nature, 2015).

Published
2019
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5. Hematopoietic Stem Cells Fail to Regenerate In VivoFollowing Inflammatory Stress

Author

Bogeska, Ruzhica, Kaschutnig, Paul, Paffenholz, Stella, Maassen, Julia, Mallm, Jan-Philipp, Wertek, Felix, Walter, Dagmar, Sandra, Blaszkiewicz, Holland-Letz, Tim, Asada, Noboru, Gräsel, Julius, Stäble, Sina, Block, Milena, Gizlenci, Özge, Prendergast, Áine M., Haas, Simon, Lipka, Daniel B, Rippe, Karsten, Brors, Benedikt, Frenette, Paul S., Essers, Marieke A.G., and Milsom, Michael D.

Abstract

An often-cited defining property of hematopoietic stem cells (HSCs) is their extensive or unlimited in vivoself-renewal capacity. We have recently described a novel mouse disease model forFanconi anemia, in which serial challenge with pro-inflammatory agonists that mimic infection, such aspolyinosinic:polycytidylic acid (pI:C), results in HSC attrition followed by a highly penetrant severe aplastic anemia, closely recapitulating the disease in patients (Walter et al., 2015, Nature).

Published
2016
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6. Altered HSC Metabolism in Response to Stress Leads to De Novodna Damage and Cellular Attrition

Author

Geiselhart, Anja, Walter, Dagmar, Lier, Amelie, Thalheimer, Frederic B., Huntscha, Sina, Brocks, David, Bayindir, Irem, Kaschutnig, Paul, Müdder, Katja, Sobotta, Mirko, Dick, Tobias, Holland-Letz, Tim, Schmezer, Peter, Schröder, Timm, Lane, Steven W, Essers, Marieke, Rieger, Michael A., Williams, David A., Trumpp, Andreas, and Milsom, Michael D.

Abstract

Hematopoietic stem cells (HSCs) reside in a quiescent state, which is thought to preserve their genomic stability during aging. HSCs are forced to exit this so-called dormant state and enter into cycle in response to stress stimuli such as infections or severe bleeding. This situation may provoke high levels of proliferative stress in HSCs and a subsequent decline in stem cell function. We recently found that de novoDNA damage can be precipitated in HSCs in vivoby enforcing cell cycle progression using agonists that mimic physiologic stress, such as interferons, G-CSF, TPO or serial bleeding, (Walter et al., Blood, 122, 21:799). The Fanconi anemia (FA) DNA repair pathway is an important route via which this replication damage is resolved in HSCs in vivo. In FA deficient mice, DNA damage repair was impaired, provoking HSC depletion and severe aplastic anemia (p<0.01) upon serial treatment with the synthetic double-stranded RNA mimetic polyI:polyC (pI:pC). Here, we sought to identify the mechanistic basis of the stress-induced DNA damage acquisition and concomitant HSC attrition in vivo.

Published
2014
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