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Li, Haiyan, Jin Jin, shao-Cong Sun und Stephanie S. Watowich. „Molecular Regulation of Adult Hematopoiesis By GATA-2“. Blood 124, Nr. 21 (06.12.2014): 4337. http://dx.doi.org/10.1182/blood.v124.21.4337.4337.
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Abstract GATA-2 is a zinc finger-containing transcriptional regulator that plays important roles in embryonic and adult hematopoiesis. Mutations in human GATA2 are associated with myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), as well as immunodeficiency disorders that present with a profound loss of monocytes, dendritic cells and other myeloid lineage populations. Recent work reveals crucial roles for GATA-2 in definitive hematopoietic stem/progenitor cell activity, vascular integrity and lymphatic development. However, the molecular mechanisms by which GATA-2 controls adult hematopoiesis via hematopoietic-cell autonomous functions are largely unknown. To address this question, we generated a tamoxifen-inducible Gata2-deficient mouse strain by breeding Gata2flox/flox mice with Cre-ER transgenic animals. Following tamoxifen treatment, Cre-ER Gata2flox/flox mice show a rapid and profound loss of circulating neutrophils, monocytes and lymphocytes, concomitant with development of anemia. These results are consistent with the requirement for GATA-2 in hematopoietic stem/progenitor cells, and may also reflect GATA-2 function in endothelial cells within the vascular niche. To explore hematopoietic-specific GATA-2 activity, we generated bone marrow chimeric mice with hematopoietic-restricted Gata2-deficiency by transplanting Cre-ER Gata2flox/flox hematopoietic cells into wild type recipients. Cre-ER Gata2flox/flox bone marrow chimeras show rapid development of cytopenias upon tamoxifen exposure, suggesting a cell autonomous role for GATA-2 in maintaining adult hematopoiesis. Strikingly, hematopoietic progenitor cells rapidly lose c-Kit expression upon inducible Gata2 deletion. Chromatin immunoprecipitation and reporter assays suggest GATA-2 cooperates with C/EBPa in regulating kit transcription. Our study suggests conditional deletion of Gata2 restricted to the hematopoietic compartment provides a model for bone marrow failure associated with MDS and mutant GATA2 human immunodeficiencies that may enable further insight into the molecular network by which GATA-2 mediates definitive hematopoiesis. Supported by grants from NIH (AI098099) and the MD Anderson Center for Cancer Epigenetics.(SSW) and the MD Anderson Center for Cancer and Inflammation (HSL). Disclosures No relevant conflicts of interest to declare.
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Zon, LI. „Developmental biology of hematopoiesis“. Blood 86, Nr. 8 (15.10.1995): 2876–91. http://dx.doi.org/10.1182/blood.v86.8.2876.bloodjournal8682876.
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The cellular and environmental regulation of hematopoiesis has been generally conserved throughout vertebrate evolution, although subtle species differences exist. The factors that regulate hematopoietic stem cell homeostasis may closely resemble the inducers of embryonic patterning, rather than the factors that stimulate hematopoietic cell proliferation and differentiation. Comparative study of embryonic hematopoiesis in lower vertebrates can generate testable hypotheses that similar mechanisms occur during hematopoiesis in higher species.
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Zon, LI. „Developmental biology of hematopoiesis“. Blood 86, Nr. 8 (15.10.1995): 2876–91. http://dx.doi.org/10.1182/blood.v86.8.2876.2876.
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Abstract The cellular and environmental regulation of hematopoiesis has been generally conserved throughout vertebrate evolution, although subtle species differences exist. The factors that regulate hematopoietic stem cell homeostasis may closely resemble the inducers of embryonic patterning, rather than the factors that stimulate hematopoietic cell proliferation and differentiation. Comparative study of embryonic hematopoiesis in lower vertebrates can generate testable hypotheses that similar mechanisms occur during hematopoiesis in higher species.
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de Rooij, Laura P. M. H., Derek C. H. Chan, Ava Keyvani Chahi und Kristin J. Hope. „Post-transcriptional regulation in hematopoiesis: RNA binding proteins take control“. Biochemistry and Cell Biology 97, Nr. 1 (Februar 2019): 10–20. http://dx.doi.org/10.1139/bcb-2017-0310.
