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101. Decoding myofibroblast origins in human kidney fibrosis

Author

Kuppe, Christoph, primary, Ibrahim, Mahmoud M., additional, Kranz, Jennifer, additional, Zhang, Xiaoting, additional, Ziegler, Susanne, additional, Perales-Patón, Javier, additional, Jansen, Jitske, additional, Reimer, Katharina C., additional, Smith, James R., additional, Dobie, Ross, additional, Wilson-Kanamori, John R., additional, Halder, Maurice, additional, Xu, Yaoxian, additional, Kabgani, Nazanin, additional, Kaesler, Nadine, additional, Klaus, Martin, additional, Gernhold, Lukas, additional, Puelles, Victor G., additional, Huber, Tobias B., additional, Boor, Peter, additional, Menzel, Sylvia, additional, Hoogenboezem, Remco M., additional, Bindels, Eric M. J., additional, Steffens, Joachim, additional, Floege, Jürgen, additional, Schneider, Rebekka K., additional, Saez-Rodriguez, Julio, additional, Henderson, Neil C., additional, and Kramann, Rafael, additional

Published
2020
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103. Human adult germline stem cells in question

Author

Ko, Kinarm, Araúzo-Bravo, Marcos J., Tapia, Natalia, Kim, Julee, Lin, Qiong, Bernemann, Christof, Han, Dong Wook, Gentile, Luca, Reinhardt, Peter, Greber, Boris, Schneider, Rebekka K., Kliesch, Sabine, Zenke, Martin, and Schöler, Hans R.

Published
2010
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105. Adult human kidney organoids originate from CD24+cells and represent an advanced model for adult polycystic kidney disease

Author

Xu, Yaoxian, Kuppe, Christoph, Perales-Patón, Javier, Hayat, Sikander, Kranz, Jennifer, Abdallah, Ali T., Nagai, James, Li, Zhijian, Peisker, Fabian, Saritas, Turgay, Halder, Maurice, Menzel, Sylvia, Hoeft, Konrad, Kenter, Annegien, Kim, Hyojin, van Roeyen, Claudia R. C., Lehrke, Michael, Moellmann, Julia, Speer, Thimoteus, Buhl, Eva M., Hoogenboezem, Remco, Boor, Peter, Jansen, Jitske, Knopp, Cordula, Kurth, Ingo, Smeets, Bart, Bindels, Eric, Reinders, Marlies E. J., Baan, Carla, Gribnau, Joost, Hoorn, Ewout J., Steffens, Joachim, Huber, Tobias B., Costa, Ivan, Floege, Jürgen, Schneider, Rebekka K., Saez-Rodriguez, Julio, Freedman, Benjamin S., and Kramann, Rafael

Abstract

Adult kidney organoids have been described as strictly tubular epithelia and termed tubuloids. While the cellular origin of tubuloids has remained elusive, here we report that they originate from a distinct CD24+epithelial subpopulation. Long-term-cultured CD24+cell-derived tubuloids represent a functional human kidney tubule. We show that kidney tubuloids can be used to model the most common inherited kidney disease, namely autosomal dominant polycystic kidney disease (ADPKD), reconstituting the phenotypic hallmark of this disease with cyst formation. Single-cell RNA sequencing of CRISPR–Cas9 gene-edited PKD1-and PKD2-knockout tubuloids and human ADPKD and control tissue shows similarities in upregulation of disease-driving genes. Furthermore, in a proof of concept, we demonstrate that tolvaptan, the only approved drug for ADPKD, has a significant effect on cyst size in tubuloids but no effect on a pluripotent stem cell-derived model. Thus, tubuloids are derived from a tubular epithelial subpopulation and represent an advanced system for ADPKD disease modeling.

