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Journal articles on the topic 'Mousse PU'

Author: Grafiati

Published: 19 October 2024

Last updated: 31 July 2025

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1

Madrange, L., P. Ehabouryi, O. Ferrandon, M. Mazeti, and J. Rodeaud. "Étude de la formation et de la stabilité des mousses chimiques de surface de la Vienne." Revue des sciences de l'eau 6, no. 3 (2005): 315–35. http://dx.doi.org/10.7202/705178ar.

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Le recensement de la charge polluante rejetée dans la rivière Vienne (France) par les usines et les stations d'épuration de Limoges à Confolens a été effectué. Des campagnes de prélèvement et d'observations visuelles ont permis de localiser les lieux d'apparition de mousses en aval d'usines de fabrication de pâte à papier et de cartons. L'étude du pouvoir moussant des mélanges des deux principaux rejets polluants (papeterie et cartonnerie) a permis de mettre en évidence des phénomènes de synergie entre certains mélanges se traduisant à la fois par une augmentation du pouvoir moussant et de la

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2

Christians, Jean-François. "Redécouverte de Schistostega pennata (Hedwig) F. Weber et D. Mohr (Schistostegaceae, Bryophyta) dans le massif du Pilat (Loire, France)." Bulletin mensuel de la Société linnéenne de Lyon 84, no. 7 (2015): 215–25. http://dx.doi.org/10.3406/linly.2015.17768.

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La redécouverte d’anciennes localités de Schistostega pennata dans le Parc naturel régional du Pilat est consécutive à des prospections ciblées, menées dans le cadre d’une enquête participative initiée par Isabelle Charissou sur le site «Bryophytes de France », également relayée par la Société Botanique du Centre-Ouest et par l’Amicale Legendre des Botanistes du Limousin. À cette occasion, de nouvelles stations ont également pu être mises en évidence. La biologie et l’écologie de cette mousse sont présentées, puis seront précisées ses répartitions ancienne et actuelle pour le massif du Pilat.

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3

Thomas, Marc, Emmanuel Discamps, Mathieu Lejay, Xavier Muth, and Jean-Guillaume Bordes. "Os qui roule n’amasse pas mousse. Une expérimentation sur le tri différentiel des vestiges lithiques et osseux dans un écoulement turbulent." Paléo 33 (2023): 146–63. http://dx.doi.org/10.4000/1296o.

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Les vestiges lithiques et fauniques constituent les principaux témoins des occupations paléolithiques. Les proportions relatives de ces matériaux au sein des assemblages sont utilisées pour définir la fonction des sites ou parties de site. Or, de nombreux processus naturels sont susceptibles d’occasionner des tris sur les ensembles de vestiges, parmi lesquels les écoulements turbulents, intervenant dans de nombreux domaines (e.g. fluviatile, ruissellement concentré). Afin d’évaluer cet impact, de nombreuses expérimentations ont déjà été réalisées, mais peu d’entre elles ont concerné à la fois

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4

Hwang, Cheol Kyu, Chun Sung Kim, Hack Sun Choi, Scott R. McKercher та Horace H. Loh. "Transcriptional Regulation of Mouse μ Opioid Receptor Gene by PU.1". Journal of Biological Chemistry 279, № 19 (2004): 19764–74. http://dx.doi.org/10.1074/jbc.m400755200.

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We previously reported that the 34-bp cis-acting element of the mouse μ opioid receptor (MOR) gene represses transcription of the MOR gene from the distal promoter. Using a yeast one-hybrid screen to identify potential transcription factors of the MOR promoter, we have identified PU.1 as one of the candidate genes. PU.1 is a member of theetsfamily of transcription factors, expressed predominantly in hematopoietic cells and microglia of brain. PU.1 plays an essential role in the development of both lymphoid and myeloid lineages. Opioids exert neuromodulatory as well as immunomodulatory effects,

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5

Gerasimo, P., C. Duserre, and H. Metivier. "Biological Behaviour of Pu Administered to Animals as Pu-Standard LICAM(C) Complex: Therapeutical Attempts to Decrease Pu Kidney Burden." Human Toxicology 5, no. 5 (1986): 309–18. http://dx.doi.org/10.1177/096032718600500503.

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The biological fate of plutonium (Pu) introduced as a Pu-standard LICAM(C) complex was investigated in male rats of two strains, in male and female mice and in the baboon. We observed that, whatever the animal species or the entry route, this complex was deposited rapidly in the kidney. In addition, more of the complex accumulated in the rat (16% of injected radioactivity) than in either the mouse (7%) or baboon (5%). This Pu deposit was cleared spontaneously with a half-life of 10 days in the rat and only 5 days in the mouse. We noted that the complex was deposited on bone during this period

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6

Zhou, Jing, Bo Li, Jun Wu, et al. "Essential Role for PU.1 in MEIS1 Activation and MLL Fusion Leukemia,." Blood 118, no. 21 (2011): 3466. http://dx.doi.org/10.1182/blood.v118.21.3466.3466.

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Abstract Abstract 3466 Down-regulation of transcription factor PU.1, a key regulator of hematopoiesis, induces myeloid leukemia in mice, demonstrating a role of PU.1 as tumor suppressor. Recent studies, however, have also suggested that PU.1 is required for repopulation/self-renewal capacity of normal hematopoietic stem cells (HSCs), and presence of PU.1 activity may be necessary to favor growth of myeloid leukemia stem cells. To explore whether PU.1 could possibly act as an oncogene in the development of certain type of myeloid leukemia, we set to look for differential up-regulation of PU.1 a

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7

Staber, Philipp B., Pu Zhang, Min Ye, et al. "Autoregulation of the Transcription Factor PU.1 Via Its Evolutionarily Conserved Upstream Regulatory Element Is Critical in Adult Mouse Hematopoiesis." Blood 114, no. 22 (2009): 1468. http://dx.doi.org/10.1182/blood.v114.22.1468.1468.