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Normal hematopoiesis is sustained through a carefully orchestrated balance between hematopoietic stem cell (HSC) self-renewal and differentiation. The functional importance of this axis is underscored by the severity of disease phenotypes initiated by abnormal HSC function, including myelodysplastic syndromes and hematopoietic malignancies. Major advances in the understanding of transcriptional regulation of primitive hematopoietic cells have been achieved; however, the post-transcriptional regulatory layer that may impinge on their behavior remains underexplored by comparison. Key players at this level include RNA-binding proteins (RBPs), which execute precise and highly coordinated control of gene expression through modulation of RNA properties that include its splicing, polyadenylation, localization, degradation, or translation. With the recent identification of RBPs having essential roles in regulating proliferation and cell fate decisions in other systems, there has been an increasing appreciation of the importance of post-transcriptional control at the stem cell level. Here we discuss our current understanding of RBP-driven post-transcriptional regulation in HSCs, its implications for normal, perturbed, and malignant hematopoiesis, and the most recent technological innovations aimed at RBP–RNA network characterization at the systems level. Emerging evidence highlights RBP-driven control as an underappreciated feature of primitive hematopoiesis, the greater understanding of which has important clinical implications.
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Chen, Sisi, und Omar Abdel-Wahab. „Splicing regulation in hematopoiesis“. Current Opinion in Hematology 28, Nr. 4 (10.05.2021): 277–83. http://dx.doi.org/10.1097/moh.0000000000000661.
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QUESENBERRY, PETER J., IAN K. MCNIECE, H. ELIZABETH MCGRATH, DANIEL S. TEMELES, GWEN B. BABER und DONNA H. DEACON. „Stromal Regulation of Hematopoiesis“. Annals of the New York Academy of Sciences 554, Nr. 1 Molecular and (Mai 1989): 116–24. http://dx.doi.org/10.1111/j.1749-6632.1989.tb22414.x.
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Sashida, Goro, und Atsushi Iwama. „Epigenetic regulation of hematopoiesis“. International Journal of Hematology 96, Nr. 4 (29.09.2012): 405–12. http://dx.doi.org/10.1007/s12185-012-1183-x.
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Wimmer, Antonia, Sophia K. Khaldoyanidi, Martin Judex, Naira Serobyan, Richard G. DiScipio und Ingrid U. Schraufstatter. „CCL18/PARC stimulates hematopoiesis in long-term bone marrow cultures indirectly through its effect on monocytes“. Blood 108, Nr. 12 (01.12.2006): 3722–29. http://dx.doi.org/10.1182/blood-2006-04-014399.
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AbstractChemokines play a role in regulating hematopoietic stem cell function, including migration, proliferation, and retention. We investigated the involvement of CCL18 in the regulation of bone marrow hematopoiesis. Treatment of human long-term bone marrow cultures (LTBMCs) with CCL18 resulted in significant stimulation of hematopoiesis, as measured by the total number of hematopoietic cells and their committed progenitors produced in culture. Monocytes/macrophages, whose survival was almost doubled in the presence of CCL18 compared with controls, were the primary cells mediating this effect. Conditioned media from CCL18-treated mature monocytes fostered colony-promoting activity that increased the number of colonies formed by hematopoietic progenitor cells. Gene expression profiling of CCL18-stimulated monocytes demonstrated more than 200 differentially expressed genes, including those regulating apoptosis (caspase-8) and proliferation (IL-6, IL-15, stem cell factor [SCF]). Up-regulation of these cytokines was confirmed on the protein expression level. The contribution of SCF and IL-6 in CCL18-mediated stimulatory activity for hematopoiesis was confirmed by SCF- and IL-6–blocking antibodies that significantly inhibited the colony-promoting activity of CCL18-stimulated conditioned medium. In addition to the effect on monocytes, CCL18 facilitated the formation of the adherent layer in LTBMCs and increased the proliferation of stromal fibroblast-like cells.