Published
2022
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106. Malignant Transformation Involving CXXC4 Mutations Identified in a Leukemic Progression Model of Severe Congenital Neutropenia

Author

Olofsen, Patricia A, Fatrai, Szabolcs, van Strien, Paulina M H, Obenauer, Julia C, de Looper, Hans W J, Hoogenboezem, Remco M, Erpelinck-Verschueren, Claudia A J, Vermeulen, Michael P W M, Roovers, Onno, Haferlach, Torsten, Jansen, Joop H, Ghazvini, Mehrnaz, Bindels, Eric M J, Schneider, Rebekka K, de Pater, Emma M, Touw, Ivo P, Olofsen, Patricia A, Fatrai, Szabolcs, van Strien, Paulina M H, Obenauer, Julia C, de Looper, Hans W J, Hoogenboezem, Remco M, Erpelinck-Verschueren, Claudia A J, Vermeulen, Michael P W M, Roovers, Onno, Haferlach, Torsten, Jansen, Joop H, Ghazvini, Mehrnaz, Bindels, Eric M J, Schneider, Rebekka K, de Pater, Emma M, and Touw, Ivo P

Abstract

Severe congenital neutropenia (SCN) patients treated with CSF3/G-CSF to alleviate neutropenia frequently develop acute myeloid leukemia (AML). A common pattern of leukemic transformation involves the appearance of hematopoietic clones with CSF3 receptor (CSF3R) mutations in the neutropenic phase, followed by mutations in RUNX1 before AML becomes overt. To investigate how the combination of CSF3 therapy and CSF3R and RUNX1 mutations contributes to AML development, we make use of mouse models, SCN-derived induced pluripotent stem cells (iPSCs), and SCN and SCN-AML patient samples. CSF3 provokes a hyper-proliferative state in CSF3R/RUNX1 mutant hematopoietic progenitors but does not cause overt AML. Intriguingly, an additional acquired driver mutation in Cxxc4 causes elevated CXXC4 and reduced TET2 protein levels in murine AML samples. Expression of multiple pro-inflammatory pathways is elevated in mouse AML and human SCN-AML, suggesting that inflammation driven by downregulation of TET2 activity is a critical step in the malignant transformation of SCN.

Published
2020

108. Transcriptional Landscape of the Microenvironment in Bone Marrow Fibrosis at Single Cell Level

Author

Leimkühler, Nils B., primary, Li, Ronghui, additional, Gleitz, Helene, additional, Snoeren, Inge, additional, Fuchs, Stijn, additional, Crysandt, Martina, additional, Koschmieder, Steffen, additional, Kuppe, Christoph, additional, Buesche, Guntram, additional, Kreipe, Hans H, additional, Costa, Ivan, additional, Kramann, Rafael, additional, and Schneider, Rebekka K., additional

Published
2019
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109. Deconstructing the Clonal Advantage and Clonal Stability of 5q- Candidate Genes in Del(5q) MDS on a Single Cell Level

Author

Stalmann, Ursula S.A., primary, Ticconi, Fabio, primary, Li, Ronghui, primary, Wong, Aaron B., primary, Cowley, Glenn, primary, Root, David E., primary, Heckl, Dirk, primary, Snoeren, Inge, primary, Martinez, Sergio, primary, Brümmendorf, Tim H, primary, Schuppert, Andreas, primary, Costa, Ivan, primary, Ebert, Benjamin L., primary, and Schneider, Rebekka K., primary

Published
2019
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111. Dissecting the Functional Reprogramming of the Microenvironment in Bone Marrow Fibrosis at the Single Cell Level

Author

Leimkühler, Nils B., primary, Ronghui, Li, additional, Gleitz, Hélène F.E., additional, Snoeren, Inge A. M., additional, Fuchs, Stijn N.R., additional, Kuppe, Christoph, additional, Stalmann, Ursula S. A., additional, Buesche, Guntram, additional, Kreipe, Hans, additional, Gütgemann, Ines, additional, Krebs, Philippe, additional, Banz, Yara, additional, Boor, Peter, additional, Tai, Evelyn Wing-Ying, additional, Brümmendorf, Tim H., additional, Koschmieder, Steffen, additional, Crysandt, Martina, additional, Bindels, Eric, additional, Kramann, Rafael, additional, Costa, Ivan G., additional, and Schneider, Rebekka K., additional