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Abstract Abstract 1468 Poster Board I-491 Background: Levels of the Ets transcription factor PU.1 control normal hematopoietic differentiation and even modest alterations can lead to leukemia and lymphoma. Regulation of PU.1 levels at different stages of hematopoiesis requires multiple interactions between several regulatory elements and transcription factors. Our previous studies identified a potential autoregulatory mechanism of the PU.1 gene through the combined activity of the proximal promoter and an evolutionarily conserved upstream regulatory element (URE), located at –14 kb relative to

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8

Bonfield, Tracey L., Baisakhi Raychaudhuri, Anagha Malur, et al. "PU.1 regulation of human alveolar macrophage differentiation requires granulocyte-macrophage colony-stimulating factor." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 5 (2003): L1132—L1136. http://dx.doi.org/10.1152/ajplung.00216.2003.

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is critically implicated in lung homeostasis in the GM-CSF knockout mouse model. These animals develop an isolated lung lesion reminiscent of pulmonary alveolar proteinosis (PAP) seen in humans. The development of the adult form of human alveolar proteinosis is not due to the absence of a GM-CSF gene or receptor defect but to the development of an anti-GM-CSF autoimmunity. The role of GM-CSF in the development of PAP is unknown. Studies in the GM-CSF knockout mouse have shown that lack of PU.1 protein expression in alveolar macrophages

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9

Mak, Ka Sin, Alister P. W. Funnell, Richard C. M. Pearson, and Merlin Crossley. "PU.1 and Haematopoietic Cell Fate: Dosage Matters." International Journal of Cell Biology 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/808524.

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The ETS family transcription factor PU.1 is a key regulator of haematopoietic differentiation. Its expression is dynamically controlled throughout haematopoiesis in order to direct appropriate lineage specification. Elucidating the biological role of PU.1 has proved challenging. This paper will discuss how a range of experiments in cell lines and mutant and transgenic mouse models have enhanced our knowledge of the mechanisms by which PU.1 drives lineage-specific differentiation during haematopoiesis.

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10

Ghisi, Margherita, Mark D. McKenzie, Ethan P. Oxley, et al. "Uncovering Key Downstream Effectors of PU.1 Tumor Suppression in Acute Myeloid Leukemia." Blood 128, no. 22 (2016): 2698. http://dx.doi.org/10.1182/blood.v128.22.2698.2698.

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Abstract Mutation or altered expression of key transcription factors resulting in aberrant myeloid differentiation is a critical step in the pathogenesis of acute myeloid leukemia (AML). The ETS-domain hematopoietic transcription factor PU.1 (SPI1) is an essential regulator of myeloid differentiation. While genetic mutation of PU.1 is rare, PU.1 is down-regulated or functionally repressed in about 50% of AML patients as a consequence of recurrent translocations (such as AML1-ETO and PML-RARα) or mutations (such as FLT3-ITD). While it is well-established that the inhibition of PU.1 function pro

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11

Vangala, Rajani K., Marion S. Heiss-Neumann, Janki S. Rangatia, et al. "The myeloid master regulator transcription factor PU.1 is inactivated by AML1-ETO in t(8;21) myeloid leukemia." Blood 101, no. 1 (2003): 270–77. http://dx.doi.org/10.1182/blood-2002-04-1288.

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Abstract The transcription factor PU.1 plays a pivotal role in normal myeloid differentiation. PU.1−/− mice exhibit a complete block in myeloid differentiation. Heterozygous PU.1 mutations were reported in some patients with acute myeloid leukemia (AML), but not in AML with translocation t(8;21), which gives rise to the fusion geneAML1-ETO. Here we report a negative functional impact of AML1-ETO on the transcriptional activity of PU.1. AML1-ETO physically binds to PU.1 in t(8;21)+ Kasumi-1 cells. AML1-ETO binds to the β3β4 region in the DNA-binding domain of PU.1 and displaces the coactivator

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12

Pospisil, Vitek, Emanuel Necas, and Tomas Stopka. "PU.1 Activity Determines Fate of Myeloid Progenitor Cells during Lineage Commitment." Blood 108, no. 11 (2006): 4207. http://dx.doi.org/10.1182/blood.v108.11.4207.4207.

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Abstract Myeloid cell commitment is regulated by factors interacting with chromatin in a progenitor cell entering differentiation. PU.1 is an ETS family transcription factor that has been well characterized in inducing myelopoiesis and blocking erythroid differentiation. Conditionally activated PU.1-Estrogen Receptor transgene in mouse PU.1 knockout-derived hematopoietic progenitors is known to induce macrophage differentiation. We observed that manipulation of PU.1 activity by using different levels of PU.1-ER activator, tamoxifen, was capable of producing major populations of myeloid progeny

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13

Chavez, James S., Jennifer L. Rabe, Giovanny Hernandez, et al. "PU.1 Expression Defines Distinct Functional Activities in the Phenotypic HSC Compartment of a Murine Inflammatory Stress Model." Cells 11, no. 4 (2022): 680. http://dx.doi.org/10.3390/cells11040680.