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The initiation of the hematopoietic program is orchestrated by key transcription factors that recruit chromatin regulators in order to activate or inhibit blood target gene expression. To generate a complete compendium of chromatin factors that establish the genetic code during developmental hematopoiesis, we conducted a large-scale reverse genetic screen targeting 425 chromatin factors in zebrafish and identified over 30 novel chromatin regulators that function at distinct steps of embryonic hematopoiesis. In vertebrates, developmental hematopoiesis occurs in two waves. During the first and primitive wave, mainly erythrocytes are produced, and we identified at least 15 chromatin factors that decrease or increase formation of \(scl^+\), \(gata1^+\), and \(\beta-globin e3^+\) erythroid progenitors. In the definitive wave, HSCs capable of self-renewal and differentiation into multiple lineages are induced, and we identified at least 18 chromatin factors that decrease or increase the formation of \(c-myb^+\) and \(runx1^+\) stem and progenitor cells in the aorta gonad mesonephros (AGM) region, without disruption of vascular development. The majority of the chromatin factors identified from the screen are involved in histone acetylation, histone methylation, and nucleosome remodeling, the same modifications that are hypothesized to have the most functional impact on the transcriptional status of a gene. Moreover, these factors can be mapped to subunits of chromatin complexes that modify these marks, such as HBO/HAT, HDAC/NuRD, SET1A/MLL, ISWI, and SWI/SNF. One of the strongest phenotypes identified from the screen came from knockdown of chromodomain helicase DNA binding domain 7 (chd7). Morpholino knockdown of chd7 resulted in increased primitive and definitive blood production from the induction of stem and progenitor cells to the differentiation of myeloid and erythroid lineages. This expansion of the blood lineage is cell autonomous as determined by blastula transplantation experiments. Though chromatin factors are believed to function broadly and are often expressed ubiquitously, the combined results of the screen and chd7 analysis show that individual factors have very tissue specific functions. These studies implicate chromatin factors as playing a major role in establishing the programs of gene expression for self-renewal and differentiation of hematopoietic cells.
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Ullrich, Sebastian 1984. „Alternative mechanisms of gene regulation during hematopoiesis“. Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/665801.
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Gene regulation orchestrates the development of different cell types and organs from the same genetic blueprint. While the basic mode of gene regulation is driven by transcription factors, there are a variety of other mechanisms that determine the amount of RNA produced per genes. In this work we first investigate specifically intron retention as a mode of alternative splicing that alters the cellular transcriptomes. As a model, we use hematopoiesis. We compare intron retention in different stages of human and mouse B-cell development to granulocyte differentiation. We further explore expression and binding patterns of splicing regulatory factors. Second, we investigate the role of lncRNAs in the transdifferentiation of B-cell related lymphoma cells to macrophages. We specifically explore the role of a set of upregulated lncRNAs during this process. We deplete their expression during transdifferentiation with CRISPR/Cas9 to identify potential genes that retard or block the process and therefore are crucial for changing cell identity. La regulació gènica determina el desenvolupament dels diferents tipus cel·lulars, teixits i òrgans. Tot i que el mode bàsic de regulació és dirigit per factors de transcripció, existeixen una gran varietat de mecanismes que contribueixen a determinar la quantitat de RNA produïda pels gens. En aquest treball, investiguem en primer lloc la retenció d’introns com un tipus d’splicing alternatiu que altera el transcriptome cel·lular. Com a model biològic, ens centrem en la hematopoesi. Comparem la retenció d’introns en diferents estadis del desenvolupament de limfòcits B en humà i ratolí amb la retenció durant la diferenciació del granulòcits. Estudiem també el patró d’expressió i d’unió (binding) dels factors de regulació de l’splicing. En segon lloc, investiguem el paper dels RNA llargs no codificants (long non coding RNAs, lncRNAs) en la transdiferenciació de limfòcits B a macròfags. En particular, el paper d’aquells lncRNAs que son regulats positivament durant aquest procés. Reduïm la seva expressió durant la transdiferenciació mitjançant la tècnica CRISPR/Cas9 amb l’objectiu d’identificar gens amb el potencial de retardar o de bloquejar el procés i que, en conseqüència, pugui jugar un paper crucial en el canvi de la identitat cel·lular.
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Durand, Ellen Marie. „Regulation of hematopoietic stem cell migration and function“. Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11550.
