Relevant bibliographies by topics / NF-E2

Academic literature on the topic 'NF-E2'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'NF-E2.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "NF-E2"

1

Ney, P. A., N. C. Andrews, S. M. Jane, B. Safer, M. E. Purucker, S. Weremowicz, C. C. Morton, S. C. Goff, S. H. Orkin, and A. W. Nienhuis. "Purification of the human NF-E2 complex: cDNA cloning of the hematopoietic cell-specific subunit and evidence for an associated partner." Molecular and Cellular Biology 13, no. 9 (September 1993): 5604–12. http://dx.doi.org/10.1128/mcb.13.9.5604.

Full text
Abstract:
The human globin locus control region-binding protein, NF-E2, was purified by DNA affinity chromatography. Its tissue-specific component, p45 NF-E2, was cloned by use of a low-stringency library screen with murine p45 NF-E2 cDNA (N. C. Andrews, H. Erdjument-Bromage, M. B. Davidson, P. Tempst, and S. H. Orkin, Nature [London] 362:722-728, 1993). The human p45 NF-E2 gene was localized to chromosome 12q13 by fluorescent in situ hybridization. Human p45 NF-E2 and murine p45 NF-E2 are highly homologous basic region-leucine zipper (bZIP) proteins with identical DNA-binding domains. Immunoprecipitation experiments demonstrated that p45 NF-E2 is associated in vivo with an 18-kDa protein (p18). Because bZIP proteins bind DNA as dimers, we infer that native NF-E2 must be a heterodimer of 45- and 18-kDa subunits. Although AP-1 and CREB copurified with NF-E2, no evidence was found for heterodimer formation between p45 NF-E2 and proteins other than p18. Thus, p18 appears to be the sole specific partner of p45 NF-E2 in erythroid cells. Cloning of human p45 NF-E2 should permit studies of the role of NF-E2 in globin gene regulation and erythroid differentiation.
APA, Harvard, Vancouver, ISO, and other styles
2

Ney, P. A., N. C. Andrews, S. M. Jane, B. Safer, M. E. Purucker, S. Weremowicz, C. C. Morton, S. C. Goff, S. H. Orkin, and A. W. Nienhuis. "Purification of the human NF-E2 complex: cDNA cloning of the hematopoietic cell-specific subunit and evidence for an associated partner." Molecular and Cellular Biology 13, no. 9 (September 1993): 5604–12. http://dx.doi.org/10.1128/mcb.13.9.5604-5612.1993.

Full text
Abstract:
The human globin locus control region-binding protein, NF-E2, was purified by DNA affinity chromatography. Its tissue-specific component, p45 NF-E2, was cloned by use of a low-stringency library screen with murine p45 NF-E2 cDNA (N. C. Andrews, H. Erdjument-Bromage, M. B. Davidson, P. Tempst, and S. H. Orkin, Nature [London] 362:722-728, 1993). The human p45 NF-E2 gene was localized to chromosome 12q13 by fluorescent in situ hybridization. Human p45 NF-E2 and murine p45 NF-E2 are highly homologous basic region-leucine zipper (bZIP) proteins with identical DNA-binding domains. Immunoprecipitation experiments demonstrated that p45 NF-E2 is associated in vivo with an 18-kDa protein (p18). Because bZIP proteins bind DNA as dimers, we infer that native NF-E2 must be a heterodimer of 45- and 18-kDa subunits. Although AP-1 and CREB copurified with NF-E2, no evidence was found for heterodimer formation between p45 NF-E2 and proteins other than p18. Thus, p18 appears to be the sole specific partner of p45 NF-E2 in erythroid cells. Cloning of human p45 NF-E2 should permit studies of the role of NF-E2 in globin gene regulation and erythroid differentiation.
APA, Harvard, Vancouver, ISO, and other styles
3

Wang, Wei, Sven Schwemmers, Elizabeth O. Hexner, and Heike L. Pahl. "AML1 is overexpressed in patients with myeloproliferative neoplasms and mediates JAK2V617F-independent overexpression of NF-E2." Blood 116, no. 2 (July 15, 2010): 254–66. http://dx.doi.org/10.1182/blood-2009-11-254664.

