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219 results on '"Lacorazza, H. Daniel"'

8. Data from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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9. Supplementary Dataset 1 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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10. Supplementary Data from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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11. Supplementary Dataset 2 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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12. Supplementary Dataset 4 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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13. Supplementary Dataset 3 from SWI/SNF Blockade Disrupts PU.1-Directed Enhancer Programs in Normal Hematopoietic Cells and Acute Myeloid Leukemia

Author

Chambers, Courtney, primary, Cermakova, Katerina, primary, Chan, Yuen San, primary, Kurtz, Kristen, primary, Wohlan, Katharina, primary, Lewis, Andrew Henry, primary, Wang, Christiana, primary, Pham, Anh, primary, Dejmek, Milan, primary, Sala, Michal, primary, Loeza Cabrera, Mario, primary, Aguilar, Rogelio, primary, Nencka, Radim, primary, Lacorazza, H. Daniel, primary, Rau, Rachel E., primary, and Hodges, H. Courtney, primary

Published
2023
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14. An ELF4 hypomorphic variant results in NK cell deficiency

Author

Salinas, Sandra Andrea, primary, Mace, Emily M., additional, Conte, Matilde I., additional, Park, Chun Shik, additional, Li, Yu, additional, Rosario-Sepulveda, Joshua I., additional, Mahapatra, Sanjana, additional, Moore, Emily K., additional, Hernandez, Evelyn R., additional, Chinn, Ivan K., additional, Reed, Abigail E., additional, Lee, Barclay J., additional, Frumovitz, Alexander, additional, Gibbs, Richard A., additional, Posey, Jennifer E., additional, Forbes Satter, Lisa R., additional, Thatayatikom, Akaluck, additional, Allenspach, Eric J., additional, Wensel, Theodore G., additional, Lupski, James R., additional, Lacorazza, H. Daniel, additional, and Orange, Jordan S., additional

Published
2022
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15. Relocalization of PU.1 Underlies the On- and Off-Tumor Effects of SWI/SNF Blockade in AML

Author

Chambers, Courtney, primary, Kurtz, Kristen, additional, Lewis, Andrew Henry, additional, Wohlan, Katharina, additional, Chan, Yuen San, additional, Cermakova, Katerina, additional, Dejmek, Milan, additional, Sala, Michal, additional, Aguilar, Rogelio, additional, Loeza Cabrera, Mario, additional, Nencka, Radim, additional, Lacorazza, H. Daniel, additional, Rau, Rachel E., additional, and Hodges, H. Courtney, additional

Published
2022
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33. The Transcription Factor ELF4 Suppresses Differentiation of Proliferating CD4+ T Cells to the Th17 Lineage

Author

Lee, Ping-Hsien, Puppi, Monica, Schluns, Kimberly S., Yu-Lee, Li-Yuan, Dong, Chen, and Lacorazza, H. Daniel

Subjects
CD4-Positive T-Lymphocytes, Mice, Knockout, Cell Survival, Cell Differentiation, Lymphocyte Activation, Article, Cell Line, DNA-Binding Proteins, Mice, Animals, Cytokines, Humans, Th17 Cells, Transcription Factors
Abstract

The differentiation of CD4(+) T cells into different Th lineages is driven by cytokine milieu in the priming site and the underlying transcriptional circuitry. Even though many positive regulators have been identified, it is not clear how this process is inhibited at transcriptional level. In this study, we report that the E-twenty six (ETS) transcription factor E74-like factor 4 (ELF4) suppresses the differentiation of Th17 cells both in vitro and in vivo. Culture of naive Elf4(-/-) CD4(+) T cells in the presence of IL-6 and TGF-β (or IL-6, IL-23, and IL-1β) resulted in increased numbers of IL-17A-positive cells compared with wild-type controls. In contrast, the differentiation to Th1, Th2, or regulatory T cells was largely unaffected by loss of ELF4. The increased expression of genes involved in Th17 differentiation observed in Elf4(-/-) CD4(+) T cells suggested that ELF4 controls their programming into the Th17 lineage rather than only IL-17A gene expression. Despite normal proliferation of naive CD4(+) T cells, loss of ELF4 lowered the requirement of IL-6 and TGF-β signaling for IL-17A induction in each cell division. ELF4 did not inhibit Th17 differentiation by promoting IL-2 production as proposed for another ETS transcription factor, ETS1. Elf4(-/-) mice showed increased numbers of Th17 cells in the lamina propria at steady state, in lymph nodes after immunization, and, most importantly, in the CNS following experimental autoimmune encephalomyelitis induction, contributing to the increased disease severity. Collectively, our findings suggest that ELF4 restrains Th17 differentiation in dividing CD4(+) T cells by regulating commitment to the Th17 differentiation program.

Published
2013

35. The transcription factor ELF4 controls quiescence of endothelial cells and their resistance to myeloablative treatments in bone marrow

Author

Sivina, Mariela, Yamada, Takeshi, Park, Chun Shik, Puppi, Monica, Coskun, Suleyman, Hirschi, Karen, and Lacorazza, H. Daniel

Subjects
Mice, Knockout, Time Factors, Cell Cycle, Drug Resistance, Cyclin-Dependent Kinase 4, Endothelial Cells, Neovascularization, Physiologic, Bone Marrow Cells, Myeloablative Agonists, Transfection, Article, DNA-Binding Proteins, Mice, Inbred C57BL, Mice, COS Cells, Chlorocebus aethiops, NIH 3T3 Cells, Animals, Humans, RNA Interference, Fluorouracil, Promoter Regions, Genetic, Cellular Senescence, Cell Proliferation, Transcription Factors
Abstract

The regeneration of the hematopoietic system in bone marrow after chemotherapy depends on a balance between the quiescence and proliferation of lineage-specific progenitor cells. Even though the vascular network in bone is damaged by cytoablation, the transcriptional control of quiescence in endothelial cells is not well known. In this study, we investigated the role of the transcription factor E74-like factor (ELF4) in the proliferation of endothelial cells in bone marrow.Loss-of-function models were used to study the role of ELF4 in human and murine endothelial cells. ELF4 promotes cell cycle entry by activating cyclin-dependent kinase-4 in human umbilical vein endothelial cells. Elf4-null mice exhibited enhanced recovery of bone marrow CD45- CD31+ endothelial cells and sinusoidal blood vessels following administration of 5-fluorouracil.Loss of ELF4 leads to increased quiescence in bone marrow endothelial cells by the deregulation of cyclin-dependent kinase-4 expression and to enhanced regeneration of sinusoidal blood vessels.

Published
2011

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