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Hematopoietic stem cell transplantation (HSCT) is an effective treatment for blood disorders and autoimmune diseases. Following HSCT, these cells must successfully migrate to the marrow niche and replenish the blood system of the recipient. This process requires both non-cell and cell-autonomous regulation of hematopoietic stem and progenitor cells (HSPCs). A transgenic reporter line in zebrafish allowed the investigation of factors that regulate HSPC migration and function. To directly observe cells in their endogenous microenvironment, confocal live imaging was used to track runx1:GFP+ HSPCs as they arrive and lodge in the niche. A novel cellular interaction was observed that involves triggered remodeling of perivascular endothelial cells during niche formation. A chemical screen identified the TGF-beta pathway as a regulator of HSPC and niche interactions. Chemical manipulation of HSPCs was used to improve engraftment and repopulation capability following transplantation. Runx1:GFP fish treated with prostaglandin E2 (PGE2) during embryogenesis exhibit increased runx1+ cells in the AGM and CHT, consistent with previous in situ data. This increase in HSPCs is maintained into adulthood, even in the absence of prolonged PGE2 exposure. Kidney marrow from these treated fish can outcompete control marrow in transplantation assays. The ability of PGE2 to confer a long-term advantage on sorted mouse marrow populations in competitive transplantation assays was tested. I found that PGE2-treated short-term (ST)-HSCs, but not long-term (LT)-HSCs show enhanced transplantability in recipients compared to control animals. My studies demonstrate that the effects of PGE2 on HSC function persist over substantial time despite transient exposure. A population of short-term HSCs can engraft and give rise to long-term multilineage reconstitution following PGE2 treatment. Collectively, our studies have led to novel insights regarding the pathways involved in HSC migration, homing, and repopulation.
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Martin, Richard. „Regulation of SCL expression and function in hematopoiesis“. Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85582.
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The development of the hematopoietic system occurs in two waves: a first wave of primitive erythropoiesis, which consists in the production of a single lineage, primitive erythrocytes, and a second wave of definitive hematopoiesis, which describes the generation of many specialized blood cell types from common hematopoietic stem cells. Whereas definitive hematopoiesis is fairly well understood, involves signals from the environment and the expression of lineage-specific transcription factors, the molecular mechanisms regulating primitive erythropoiesis remain to be defined. The aim of this thesis was to clarify the roles of the Stem Cell Leukemia (SCL) gene and Vascular Endothelial Growth Factor (VEGF) during primitive and definitive hematopoiesis. Although gene targeting experiments indicate essential roles for VEGF/Flk-1 signaling and SCL at the onset of hematopoiesis, their exact functions remain elusive. This work has revealed that different thresholds of VEGF are required for the migration of hematopoietic precursors from mesoderm to sites of hematopoiesis and for their subsequent expansion. Furthermore, it shows that SCL, a basic helix-loop-helix transcription factor, acts downstream of VEGF signaling to ensure the survival of primitive erythrocytes. During definitive hematopoiesis, conditional knock-out experiments establish a non-redundant role for SCL during erythroid and megakaryocytic differentiation. Yet, it remains unclear whether SCL is essential for commitment to these lineages. Results presented in this thesis suggest that SCL is not involved in commitment to these pathways, but rather acts to consolidate and expand the erythroid and megakaryocytic compartments, following lineage choice. Finally, despite the central role for SCL during hematopoietic development, the mechanisms regulating its tissue specific expression remain unknown. This work provides molecular and functional evidence that demonstrate that the homeodomain- Taken together, this work has elucidated molecular mechanisms which underlie cell fate decisions. It describes how the activity of a master regulator of erythroid differentiation, SCL, is regulated both by signals from the environment and at the transcriptional level, through combinatorial interactions between lineage-specific transcription factors.
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Smith, Molly. „Alternative Splicing and Regulation of Innate Immune Mediators in Normal and Malignant Hematopoiesis“. University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1563527303459942.
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Gronthos, Stan. „Stromal precursor cells : purification and the development of bone tissue“. Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phg8757.pdf.
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Bibliography: leaves 152-223. Experiments were designed to identify and purify human bone marrow stromal precursor cells by positive immunoselection, based on the cell surface expression of the VCAM-1 and STRO-1 antigens. The data presented demonstrates a hierarchy of bone cell development in vitro.