Published
2019
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112. Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., primary, Mullally, Ann, additional, Dugourd, Aurelien, additional, Peisker, Fabian, additional, Hoogenboezem, Remco, additional, Van Strien, Paulina M.H., additional, Bindels, Eric M., additional, Heckl, Dirk, additional, Büsche, Guntram, additional, Fleck, David, additional, Müller-Newen, Gerhard, additional, Wongboonsin, Janewit, additional, Ventura Ferreira, Monica, additional, Puelles, Victor G., additional, Saez-Rodriguez, Julio, additional, Ebert, Benjamin L., additional, Humphreys, Benjamin D., additional, and Kramann, Rafael, additional

Published
2018
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116. Increased neutrophil extracellular trap formation promotes thrombosis in myeloproliferative neoplasms

Author

Wolach, Ofir, primary, Sellar, Rob S., additional, Martinod, Kimberly, additional, Cherpokova, Deya, additional, McConkey, Marie, additional, Chappell, Ryan J., additional, Silver, Alexander J., additional, Adams, Dylan, additional, Castellano, Cecilia A., additional, Schneider, Rebekka K., additional, Padera, Robert F., additional, DeAngelo, Daniel J., additional, Wadleigh, Martha, additional, Steensma, David P., additional, Galinsky, Ilene, additional, Stone, Richard M., additional, Genovese, Giulio, additional, McCarroll, Steven A., additional, Iliadou, Bozenna, additional, Hultman, Christina, additional, Neuberg, Donna, additional, Mullally, Ann, additional, Wagner, Denisa D., additional, and Ebert, Benjamin L., additional

Published
2018
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117. Core Circadian Clock Genes Regulate Leukemia Stem Cells in AML

Author

Massachusetts Institute of Technology. Department of Biology, Regev, Aviv, Puram, Rishi V., Kowalczyk, Monika S., de Boer, Carl G., Schneider, Rebekka K., Miller, Peter G., McConkey, Marie, Tothova, Zuzana, Tejero, Héctor, Heckl, Dirk, Järås, Marcus, Chen, Michelle C., Li, Hubo, Tamayo, Alfred, Cowley, Glenn S., Rozenblatt-Rosen, Orit, Al-Shahrour, Fatima, Ebert, Benjamin L., Massachusetts Institute of Technology. Department of Biology, Regev, Aviv, Puram, Rishi V., Kowalczyk, Monika S., de Boer, Carl G., Schneider, Rebekka K., Miller, Peter G., McConkey, Marie, Tothova, Zuzana, Tejero, Héctor, Heckl, Dirk, Järås, Marcus, Chen, Michelle C., Li, Hubo, Tamayo, Alfred, Cowley, Glenn S., Rozenblatt-Rosen, Orit, Al-Shahrour, Fatima, and Ebert, Benjamin L.

Abstract

Leukemia stem cells (LSCs) have the capacity to self-renew and propagate disease upon serial transplantation in animal models, and elimination of this cell population is required for curative therapies. Here, we describe a series of pooled, in vivo RNAi screens to identify essential transcription factors (TFs) in a murine model of acute myeloid leukemia (AML) with genetically and phenotypically defined LSCs. These screens reveal the heterodimeric, circadian rhythm TFs Clock and Bmal1 as genes required for the growth of AML cells in vitro and in vivo. Disruption of canonical circadian pathway components produces anti-leukemic effects, including impaired proliferation, enhanced myeloid differentiation, and depletion of LSCs. We find that both normal and malignant hematopoietic cells harbor an intact clock with robust circadian oscillations, and genetic knockout models reveal a leukemia-specific dependence on the pathway. Our findings establish a role for the core circadian clock genes in AML., National Institutes of Health (U.S.) (Grant P01 CA066996), National Institutes of Health (U.S.) (Grant R01 HL082945), National Cancer Institute (U.S.) (Grant P30-CA14051)