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The transcription factor PU.1 is a critical regulator of lineage fate in blood-forming hematopoietic stem cells (HSC). In response to pro-inflammatory signals, such as the cytokine IL-1β, PU.1 expression is increased in HSC and is associated with myeloid lineage expansion. To address potential functional heterogeneities arising in the phenotypic HSC compartment due to changes in PU.1 expression, here, we fractionated phenotypic HSC in mice using the SLAM surface marker code in conjunction with PU.1 expression levels, using the PU.1-EYFP reporter mouse strain. While PU.1lo SLAM cells contain ex

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14

Ghani, Saeed, Pia Riemke, Jörg Schönheit, et al. "Macrophage development from HSCs requires PU.1-coordinated microRNA expression." Blood 118, no. 8 (2011): 2275–84. http://dx.doi.org/10.1182/blood-2011-02-335141.

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Abstract The differentiation of HSCs into myeloid lineages requires the transcription factor PU.1. Whereas PU.1-dependent induction of myeloid-specific target genes has been intensively studied, negative regulation of stem cell or alternate lineage programs remains incompletely characterized. To test for such negative regulatory events, we searched for PU.1-controlled microRNAs (miRs) by expression profiling using a PU.1-inducible myeloid progenitor cell line model. We provide evidence that PU.1 directly controls expression of at least 4 of these miRs (miR-146a, miR-342, miR-338, and miR-155)

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15

Lin, Ligen, Weijun Pang, Keyun Chen, et al. "Adipocyte expression of PU.1 transcription factor causes insulin resistance through upregulation of inflammatory cytokine gene expression and ROS production." American Journal of Physiology-Endocrinology and Metabolism 302, no. 12 (2012): E1550—E1559. http://dx.doi.org/10.1152/ajpendo.00462.2011.

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We have reported previously that ETS family transcription factor PU.1 is expressed in mature adipocytes of white adipose tissue. PU.1 expression is increased greatly in mouse models of genetic or diet-induced obesity. Here, we show that PU.1 expression is increased only in visceral but not subcutaneous adipose tissues of obese mice, and the adipocytes are responsible for this increase in PU.1 expression. To further address PU.1's physiological function in mature adipocytes, PU.1 was knocked down in 3T3-L1 cells using retroviral-mediated expression of PU.1-targeting shRNA. Consistent with previ

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16

Karpurapu, Manjula, Kavita Kumari Kakarala, Sangwoon Chung, et al. "Epigallocatechin gallate regulates the myeloid-specific transcription factor PU.1 in macrophages." PLOS ONE 19, no. 4 (2024): e0301904. http://dx.doi.org/10.1371/journal.pone.0301904.

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Our previous research demonstrated that PU.1 regulates expression of the genes involved in inflammation in macrophages. Selective knockdown of PU.1 in macrophages ameliorated LPS-induced acute lung injury (ALI) in bone marrow chimera mice. Inhibitors that block the transcriptional activity of PU.1 in macrophages have the potential to mitigate the pathophysiology of LPS-induced ALI. However, complete inactivation of PU.1 gene disrupts normal myelopoiesis. Although the green tea polyphenol Epigallocatechin gallate (EGCG) has been shown to regulate inflammatory genes in various cell types, it is

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17

Lian, Ming, Yu Fang Jiang, Shi Dong Lv, Yi Long He, Jiang Sheng Zhou, and Qing Xiong Meng. "The Anti-Obesity Effect of Instant Pu-Erh Black Tea in Mice with Hydrogenated Oil Diet-Induced Obesity." Applied Mechanics and Materials 644-650 (September 2014): 5248–51. http://dx.doi.org/10.4028/www.scientific.net/amm.644-650.5248.

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Obesity is becoming a worldwide epidemic disease, and the incidence is increasing year by year. Drinking tea has been demonstrated to have multiple beneficial effects to obese patients. This article tested the effect of instant Pu-erh black tea on weight loss in diet-induced obese (DIO) mice. The results demonstrated that instant Pu-erh black tea was be able to reduce the mouse weight dose-dependently. Its effect is stronger than that of L-carnitine, a weight loss drug currently on the market. Instant Pu-erh black tea also accelerated lipid metabolism and eased the high-fat diet-induced liver

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18

Antony-Debre, Ileana, Ananya Paul, Joana Leite, et al. "Direct Pharmacological Inhibition of the Transcription Factor PU.1 in Acute Myeloid Leukemia." Blood 130, Suppl_1 (2017): 858. http://dx.doi.org/10.1182/blood.v130.suppl_1.858.858.

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Abstract Functionally critical decreases in levels or activity of the ETS family transcription factor PU.1 are present in approximately 2/3 of patients with acute myeloid leukemia (AML), across different AML subtypes (Sive, Leukemia 2016) including at the stem cell level (Steidl, Nat Genet 2006; Will, Nat Med 2015). Thus, targeting PU.1 could be an appealing option for treatment. As complete loss of PU.1 leads to stem cell failure (Iwasaki, Blood 2005), we hypothesized that PU.1 inhibition could eradicate leukemic cells harboring already low levels of PU.1, with modest effects on normal cells.

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19

Rekhtman, Natasha, Kevin S. Choe, Igor Matushansky, Stuart Murray, Tomas Stopka, and Arthur I. Skoultchi. "PU.1 and pRB Interact and Cooperate To Repress GATA-1 and Block Erythroid Differentiation." Molecular and Cellular Biology 23, no. 21 (2003): 7460–74. http://dx.doi.org/10.1128/mcb.23.21.7460-7474.2003.