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Gaboury, Louis A. „Studies of the role of mesenchymal cells in the regulation of hemopoiesis“. Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28784.
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Hemopoiesis is thought to be regulated in part by specific, but as yet undefined, interactions between primitive hemopoietic cells and fixed, non-hemopoietic marrow elements collectively referred to as the stroma. Recently, a marrow culture system has been described that allows the maintenance of primitive human hemopoietic progenitor cells for many weeks in the absence of exogenously added hemopoietic growth factors. The formation of a heterogeneous adherent layer in which many stromal elements are found appears to be important to the maintenance of hemopoiesis in this system. As part of the overall goal of delineating the cellular and molecular interactions involved, my first objective was to develop an experimental system for assessing the hemopoiesis-sustaining function of the adherent layer of long-term human marrow cultures. This required the identification of a suitable procedure for separating the hemopoietic and non-hemopoietic regulatory components so that the former could be used to quantitate the function of the latter. This was achieved using irradiation to selectively inactivate residual hemopoietic cells in long-term culture adherent layers, and using a medium containing cis-4-hydroxy-L-proline to selectively inactivate stromal cells and their precursors present in suspensions of unseparated human marrow which were then added back in co-culture experiments.
My second objective was to develop a strategy for obtaining purified populations of cells corresponding to the various mesenchymal cell types in long-term adherent layers. I therefore prepared a high titre SV-40 virus stock and used it to establish permanent, cloned lines from human marrow "fibroblast" colonies, long-term culture adherent layers, and umbilical cord endothelial cells. Characterization of the transformants generated showed that they were all positive for SV-40, and in general expressed the phenotypic characteristics of the cells originally infected. Functional studies showed that these transformants, like their normal counterparts, respond to activation by producing two types of hemopoietic growth factors.
These studies suggest that marrow mesenchymal cells may regulate the growth and maintenance of primitive hemopoietic cells by producing hemopoietic growth factors in response to appropriate perturbation. The availability of permanent cloned lines of human marrow stromal cells should facilitate future analysis of these events at the molecular level. Medicine, Faculty of Pathology and Laboratory Medicine, Department of Graduate
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Serbanovic-Canic, Jovana. „Using zebrafish to identify new regulators of haematopoiesis“. Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607950.
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Rothberg, Janet L. „Polycomb-like 2 (Mtf2/Pcl2) is Required for Epigenetic Regulation of Hematopoiesis“. Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/35323.
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Polycomb proteins are epigenetic regulators that are critical in mediating gene repression at critical stages during development. Core and accessory proteins make up the Polycomb Repressive Complex 2 (PRC2), which is responsible for trimethylation of lysine 27 on histone 3 (H3K27me3), leading to maintenance of chromatin compaction and sustained gene repression. Classically, Polycomb accessory proteins are often thought of as having minor roles in fine-tuning the repressive action of PRC2. Their actions have often been attributed to chromatin recognition, targeting to specific loci and enhancing methyltransferase activity. In our previous work in mouse embryonic stem cells (ESCs), we showed that Polycomb-like 2 (Mtf2/Pcl2) is critical for PRC2-mediated regulation of stem cell self-renewal through feed-forward control of the pluripotency network. In moving beyond the ESC model system, we sought to interrogate the role of Mtf2 in vivo by creating a gene-targeted knockout mouse model. Surprisingly, we discovered a tissue-specific role for Mtf2 in controlling erythroid maturation and hematopoietic stem cell self-renewal. Via its regulation of other PRC2 members, Mtf2 is critical for global H3K27me3 methylation at promoter-proximal sites in developing erythroblasts. Thus, Mtf2 is required for proper maturation of erythroblasts. Loss of Mtf2 also reduces HSC self-renewal leading to stem cell pool exhaustion. Additionally, misregulation of Mtf2 in leukemia models contributes to massive leukemic blast expansion at the expense of leukemic stem cell self-renewal. In the developing hematopoietic system, Mtf2 functions as a core complex member, controlling epigenetic regulation of self-renewal and maturation of both stem and committed cells.
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Jarratt, Andrew. „Locus-wide studies into the transcriptional regulation of Runx1 in developmental hematopoiesis“. Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572521.