Published
2018

119. Gli1 + Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target

Author

Schneider, Rebekka K., primary, Mullally, Ann, additional, Dugourd, Aurelien, additional, Peisker, Fabian, additional, Hoogenboezem, Remco, additional, Van Strien, Paulina M.H., additional, Bindels, Eric M., additional, Heckl, Dirk, additional, Büsche, Guntram, additional, Fleck, David, additional, Müller-Newen, Gerhard, additional, Wongboonsin, Janewit, additional, Ventura Ferreira, Monica, additional, Puelles, Victor G., additional, Saez-Rodriguez, Julio, additional, Ebert, Benjamin L., additional, Humphreys, Benjamin D., additional, and Kramann, Rafael, additional

Published
2017
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120. Single-cell RNA-seq reveals changes in cell cycle and differentiation programs upon aging of hematopoietic stem cells

Author

Massachusetts Institute of Technology. Department of Biology, Regev, Aviv, Kowalczyk, Monika S., Tirosh, Itay, Heckl, Dirk, Rao, Tata Nageswara, Dixit, Atray, Haas, Brian J., Schneider, Rebekka K., Wagers, Amy J., Ebert, Benjamin L., Massachusetts Institute of Technology. Department of Biology, Regev, Aviv, Kowalczyk, Monika S., Tirosh, Itay, Heckl, Dirk, Rao, Tata Nageswara, Dixit, Atray, Haas, Brian J., Schneider, Rebekka K., Wagers, Amy J., and Ebert, Benjamin L.

Abstract

Both intrinsic cell state changes and variations in the composition of stem cell populations have been implicated as contributors to aging. We used single-cell RNA-seq to dissect variability in hematopoietic stem cell (HSC) and hematopoietic progenitor cell populations from young and old mice from two strains. We found that cell cycle dominates the variability within each population and that there is a lower frequency of cells in the G1 phase among old compared with young long-term HSCs, suggesting that they traverse through G1 faster. Moreover, transcriptional changes in HSCs during aging are inversely related to those upon HSC differentiation, such that old short-term (ST) HSCs resemble young long-term (LT-HSCs), suggesting that they exist in a less differentiated state. Our results indicate both compositional changes and intrinsic, population-wide changes with age and are consistent with a model where a relationship between cell cycle progression and self-renewal versus differentiation of HSCs is affected by aging and may contribute to the functional decline of old HSCs., Howard Hughes Medical Institute, National Institutes of Health (U.S.) (Centers of Excellence in Genomic Science Award 1P50HG006193-01), National Cancer Institute (U.S.) (Koch Institute Support (Core) Grant P30-CA14051), Klarman Cell Observatory

Published
2016

122. Thrombosis in Myeloproliferative Neoplasms Is Linked to Increased Neutrophil Extracellular Trap (NET) Formation

Author

Wolach, Ofir, primary, Sellar, Rob S, additional, Martinod, Kimberly, additional, McConkey, Marie E., additional, Silver, Alexander J., additional, Chappell, Ryan, additional, Stone, Richard M., additional, Wadleigh, Martha, additional, Steensma, David P, additional, DeAngelo, Daniel J., additional, Galinsky, Ilene, additional, Schneider, Rebekka K., additional, Padera, Robert F., additional, Mullally, Ann, additional, Wagner, Denisa D., additional, and Ebert, Benjamin L., additional

Published
2016
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123. Physiologic Expression of Sf3b1 K700E Causes Impaired Erythropoiesis, Aberrant Splicing, and Sensitivity to Therapeutic Spliceosome Modulation