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ABSTRACT PU.1 and GATA-1 are two hematopoietic specific transcription factors that play key roles in development of the myeloid and erythroid lineages, respectively. The two proteins bind to one another and inhibit each other's function in transcriptional activation and promotion of their respective differentiation programs. This mutual antagonism may be an important aspect of lineage commitment decisions. PU.1 can also act as an oncoprotein since deregulated expression of PU.1 in erythroid precursors causes erythroleukemias in mice. Studies of cultured mouse erythroleukemia cell lines indicat

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20

Ye, Min, Olga Ermaermakova-Cirilli, and Thomas Graf. "B Cell Development in the Absence of PU.1." Blood 104, no. 11 (2004): 226. http://dx.doi.org/10.1182/blood.v104.11.226.226.

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Abstract Mice deficient of the ETS-family transcription factor PU.1 lack B cells as well as macrophages. While most macrophage specific genes are known to be regulated by high levels of PU.1, the reason for the defect in B cell formation is not known. Here we analyzed a mouse strain in which a floxed version of the PU.1 gene, surrounding exon 4 and 5, which encode the DNA, binding and PEST domains (developed by C. Somoza and D. Tenen), was excised by Cre mediated recombination. As expected, this strain lacks both B cells and macrophages and die at birth. Surprisingly, however, we were able to

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Saunthararajah, Yogenthiran, SiJun Yang, ShriHari Kadkol, Marie Baraoidan, Vinzon Ibanez, and Fariborz Mortazavi. "GATA-1, but Not GATA-2, Antagonizes PU.1 Mediated Transcriptional Activity at the CBFA2T3 (ETO2, MTG16) Promoter through a Mechanism Dependent on GATA DNA Binding." Blood 106, no. 11 (2005): 1749. http://dx.doi.org/10.1182/blood.v106.11.1749.1749.

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Abstract CBFA2T3 (ETO2, MTG16), a target of chromosomal translocation in acute myeloid leukemia, has its highest expression in hematopoietic cells compared to other tissues. This suggests that its expression is regulated by major hematopoietic transcription factors. The proximal promoter from −171 to −65 bp has greater than 90% identity between mouse and human and contains recognition sites for major hematopoietic transcription factors PU.1, GATA-1 and GATA-2. Using chromatin immuno-precipitation and the MPD hematopoietic cell-line, this segment was pulled down with endogenous PU.1, GATA-1 and

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22

Yona, Simon, and Alexander Mildner. "Good things come in threes." Science Immunology 3, no. 30 (2018): eaav5545. http://dx.doi.org/10.1126/sciimmunol.aav5545.

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23

Bartholdy, Boris, Yukiya Yamamoto, Erica Evans, John Crispino, and Daniel G. Tenen. "PU.1 - c-Jun Interactions Are Crucial for PU.1 Function in Myeloid Development." Blood 114, no. 22 (2009): 3651. http://dx.doi.org/10.1182/blood.v114.22.3651.3651.

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Abstract Abstract 3651 Poster Board III-587 The Ets transcription factor PU.1 is a master regulator absolutely required for the differentiation of monocytes, macrophages, and B cells in the fetal liver and in the adult bone marrow. PU.1 drives hematopoietic differentiation partly through direct protein-protein interactions with other transcription factors, such as the AP-1 transcription factor c-Jun. We have shown that c-Jun can be recruited to promoters which do not include AP-1 binding sites, such as the MCSFR promoter, and act as a PU.1-dependent co-activator. To address the functional impo

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24

Iino, Tadafumi, Hiromi Iwasaki, Kentaro Kohno, et al. "Selective Disruption of PU.1 in Mature Dendritic Cells Affects Their Tissue Distribution and T Cell Homeostasis." Blood 118, no. 21 (2011): 518. http://dx.doi.org/10.1182/blood.v118.21.518.518.

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Abstract Abstract 518 PU.1, a hematopoietic transcription factor, is indispensable for development of conventional dendritic cells (cDCs) from hematopoietic stem cells. However, the function of PU.1 in mature cDC remains unclear. To test the possible role of PU.1 in mature cDCs, we developed mice lacking PU.1 selectively in mature cDCs (DC-PU.1D/D mice) by crossing a PU.1flox mouse line with a transgenic Itgax (CD11c)-Cre strain. In these mice, cDCs were dramatically reduced in spleen, thymus, lymph node, and skin, down to <40%, <25%, <10% and <5% of DCs in control mice respectivel

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25

Wei, Fang, Kristina Zaprazna, Junwen Wang, and Michael L. Atchison. "PU.1 Can Recruit BCL6 to DNA To Repress Gene Expression in Germinal Center B Cells." Molecular and Cellular Biology 29, no. 17 (2009): 4612–22. http://dx.doi.org/10.1128/mcb.00234-09.

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ABSTRACT BCL6 is a transcriptional repressor crucial for germinal center formation. BCL6 represses transcription by a variety of mechanisms by binding to specific DNA sequences or by recruitment to DNA by protein interactions. We found that BCL6 can inhibit activities of the immunoglobulin kappa (Igκ) intron and 3′ enhancers. At the Igκ 3′ enhancer, BCL6 repressed enhancer activity through the PU.1 binding site. We found that BCL6 physically interacted with PU.1 in vivo and in vitro, and the results of sequential chromatin immunoprecipitation assays and transient-expression assays suggested th

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26

O’Brien, Gráinne, Lourdes Cruz-Garcia, Joanna Zyla, et al. "Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML." Carcinogenesis 41, no. 8 (2019): 1104–12. http://dx.doi.org/10.1093/carcin/bgz175.