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Developmental hematopoiesis sees the generation of the first blood cells and definitive blood during embryonic development. The founding cell of definitive hematopoiesis, the hematopoietic stem cell (HSC), gives rise to all adult blood :I: ]] 1:: t '.1 '4 !..:. : 1 1 '.! . lineages throughout the the life span or an orgamism. It IS expected that future ex-vivo manipulation ofHSCs for therapeutic uses will benefit from a thorough understanding of the mechanisms, both cellular and genetic, that give rise to HSCs. One of the most critical regulators of HSC emergence in the embryo is the transcription factor (TF) Runxl. One aim of our lab is to decipher what controls the cis-regulation of Runxl to understand better how it exerts its function in the emergence of HSCs. In this thesis, chromatin assays were used to identify putative enhancers within the 1.3 Mb Runxl syntenic region. Seven novel enhancers were identified that mediate reporter gene expression in discrete patterns of Runx1-specific hematopoietic expression in transient transgenic embryos. Characterization of the cells marked by one of these enhancers, the + 11 0 enhancer in a transgenic mouse line, showed that it is active in clonogenic progenitors at Ell.5, but, interestingly, not HSCs. Finally, chromosome conformation capture (3C) assays showed physical interactions between the Runxl PI and P2 promoters and between the Runxl PI and P2 promoters and putative regulatory elements in the 1.3 Mb syntenic region. Together, these data increase our understanding of the complexity of Runxl cis-regulation during development and provide a starting point for characterizing what upstream trans-acting factors converge on Runxl to specify blood.
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I͡Astrebov, A. P. Reguli͡at͡sii͡a gemopoėza pri vozdeĭstvii na organizm ėkstremalʹnykh faktorov. Sverdlovsk: Akademii͡a nauk SSSR, Uralʹskoe otd-nie, 1988.
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Pezcoller Symposium on Normal and Malignant Hematopoiesis: New Advances (6th 1994 Rovereto, Italy). Normal and malignant hematopoiesis: New advances. New York: Plenum Press, 1995.
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International Symposium on Inhibitory Factors in the Regulation of Hematopoiesis. (1st 1987 Paris, France). The inhibitors of hematopoiesis =: Les inhibiteurs de l'hématopoïèse : proceedings of the First International Symposium on Inhibiting Factors in the Regulation of Hematopoiesis, Paris, (France), 26-28 April, 1987). [Paris]: INSERM, 1987.
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Conference, on Hemoglobin Switching (5th 1986 Airlie Va ). Developmental control of globin gene expression: Proceedings of the Fifth Conference on Hemoglobin Switching, held in Airlie, Virginia, September 28-October 1, 1986. New York: Liss, 1987.
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International Conference on Negative Regulation of Hematopoiesis (3rd 1993 Paris, France). The negative regulation of hematopoiesis: From fundamental aspects to clinical applications : Régulation négative de l'hématopïèse : des aspects fondamentaux à l'application clinique : proceedings of the third International Conference on Negative Regulation of Hematopoiesis, Paris, France, 18-22 April, 1993. Paris: Editions INSERM, 1993.
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Metcalf, Donald. „Regulation of Normal Hemopoiesis“. In Normal and Malignant Hematopoiesis, 1–10. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1927-0_1.
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Ogawa, Makio, und Fumiya Hirayama. „Cytokine Regulation of Lymphohemopoietic Progenitors“. In Normal and Malignant Hematopoiesis, 11–14. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1927-0_2.
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Mustjoki, Satu, Riitta Alitalo und Antti Vaheri. „Role of Plasminogen Activation in Hematopoietic Malignancies and in Normal Hematopoiesis“. In Plasminogen: Structure, Activation, and Regulation, 217–35. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0165-7_13.
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Rameshwar, Pranela, und Pedro Gascón. „Neural Regulation of Hematopoiesis by the Tachykinins“. In Molecular Biology of Hematopoiesis 5, 463–70. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0391-6_56.
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Cantrell, D. A., M. Izquierdo, J. Nunes, N. Osman, K. Reif und M. Woodrow. „The Regulation and Function of p21Ras in T Cell Activation and Growth“. In Normal and Malignant Hematopoiesis, 61–76. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1927-0_7.