Author

Obeng, Esther A., primary, Chappell, Ryan J., additional, Seiler, Michael, additional, Chen, Michelle C., additional, Campagna, Dean R., additional, Schmidt, Paul J., additional, Schneider, Rebekka K., additional, Lord, Allegra M., additional, Wang, Lili, additional, Gambe, Rutendo G., additional, McConkey, Marie E., additional, Ali, Abdullah M., additional, Raza, Azra, additional, Yu, Lihua, additional, Buonamici, Silvia, additional, Smith, Peter G., additional, Mullally, Ann, additional, Wu, Catherine J., additional, Fleming, Mark D., additional, and Ebert, Benjamin L., additional

Published
2016
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124. Mutant Calreticulin Requires Both Its Mutant C-terminus and the Thrombopoietin Receptor for Oncogenic Transformation

Author

Elf, Shannon, primary, Abdelfattah, Nouran S., additional, Chen, Edwin, additional, Perales-Patón, Javier, additional, Rosen, Emily A., additional, Ko, Amy, additional, Peisker, Fabian, additional, Florescu, Natalie, additional, Giannini, Silvia, additional, Wolach, Ofir, additional, Morgan, Elizabeth A., additional, Tothova, Zuzana, additional, Losman, Julie-Aurore, additional, Schneider, Rebekka K., additional, Al-Shahrour, Fatima, additional, and Mullally, Ann, additional

Published
2016
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125. Sequentially inducible mouse models reveal that Npm1mutation causes malignant transformation of Dnmt3a-mutant clonal hematopoiesis

Author

Loberg, Matthew A., Bell, Rebecca K., Goodwin, Leslie O., Eudy, Elizabeth, Miles, Linde A., SanMiguel, Jennifer M., Young, Kira, Bergstrom, David E., Levine, Ross L., Schneider, Rebekka K., and Trowbridge, Jennifer J.

Abstract

Clonal hematopoiesis (CH) is a common aging-associated condition with increased risk of hematologic malignancy. Knowledge of the mechanisms driving evolution from CH to overt malignancy has been hampered by a lack of in vivo models that orthogonally activate mutant alleles. Here, we develop independently regulatable mutations in DNA methyltransferase 3A (Dnmt3a) and nucleophosmin 1 (Npm1), observed in human CH and AML, respectively. We find Dnmt3amutation expands hematopoietic stem and multipotent progenitor cells (HSC/MPPs), modeling CH. Induction of mutant Npm1after development of Dnmt3a-mutant CH causes progression to myeloproliferative disorder (MPD), and more aggressive MPD is observed with longer latency between mutations. MPDs uniformly progress to acute myeloid leukemia (AML) following transplant, accompanied by a decrease in HSC/MPPs and an increase in myeloid-restricted progenitors, the latter of which propagate AML in tertiary recipient mice. At a molecular level, progression of CH to MPD is accompanied by selection for mutations activating Ras/Raf/MAPK signaling. Progression to AML is characterized by additional oncogenic signaling mutations (Ptpn11, Pik3r1, Flt3) and/or mutations in epigenetic regulators (Hdac1, Idh1, Arid1a). Together, our study demonstrates that Npm1mutation drives evolution of Dnmt3a-mutant CH to AML and rate of disease progression is accelerated with longer latency of CH.

Published
2019
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126. Rps14, Csnk1a1and miRNA145/miRNA146adeficiency cooperate in the clinical phenotype and activation of the innate immune system in the 5q- syndrome

Author

Ribezzo, Flavia, Snoeren, Inge A. M., Ziegler, Susanne, Stoelben, Jacques, Olofsen, Patricia A., Henic, Almira, Ferreira, Monica Ventura, Chen, Si, Stalmann, Ursula S. A., Buesche, Guntram, Hoogenboezem, Remco M., Kramann, Rafael, Platzbecker, Uwe, Raaijmakers, Marc H. G. P., Ebert, Benjamin L., and Schneider, Rebekka K.