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Abstract Therapy-related and more specifically radiotherapy-associated acute myeloid leukaemia (AML) is a well-recognized potential complication of cytotoxic therapy for the treatment of a primary cancer. The CBA mouse model is used to study radiation leukaemogenesis mechanisms with Sfpi1/PU.1 deletion and point mutation already identified as driving events during AML development. To identify new pathways, we analysed 123 mouse radiation-induced AML (rAML) samples for the presence of mutations identified previously in human AML and found three genes to be mutated; Sfpi1 R235 (68%), Flt3-ITD (4

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27

Welner, Robert S., Danielle E. Tenen, Henry Yang, Deepak Bararia, Giovanni Amabile, and Daniel G. Tenen. "Relationship Between Self-Renewal and Differentiation Pathways in Stem Cells and Leukemia." Blood 124, no. 21 (2014): 4789. http://dx.doi.org/10.1182/blood.v124.21.4789.4789.

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Abstract Hematopoietic stem cells are capable of perpetual self-renewal and multi-lineage differentiation, properties that are maintained throughout life by minimal cell cycle activity. Our work has focused on deciphering transcriptional driven differentiation versus self-renewal pathways in stem and progenitor cells. To this end, we have studied transcription factors that control the fate of hematopoietic stem cells by combining mouse models of activated self-renewal with models that can report transcription factor expression. We chose to study the Wnt pathway, activated in several types of l

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Ha, Soon-Duck, Woohyun Cho, Rodney P. DeKoter та Sung Ouk Kim. "The transcription factor PU.1 mediates enhancer-promoter looping that is required for IL-1β eRNA and mRNA transcription in mouse melanoma and macrophage cell lines". Journal of Biological Chemistry 294, № 46 (2019): 17487–500. http://dx.doi.org/10.1074/jbc.ra119.010149.

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The DNA-binding protein PU.1 is a myeloid lineage–determining and pioneering transcription factor due to its ability to bind “closed” genomic sites and maintain “open” chromatin state for myeloid lineage–specific genes. The precise mechanism of PU.1 in cell type–specific programming is yet to be elucidated. The melanoma cell line B16BL6, although it is nonmyeloid lineage, expressed Toll-like receptors and activated the transcription factor NF-κB upon stimulation by the bacterial cell wall component lipopolysaccharide. However, it did not produce cytokines, such as IL-1β mRNA. Ectopic PU.1 expr

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Shin, Dong-Mi, Chang-Hoon Lee, and Herbert Morse. "The Transcriptional Network Governed by Interferon Regulatory Factor (IRF8) In Germinal Center B Cell Lymphomas." Blood 116, no. 21 (2010): 3638. http://dx.doi.org/10.1182/blood.v116.21.3638.3638.

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Abstract Abstract 3638 The transcription factor IRF8, is highly expressed in germinal center (GC) centroblastic B cells and diffuse large B cell lymphomas (DLBCL). IRF8 is known to play roles in GC formation as well as in early B cell fate commitment, functioning both as a transcriptional activator and repressor; however, the transcriptional network regulated by IRF8 has not been elucidated yet. To identify direct targets of IRF8 on a genome-wide scale, we used ChIP-chip and expression profiling to study human and mouse lymphoma cell lines of GC origin – human Ly1, Odh1 and Val and mouse NFS20

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30

Lian, Ming, Yu Fang Jiang, Shi Dong Lv, Yi Long He, Jiang Sheng Zhou, and Qing Xiong Meng. "The Anti-Obesity Effect of Instant Pu-Erh Ripe Tea in Mice with Hydrogenated Oil Diet-Induced Obesity." Applied Mechanics and Materials 644-650 (September 2014): 5239–43. http://dx.doi.org/10.4028/www.scientific.net/amm.644-650.5239.

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Obesity has become a fast growing epidemic in developing countries, as well as in some of the developing countries. Drinking Chinese tea has been demonstrated to have multiple beneficial effects to obese patients. It showed strong effect in reducing body fat and lowering blood sugar. This article tested the effect of instant Pu-erh ripe tea on weight loss in diet-induced obese (DIO) mice. The results demonstrated that instant Pu-erh ripe tea was be able to reduce the mouse weight dose-dependently. Its effect is stronger than that of L-carnitine, a weight loss drug currently on the market. Inst

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31

Koc, Hazal, Ebru Kilicay, Zeynep Karahaliloglu, Baki Hazer, and Emir B. Denkbas. "Prevention of urinary infection through the incorporation of silver–ricinoleic acid–polystyrene nanoparticles on the catheter surface." Journal of Biomaterials Applications 36, no. 3 (2021): 385–405. http://dx.doi.org/10.1177/0885328220983552.

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Nosocominal infections associated with biofilm formation on urinary catheters cause serious complications. The aim of this study was to investigate the feasibility of the polyurethane (PU) catheter modified with tetracycline hydrochloride (TCH) attached Ag nanoparticles embedded PolyRicinoleic acid-Polystyrene Nanoparticles (PU-TCH-AgNPs-PRici-PS NPs) and the influence on antimicrobial and antibiofilm activity of urinary catheters infected by Escherichia coli and Staphylococcus aureus. For this purpose, AgNPs embedded PRici graft PS graft copolymers (AgNPs-PRici-g-PS) were synthesized via free

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32

Musikacharoen, Tipayaratn, Asako Oguma, Yasunobu Yoshikai, Norika Chiba, Akio Masuda та Tetsuya Matsuguchi. "Interleukin-15 induces IL-12 receptor β1 gene expression through PU.1 and IRF 3 by targeting chromatin remodeling". Blood 105, № 2 (2005): 711–20. http://dx.doi.org/10.1182/blood-2004-03-0842.