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Miller, Alan M. „Lipoxygenase Metabolism in the Regulation of Hematopoiesis“. In Prostaglandins, Leukotrienes, Lipoxins, and PAF, 339–51. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-0727-1_33.
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Link, Daniel C. „Regulation of Hematopoiesis by CXCL12/CXCR4 Signaling“. In Targeted Therapy of Acute Myeloid Leukemia, 593–605. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1393-0_30.
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Marziali, Giovanna, Edvige Perrotti, Ramona Ilari, Eliana M. Coccia, Ugo Testa und Angela Battistini. „Transcriptional Regulation of the Ferritin H-Chain and Transferrin Receptor in Hematopoietic Cells“. In Molecular Biology of Hematopoiesis 6, 391–402. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4797-6_48.
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Konferenzberichte zum Thema "Hematopoiesis Regulation":
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Greenwood, Dalton L., und Jeffrey C. Rathmell. „Abstract PR07: Connecting acetate and citrate metabolism with epigenetic regulation of hematopoiesis“. In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-pr07.
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Jiang, Qingfei, Maria Anna Zipeto, Nathan Delos Santos, Sheldon Morris und Catriona Jamieson. „Abstract 299: RNA editing enzyme ADAR1 accelerates normal hematopoiesis cell cycle by regulation microRNA biogenesis“. In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-299.
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Lee, Jennifer, Jae-Hung Shieh, Jianxuan Zhang, Liren Liu, Giovanni Morrone, Malcolm A. S. Moore und Pengbo Zhou. „Abstract 211: Ubiquitin-proteolytic regulation of hematopoietic stem cell expansion“. In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-211.
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Asch, Adam S., Maria J. Ruiz-Echevarria, Jared Whelan, Thomas Green, Biree Andemariam, Douglas Weidner und Nance Hamel. „Abstract 4234: Translational regulation mediates hematopoietic progenitor cell generation in embryonic stem cell culture“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4234.
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Wu, Siyuan, Tiangang Cui und Tianhai Tian. „Mathematical Modelling of Genetic Network for Regulating the Fate Determination of Hematopoietic Stem Cells“. In 2018 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2018. http://dx.doi.org/10.1109/bibm.2018.8621476.
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Dorokhina, Yu A., und G. F. Ryzhkova. „Morphological and biochemical parameters of blood in rabbits when using energymetabolic compositions“. In SPbVetScience. FSBEI HE St. Petersburg SUVM, 2023. http://dx.doi.org/10.52419/3006-2022-7-18-23.
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Annotation:
Modern animal husbandry can no longer be imagined without special biologically active additives and a variety of protein, vitamin and mineral complexes. Among all additives, a special place is occupied by energy-metabolic compositions that give animals all the most necessary and important substances. The composition of the EC includes: yantaric acid is a universal intracellular metabolite, widely involved in metabolic reactions in the body; citric acid is the main intermediate product of the metabolic cycle of tricarboxylic acids, plays an important role in the system of biochemical reactions of cellular respiration of living organisms; iodinol – uniquea fecal medicinal substance, it determines high biological activity, regulates immunity and metabolism in the body; cyanocoalamin (vitamin B12) - prevents the appearance of anemia, enhances immunity, plays an important role in regulating the function of hematopoietic organs; glycerin has antiseptic and preservative properties.
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Grigoriou, M., P. Verginis, C. Nikolaou, P. Pavlidis, E. Dermitzakis, G. Bertsias, D. Boumpas und A. Banos. „S4D:7 Next generation sequencing in hematopoietic progenitors of murine sle model reveals aberrant regulation of cebp/a expression“. In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.26.
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Khella, Christen A., und Michael L. Gatza. „Abstract 5858: Multiplatform analyses identify upregulated hematopoietic cell kinase activity in poorly prognostic high-grade serous ovarian cancer and its role in regulating tumor aggressiveness“. In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5858.
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Berichte der Organisationen zum Thema "Hematopoiesis Regulation":
1
Taub, Floyd E., und Richard E. Weller. Proline-Rich Polypeptide 1 and GX-NH2: Molecular and Genetic Mechanisms of Hematopoiesis Regulation. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1025686.