Abstract

RPS14, CSNK1A1, and miR-145are universally co-deleted in the 5q- syndrome, but mouse models of each gene deficiency recapitulate only a subset of the composite clinical features. We analyzed the combinatorial effect of haploinsufficiency for Rps14, Csnk1a1, and miRNA-145, using mice with genetically engineered, conditional heterozygous inactivation of Rps14and Csnk1a1and stable knockdown of miR-145/miR-146a. Combined Rps14/Csnk1a1/miR-145/146adeficiency recapitulated the cardinal features of the 5q- syndrome, including (1) more severe anemia with faster kinetics than Rps14haploinsufficiency alone and (2) pathognomonic megakaryocyte morphology. Macrophages, regulatory cells of erythropoiesis and the innate immune response, were significantly increased in Rps14/Csnk1a1/miR-145/146adeficient mice as well as in 5q- syndrome patient bone marrows and showed activation of the innate immune response, reflected by increased expression of S100A8, and decreased phagocytic function. We demonstrate that Rps14/Csnk1a1/miR-145 and miR-146adeficient macrophages alter the microenvironment and induce S100A8 expression in the mesenchymal stem cell niche. The increased S100A8 expression in the mesenchymal niche was confirmed in 5q- syndrome patients. These data indicate that intrinsic defects of the 5q- syndrome hematopoietic stem cell directly alter the surrounding microenvironment, which in turn affects hematopoiesis as an extrinsic mechanism.

Published
2019
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127. An engineered multicomponent bone marrow niche for the recapitulation of hematopoiesis at ectopic transplantation sites

Author

Ventura Ferreira, Mónica S., primary, Bergmann, Christian, additional, Bodensiek, Isabelle, additional, Peukert, Kristina, additional, Abert, Jessica, additional, Kramann, Rafael, additional, Kachel, Paul, additional, Rath, Björn, additional, Rütten, Stephan, additional, Knuchel, Ruth, additional, Ebert, Benjamin L., additional, Fischer, Horst, additional, Brümmendorf, Tim H., additional, and Schneider, Rebekka K., additional

Published
2016
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128. Physical Interaction Between Mutant Calreticulin and the Thrombopoietin Receptor Is Required for Hematopoietic Transformation

Author

Elf, Shannon, primary, Abdelfattah, Nouran, additional, Chen, Edwin, additional, Perales-Patón, Javier, additional, Rosen, Emily, additional, Ko, Amy, additional, Peisker, Fabian, additional, Florescu, Natalie, additional, Giannini, Silvia, additional, Wolach, Ofir, additional, Morgan, Elizabeth A., additional, Losman, Julie-Aurore, additional, Schneider, Rebekka K., additional, Al-Shahrour, Fatima, additional, and Mullally, Ann, additional

Published
2015
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129. A Novel Conditional Knockout of the Diamond Blackfan Anemia Gene Rpl11 Shows Failure of Erythropoiesis, a Marked Increase in BFU-E Progenitors By Phenotype That Proliferate Poorly in Culture, and Activation of p53 Target Genes

Author

Joyce, Cailin E, primary, McGuinness, Meaghan, additional, Schneider, Rebekka K, additional, Fleming, Mark D., additional, Campagna, Dean R, additional, Schmidt, Paul J, additional, Ebert, Benjamin L, additional, Novina, Carl D., additional, and Sieff, Colin A., additional

Published
2015
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130. Targeting megakaryocytic-induced fibrosis in myeloproliferative neoplasms by AURKA inhibition

Author

Jeremy Wen, Qiang, primary, Yang, Qiong, additional, Goldenson, Benjamin, additional, Malinge, Sébastien, additional, Lasho, Terra, additional, Schneider, Rebekka K, additional, Breyfogle, Lawrence J, additional, Schultz, Rachael, additional, Gilles, Laure, additional, Koppikar, Priya, additional, Abdel-Wahab, Omar, additional, Pardanani, Animesh, additional, Stein, Brady, additional, Gurbuxani, Sandeep, additional, Mullally, Ann, additional, Levine, Ross L, additional, Tefferi, Ayalew, additional, and Crispino, John D, additional