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AbstractInterleukin-12 receptor β1 (IL12RB1) is expressed on a variety of immune cells, including T and natural killer (NK) cells and macrophages, and is involved in innate and adaptive immune responses. Levels of IL12RB1 mRNA are dynamically regulated by various cytokines, including interferon-γ (IFN-γ) and IL-15. To reveal the regulatory mechanisms governing IL12RB1 gene expression, we analyzed the transcriptional regulatory region of the mouse IL12RB1 gene. Promoter analyses in a mouse macrophage cell line, RAW264.7, revealed that the 2508-bp region upstream of the transcriptional start sit

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Iino, Tadafumi, Yong Chong, Shin-ichi Mizuno, et al. "PU.1 Plays a Critical Role in Maintenance of Mature Dendritic Cell Pool." Blood 112, no. 11 (2008): 3554. http://dx.doi.org/10.1182/blood.v112.11.3554.3554.

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Abstract PU.1, a hematopoietic transcription factor, is absolutely required for development of myelo-lymphoid cells from hematopoietic stem cells (HSC). PU.1-deficient mice fail to develop common myeloid progenitors (CMPs) or common lymphoid progenitors (CLPs), resulting in complete loss of dendritic cells (DC) in addition to mature myeloid and lymphoid cells. In this study, by disrupting PU.1 specifically at the mature DC stage, we here show that PU.1 is necessary for maintenance of mature DC pool. By crossing PU.1 floxed/floxed mice with a mouse line harboring the Cre transgene driven by the

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Cristóbal, Lara, Nerea de los Reyes, Miguel A. Ortega, et al. "Local Growth Hormone Therapy for Pressure Ulcer Healing on a Human Skin Mouse Model." International Journal of Molecular Sciences 20, no. 17 (2019): 4157. http://dx.doi.org/10.3390/ijms20174157.

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The growth hormone is involved in skin homeostasis and wound healing. We hypothesize whether it is possible to improve pressure ulcer (PU) healing by locally applying the recombinant human growth hormone (rhGH) in a human skin mouse model. Non-obese diabetic/severe combined immunodeficient mice (n = 10) were engrafted with a full-thickness human skin graft. After 60 days with stable grafts, human skin underwent three cycles of ischemia-reperfusion with a compression device to create a PU. Mice were classified into two groups: rhGH treatment group (n = 5) and control group (n = 5). In the rhGH

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Kucine, Nicole, Sachie Marubayashi, Neha Bhagwat, et al. "Tumor-specific HSP90 inhibition as a therapeutic approach in JAK-mutant acute lymphoblastic leukemias." Blood 126, no. 22 (2015): 2479–83. http://dx.doi.org/10.1182/blood-2015-03-635821.

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Key Points PU-H71, a novel purine scaffold inhibitor, shows potent therapeutic efficacy in JAK-mutant ALL cells and mouse models. HSP90 inhibition retains therapeutic efficacy in ruxolitinib-persistent JAK-mutant ALL cells.

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Bach, Christian, Philipp B. Staber, Min Ye та ін. "PU.1 Is a Downstream Target of C/EBPα in Normal Hematopoiesis and Acute Myeloid Leukemia". Blood 118, № 21 (2011): 1353. http://dx.doi.org/10.1182/blood.v118.21.1353.1353.

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Abstract Abstract 1353 The transcription factors PU.1 and C/EBPα are key regulators of hematopoietic cell differentiation. Tight and coordinated regulation of these factors is essential for normal hematopoiesis and even moderate alterations can lead to acute myeloid leukemia (AML). Previous studies established that in PU.1 knockout mice myeloid differentiation is blocked at an earlier stage compared to C/EBPα knockouts, consistent with PU.1 acting upstream of C/EBPα during hematopoietic differentiation. Recently, however, we and others identified a PU.1 upstream regulatory element (URE) which

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Vlckova, Petra, Libor Stanek, Pavel Burda, et al. "PU.1 and p53 Double Mutant Mice Develop Aggressive AML with Dysplastic Features." Blood 120, no. 21 (2012): 769. http://dx.doi.org/10.1182/blood.v120.21.769.769.

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Abstract Abstract 769 Introduction: Downregulation of tumour suppressor transcription factor PU.1 in haematopoietic stem and progenitor cells represents primary underlying mechanism for the development of acute myeloid leukaemia (AML) in mice with homozygous deletion of the upstream regulatory element (URE) of PU.1 gene. Human AML often display differences in aggressiveness that are associated with mutations of a well known tumour suppressor p53. We produced murine model carrying mutations of p53 and URE that develops highly aggressive AML and focused on molecular mechanisms that are responsib

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Fisher, Robert C., Marilyn C. Olson, Jagan M. R. Pongubala, et al. "Normal Myeloid Development Requires Both the Glutamine-Rich Transactivation Domain and the PEST Region of Transcription Factor PU.1 but Not the Potent Acidic Transactivation Domain." Molecular and Cellular Biology 18, no. 7 (1998): 4347–57. http://dx.doi.org/10.1128/mcb.18.7.4347.

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ABSTRACT Gene targeting of transcription factor PU.1 results in an early block to fetal hematopoiesis, with no detectable lymphoid or myeloid cells produced in mouse embryos. Furthermore,PU.1 −/− embryonic stem (ES) cells fail to differentiate into Mac-1+ and F4/80+macrophages in vitro. We have previously shown that a PU.1 transgene under the control of its own promoter restores the ability ofPU.1 −/− ES cells to differentiate into macrophages. In this study, we take advantage of ourPU.1 −/− ES cell rescue system to genetically test which previously identified PU.1 functional domains are neces

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Steidl, Ulrich, Frank Rosenbauer, Xuesong Gu, et al. "Knockdown of the Transcription Factor PU.1 Causes Characteristic Transcriptional Changes in Hematopoietic Stem Cells Prior to Leukemic Transformation." Blood 104, no. 11 (2004): 1112. http://dx.doi.org/10.1182/blood.v104.11.1112.1112.

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Abstract Knockdown of the expression of the transcription factor PU.1 in mice results in an initial preleukemic expansion of myeloid progenitors and subsequent transformation to an immature acute myeloid leukemia (AML). Recent reports suggest that functional inactivation of PU.1 might also play a role in human AML. However, the molecular mechanisms underlying the malignant transformation are unknown. Examining the bone marrow of leukemic PU.1 knockdown mice we found an expansion of lin−, c-kit+, Sca1+ hematopoietic stem cells (HSC) as compared to wildtype animals. This finding prompted us to e

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Foos, Gabriele E., Kimberlee M. Fischer, Jeremiah Savage, Venkat Reddy, and Bruce E. Torbett. "Identification of PU.1 Target Genes That Are Dependent on Specific Functional Domains of the Transcription Factor PU.1." Blood 108, no. 11 (2006): 1174. http://dx.doi.org/10.1182/blood.v108.11.1174.1174.

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Abstract The expression of PU.1, a member of the ets transcription factor family, is limited to the hematopoietic lineage. Using knockout and reduced PU.1 expression and gain of function mice as a model system, it has been demonstrated that PU.1 plays a key role in early myeloid and lymphoid fate decision and at later stages of myeloid differentiation and function. In PU.1 (Sfpi1) null mice, dendritic cells and monocytes could not be identified, but early myeloid progenitors and immature neutrophils were present. In mice with reduced PU.1 expression monocyte development was hindered, immature

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Zhang, Pu, Gang Huang, Alex Ebralidze, et al. "Genetics and Epigenetics of the PU.1 Upstream Regulatory Element: AML1 Binding Sites Are Critical for Leuekmia Induced by the AML/ETO9a Fusion Oncogene." Blood 112, no. 11 (2008): 594. http://dx.doi.org/10.1182/blood.v112.11.594.594.

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Abstract The level of expression of the transcription factor PU.1 is a critical determinant of lineage commitment in normal hematopoiesis, and dysregulation of PU.1 leads to development of leukemia. In mice with targeted disruption of the PU.1 upstream regulatory element (URE), expression of PU.1 is decreased to 20% of wild type levels and results in development of acute myeloid leukemia (AML). These data suggests that tightly regulated PU.1 expression is important to maintain normal hematopoiesis and prevent leukemogenesis. Previously, we reported that AML1 (RUNX1) regulated PU.1 expression.

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Moleriu, Lavinia, Adina Octavia Duse, Florin Borcan, et al. "Formulation and Characterization of Antibacterial Hydrogels Based on Polyurethane Microstructures and 1,2,4-Triazole Derivatives." Materiale Plastice 54, no. 2 (2017): 348–52. http://dx.doi.org/10.37358/mp.17.2.4849.

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Antibacterial gels offer an efficient hygiene in the absence of soap and water. The most part of these products are based on mixtures of different antibacterial and fungicide substances dissolved in an alcohol. Unfortunately, all cosmetic products containing alcohols wash the sebum and dry the skin. In the present study, alcohol-free antibacterial hydrogels were obtained through the synthesis of polyurethane (PU) microstructures with an increased amount of surfactant; 5-mercapto-1,2,4-triazole derivatives were used as active compounds inside the PU microstructures as antibacterial agents. Ther

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Kitajima, Kenji, Makoto Tanaka, Jie Zheng, et al. "Redirecting differentiation of hematopoietic progenitors by a transcription factor, GATA-2." Blood 107, no. 5 (2006): 1857–63. http://dx.doi.org/10.1182/blood-2005-06-2527.

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GATA-2 is a zinc finger transcription factor essential for differentiation of immature hematopoietic cells. We analyzed the function of GATA-2 by a combined method of tetracycline-dependent conditional gene expression and in vitro hematopoietic differentiation from mouse embryonic stem (ES) cells using OP9 stroma cells (OP9 system). In the presence of macrophage colony-stimulating factor (M-CSF), the OP9 system induced macrophage differentiation. GATA-2 expression in this system inhibited macrophage differentiation and redirected the fate of hematopoietic differentiation to other hematopoietic

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Jenal, Mathias, Venkateshwar A. Reddy, Judith Laedrach, et al. "The Anti-Apoptotic Gene BCL2A1 Is Transcriptionally Regulated by PU.1." Blood 112, no. 11 (2008): 3579. http://dx.doi.org/10.1182/blood.v112.11.3579.3579.

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Abstract PU.1 is a hematopoietic transcriptional regulator that is necessary for the development of both myeloid and B cells. To identify new PU.1 target genes in neutrophil development PU.1 was introduced into mouse 503 PU.1-null cells using lentiviral gene transfer and microarray analyses of two independent 503 PU.1-rescued and parental 503 cells were compared. The BCL2A1 gene was found to be more than 50-fold induced in 503 PU.1- restored as compared to the parental 503-null cells. BCL2A1 (also known as BFL-1/A1) is an anti-apoptotic member of the BCL2 family. BCL2A1 was initially identifie

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Nishimura, Nao, Shinya Endo, Niina Ueno, et al. "Xenograft Models of Multiple Myeloma Reveal That PU.1 Serves As a Tumor Suppressor for Multiple Myeloma." Blood 124, no. 21 (2014): 2047. http://dx.doi.org/10.1182/blood.v124.21.2047.2047.