Published
2015
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134. Loss of TET2 Function in Myelodysplastic Syndrome Results in Intragenic Hypermethylation and Alterations in mRNA Splicing

Author

Lord, Allegra M, primary, Clement, Kendell, additional, Schneider, Rebekka K., additional, Marie, McConkey, additional, Chen, Michelle C., additional, Levine, Ross L., additional, Mullally, Ann, additional, Galili, Naomi, additional, Ali, Abdullah Mahmood, additional, Raza, Azra, additional, Bejar, Rafael, additional, Meissner, Alexander, additional, and Ebert, Benjamin L., additional

Published
2014
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136. Activated fibronectin-secretory phenotype of mesenchymal stromal cells in pre-fibrotic myeloproliferative neoplasms

Author

Schneider, Rebekka K, primary, Ziegler, Susanne, additional, Leisten, Isabelle, additional, Ferreira, Monica SV, additional, Schumacher, Anne, additional, Rath, Björn, additional, Fahrenkamp, Dirk, additional, Müller-Newen, Gerhard, additional, Crysandt, Martina, additional, Wilop, Stefan, additional, Jost, Edgar, additional, Koschmieder, Steffen, additional, Knüchel, Ruth, additional, Brümmendorf, Tim H, additional, and Ziegler, Patrick, additional

Published
2014
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137. Cell Fusion Enhances Mesendodermal Differentiation of Human Induced Pluripotent Stem Cells

Author

Qin, Jie, primary, Sontag, Stephanie, additional, Lin, Qiong, additional, Mitzka, Saskia, additional, Leisten, Isabelle, additional, Schneider, Rebekka K., additional, Wang, Xiaoying, additional, Jauch, Anna, additional, Peitz, Michael, additional, Brüstle, Oliver, additional, Wagner, Wolfgang, additional, Zhao, Robert Chunhua, additional, and Zenke, Martin, additional

Published
2014
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138. Speckle Tracking Echocardiography Detects Uremic Cardiomyopathy Early and Predicts Cardiovascular Mortality in ESRD

Author

Kramann, Rafael, primary, Erpenbeck, Johanna, additional, Schneider, Rebekka K., additional, Röhl, Anna B., additional, Hein, Marc, additional, Brandenburg, Vincent M., additional, van Diepen, Merel, additional, Dekker, Friedo, additional, Marx, Nicolaus, additional, Floege, Jürgen, additional, Becker, Michael, additional, and Schlieper, Georg, additional

Published
2014
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140. Csnk1a1 inhibition has p53-dependent therapeutic efficacy in acute myeloid leukemia

Author

Järås, Marcus, primary, Miller, Peter G., additional, Chu, Lisa P., additional, Puram, Rishi V., additional, Fink, Emma C., additional, Schneider, Rebekka K., additional, Al-Shahrour, Fatima, additional, Peña, Pablo, additional, Breyfogle, L. Jordan, additional, Hartwell, Kimberly A., additional, McConkey, Marie E., additional, Cowley, Glenn S., additional, Root, David E., additional, Kharas, Michael G., additional, Mullally, Ann, additional, and Ebert, Benjamin L., additional

Published
2014
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142. Sustained Alterations In Bone Marrow Stromal Cells From Patients With Myeloproliferative Neoplasms (MPN) Contribute To Remodelling Of The Bone Marrow Microenvironment Prior To The Manifestation Of Myelofibrosis

Author

Schneider, Rebekka K., primary, Leisten, Isabelle, additional, Ziegler, Susanne, additional, Schumacher, Anne, additional, Rath, Björn, additional, Fahrenkamp, Dirk, additional, Mueller-Newen, Gerhard, additional, Crysandt, Martina, additional, Wilop, Stefan, additional, Jost, Edgar, additional, Knuechel, Ruth, additional, Bruemmendorf, Tim H., additional, and Ziegler, Patrick, additional

Published
2013
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144. Reconsidering pluripotency tests: Do we still need teratoma assays?