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Abstract PU.1 is an essential transcription factor for hematopoiesis and important for differentiation of both myeloid and lymphoid lineages. In mice conditionally knocked-out of 3.4 kb length of the enhancer region located in14 kb 5’ upstream of the PU.1 gene (URE), PU.1 is down-regulated in myeloid cells and B cells by 20% of that of wild type, and such mice develop acute myeloid leukemia and CLL-like diseases. These data strongly suggest that PU.1 has tumor suppressor activity in hematopoietic cells. We previously reported that human PU.1 is down-regulated in the majority of myeloma cell li

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Sive, Jonathan I., Fernando J. Calero-Nieto, Rebecca Hannah, and Berthold Göttgens. "Genome-Scale Analysis of the Pu.1 Driven Transcriptional Programme That Overcomes the Differentiation Block in a Novel Pu.1-Inducible AML Cell Line." Blood 124, no. 21 (2014): 869. http://dx.doi.org/10.1182/blood.v124.21.869.869.

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Abstract Transcription factors (TFs) play a key role in determining normal haematopoiesis; haematological cancers often being characterised by TF dysregulation. Pu.1 is a TF that plays a major role in myeloid differentiation, with mutations and down regulation of Pu.1 activity described in human acute myeloid leukemia (AML). To investigate the role of Pu.1 in normal and leukemic myeloid fate, we developed a model of inducible Pu.1 rescue in a murine AML cell line, and utilised it to assess genome-wide Pu.1-DNA-binding profiles and the subsequent effects on histone remodelling, gene expression

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Hu, Tianyuan, Kiyomi Morita, Matthew C. Hill, et al. "PRDM16s transforms megakaryocyte-erythroid progenitors into myeloid leukemia–initiating cells." Blood 134, no. 7 (2019): 614–25. http://dx.doi.org/10.1182/blood.2018888255.

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Abstract Oncogenic mutations confer on cells the ability to propagate indefinitely, but whether oncogenes alter the cell fate of these cells is unknown. Here, we show that the transcriptional regulator PRDM16s causes oncogenic fate conversion by transforming cells fated to form platelets and erythrocytes into myeloid leukemia stem cells (LSCs). Prdm16s expression in megakaryocyte-erythroid progenitors (MEPs), which normally lack the potential to generate granulomonocytic cells, caused AML by converting MEPs into LSCs. Prdm16s blocked megakaryocytic/erythroid potential by interacting with super

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Iino, Tadafumi, Yong Jeong, Shin-ichi Mizuno, et al. "PU.1 Is Indispensable for Development of Mature Dendritic Cells and Their Function That Plays a Critical Role in Maintenance of Normal T Cell Pool." Blood 114, no. 22 (2009): 1471. http://dx.doi.org/10.1182/blood.v114.22.1471.1471.

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Abstract Abstract 1471 Poster Board I-494 PU.1, a hematopoietic transcription factor, is indispensable for development of myelo-lymphoid cells from hematopoietic stem cells (HSCs). PU.1-deficient mice fail to develop common myeloid progenitors (CMPs) or common lymphoid progenitors (CLPs), resulting in complete loss of dendritic cells (DC) in addition to mature myeloid and lymphoid cells. By disrupting PU.1 specifically at the mature DC stage, we here show that PU.1 is necessary for maintenance of mature DC pool and their functions. We crossed PU.1 floxed/floxed mice with a mouse line harboring

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Wang, Hongsheng, Shweta Jain, Jiafang Sun, Alexander L. Kovalchuk, and Herbert C. Morse. "An essential role of transcription factors PU.1 and IRF8 in follicular B cell development and the germinal center response." Journal of Immunology 200, no. 1_Supplement (2018): 171.19. http://dx.doi.org/10.4049/jimmunol.200.supp.171.19.

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Abstract The transcription factors PU.1 and IRF8 regulate an unknown number of gene programs for differentiation of many hematopoietic cells including B cells, dendritic cells and myeloid cells. Their roles in B cell development were previously studied using B cell-specific conditional deletion mouse models, such as PU.1flox/flox-CD19Cre, IRF8flox/flox-CD19Cre, IRF8−/−PU.1flox/flox-CD19Cre, or IRF8flox/flox-PU.1flox/flox-CD19Cre mice. While PU.1-deficient B cells are phenotypically normal, deletion of IRF8 in B cells caused a moderate expansion of marginal zone B cells. Double deletion of PU.1

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Kazianka, Lukas, Michaela Prchal-Murphy, Christiane Agreiter, et al. "Ly6C+ Inflammatory Monocytes Create a Leukemia-Initiating Niche." Blood 144, Supplement 1 (2024): 881. https://doi.org/10.1182/blood-2024-208750.

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Background Physiological hematopoiesis relies on a tightly balanced equilibrium of mature blood cell formation and stem cell maintenance that is governed by cell-intrinsic as well as cell-extrinsic stimuli. While the role of transcription factors is well established in this model, the latter are exerted by a complex network of multiple cell types (such as fibroblasts, endothelial cells, bone lining cells, monocytes/macrophages, megakaryocytes, etc.) forming a functional unit that provides the bone marrow (BM) niche. Leukemogenesis is classically perceived as a multi-step process with serial ac

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