Author

Buta, Christiane, primary, David, Robert, additional, Dressel, Ralf, additional, Emgård, Mia, additional, Fuchs, Christiane, additional, Gross, Ulrike, additional, Healy, Lyn, additional, Hescheler, Jürgen, additional, Kolar, Roman, additional, Martin, Ulrich, additional, Mikkers, Harald, additional, Müller, Franz-Josef, additional, Schneider, Rebekka K., additional, Seiler, Andrea E.M., additional, Spielmann, Horst, additional, and Weitzer, Georg, additional

Published
2013
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145. Novel insights into osteogenesis and matrix remodelling associated with calcific uraemic arteriolopathy

Author

Kramann, Rafael, primary, Brandenburg, Vincent M., additional, Schurgers, Leon J., additional, Ketteler, Markus, additional, Westphal, Saskia, additional, Leisten, Isabelle, additional, Bovi, Manfred, additional, Jahnen-Dechent, Willi, additional, Knüchel, Ruth, additional, Floege, Jürgen, additional, and Schneider, Rebekka K., additional

Published
2012
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148. Comparative Analysis of Hematopoiesis Supporting Capacity and Matrix Remodeling of Bone Marrow Stromal Cells Isolated From Patients with Myeloproliferative Neoplasms.

Author

Schneider, Rebekka K, primary, Leisten, Isabelle, additional, Ziegler, Susanne, additional, Schumacher, Anne, additional, Fahrenkamp, Dirk, additional, Mueller-Newen, Gerhard, additional, Crysandt, Martina, additional, Jost, Edgar, additional, Knuechel, Ruth, additional, Brümmendorf, Tim H, additional, and Ziegler, Patrick, additional

Published
2012
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149. Casein Kinase 1 Alpha Maintains Normal and Leukemic Stem Cells by Regulating p53 Activity

Author

Järås, Marcus, primary, Miller, Peter G., additional, Chu, Lisa, additional, Schneider, Rebekka K., additional, Puram, Rishi V, additional, Al-Shahrour, Fatima, additional, Fink, Emma, additional, Hartwell, Kimberly A., additional, McConkey, Marie, additional, Cowley, Glenn, additional, Mullally, Ann, additional, Kharas, Michael G, additional, and Ebert, Benjamin L., additional

Published
2012
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150. Met-Signaling Controls Dendritic Cell Migration in Skin by Regulating Podosome Formation and Function

Author

Hamouda, Ahmed E.I., Schalla, Carmen, Sechi, Antonio, Zenke, Martin, Schneider, Rebekka K., and Hieronymus, Thomas

Abstract

Signaling through the HGF receptor/Met in skin-resident Langerhans cells (LCs) and dermal dendritic cells (DCs) is essential for their emigration toward draining lymph nodes upon inflammation-induced activation. In this study, we addressed the role of Met signaling in distinct steps of LC/dermal DC emigration from the skin by employing a conditionally Met-deficient mouse model (Metflox/flox). We found that Met deficiency severely impaired podosome formation in DCs and concomitantly decreased the proteolytic degradation of gelatin. Accordingly, Met-deficient LCs failed to efficiently cross the extracellular matrix−rich basement membrane between the epidermis and the dermis. We further observed that HGF-dependent Met activation reduced the adhesion of bone marrow−derived LCs to various extracellular matrix factors and enhanced the motility of DCs in three-dimensional collagen matrices, which was not the case for Met-deficient LCs/DCs. We found no impact of Met signaling on the integrin-independent amoeboid migration of DCs in response to the CCR7 ligand CCL19. Collectively, our data show that the Met-signaling pathway regulates the migratory properties of DC in HGF-dependent and HGF-independent manners.

Published
2023
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