Full text
Abstract:
Abstract The transcription factor NF-E2 is overexpressed in the majority of patients with polycythemia vera (PV). Concomitantly, 95% of these patients carry the JAK2V617F mutation. Although NF-E2 levels correlate with JAK2V671F allele burden in some PV cohorts, the molecular mechanism causing aberrant NF-E2 expression has not been described. Here we show that NF-E2 expression is also increased in patients with essential thrombocythemia and primary myelofibrosis independent of the presence of the JAK2V617F mutation. Characterization of the NF-E2 promoter revealed multiple functional binding sites for AML1/RUNX-1. Chromatin immunoprecipitation demonstrated AML1 binding to the NF-E2 promoter in vivo. Moreover, AML1 binding to the NF-E2 promoter was significantly increased in granulocytes from PV patients compared with healthy controls. AML1 mRNA expression was elevated in patients with PV, essential thrombocythemia, and primary myelofibrosis both in the presence and absence of JAK2V617F. In addition, AML1 and NF-E2 expression were highly correlated. RNAi-mediated suppression of either AML1 or of its binding partner CBF-β significantly decreased NF-E2 expression. Moreover, expression of the leukemic fusion protein AML/ETO drastically decreased NF-E2 protein levels. Our data identify NF-E2 as a novel AML1 target gene and delineate a role for aberrant AML1 expression in mediating elevated NF-E2 expression in MPN patients.
APA, Harvard, Vancouver, ISO, and other styles
4

Martin, Florence, Jan M. van Deursen, Ramesh A. Shivdasani, Carl W. Jackson, Amber G. Troutman, and Paul A. Ney. "Erythroid Maturation and Globin Gene Expression in Mice With Combined Deficiency of NF-E2 and Nrf-2." Blood 91, no. 9 (May 1, 1998): 3459–66. http://dx.doi.org/10.1182/blood.v91.9.3459.

Full text
Abstract:
Abstract NF-E2 binding sites, located in distant regulatory sequences, may be important for high level α- and β-globin gene expression. Surprisingly, targeted disruption of each subunit of NF-E2 has either little or no effect on erythroid maturation in mice. For p18 NF-E2, this lack of effect is due, at least in part, to the presence of redundant proteins. For p45 NF-E2, one possibility is that NF-E2–related factors, Nrf-1 or Nrf-2, activate globin gene expression in the absence of NF-E2. To test this hypothesis for Nrf-2, we disrupted the Nrf-2 gene by homologous recombination. Nrf-2–deficient mice had no detectable hematopoietic defect. In addition, no evidence was found for reciprocal upregulation of NF-E2 or Nrf-2 protein in fetal liver cells deficient for either factor. Fetal liver cells deficient for both NF-E2 and Nrf-2 expressed normal levels of α- and β-globin. Mature mice with combined deficiency of NF-E2 and Nrf-2 did not exhibit a defect in erythroid maturation beyond that seen with loss of NF-E2 alone. Thus, the presence of a mild erythroid defect in NF-E2–deficient mice is not the result of compensation by Nrf-2.
APA, Harvard, Vancouver, ISO, and other styles
5

Martin, Florence, Jan M. van Deursen, Ramesh A. Shivdasani, Carl W. Jackson, Amber G. Troutman, and Paul A. Ney. "Erythroid Maturation and Globin Gene Expression in Mice With Combined Deficiency of NF-E2 and Nrf-2." Blood 91, no. 9 (May 1, 1998): 3459–66. http://dx.doi.org/10.1182/blood.v91.9.3459.3459_3459_3466.

Full text
Abstract:
NF-E2 binding sites, located in distant regulatory sequences, may be important for high level α- and β-globin gene expression. Surprisingly, targeted disruption of each subunit of NF-E2 has either little or no effect on erythroid maturation in mice. For p18 NF-E2, this lack of effect is due, at least in part, to the presence of redundant proteins. For p45 NF-E2, one possibility is that NF-E2–related factors, Nrf-1 or Nrf-2, activate globin gene expression in the absence of NF-E2. To test this hypothesis for Nrf-2, we disrupted the Nrf-2 gene by homologous recombination. Nrf-2–deficient mice had no detectable hematopoietic defect. In addition, no evidence was found for reciprocal upregulation of NF-E2 or Nrf-2 protein in fetal liver cells deficient for either factor. Fetal liver cells deficient for both NF-E2 and Nrf-2 expressed normal levels of α- and β-globin. Mature mice with combined deficiency of NF-E2 and Nrf-2 did not exhibit a defect in erythroid maturation beyond that seen with loss of NF-E2 alone. Thus, the presence of a mild erythroid defect in NF-E2–deficient mice is not the result of compensation by Nrf-2.
APA, Harvard, Vancouver, ISO, and other styles
6

Kotkow, K. J., and S. H. Orkin. "Dependence of globin gene expression in mouse erythroleukemia cells on the NF-E2 heterodimer." Molecular and Cellular Biology 15, no. 8 (August 1995): 4640–47. http://dx.doi.org/10.1128/mcb.15.8.4640.

Full text
Abstract:
High-level, tissue-specific expression of the beta-globin genes requires the presence of an upstream locus control region (LCR). The overall enhancer activity of the beta-globin complex LCR (beta-LCR) is dependent on the integrity of the tandem NF-E2 sites of HS-2. The NF-E2 protein which binds these sites is a heterodimeric basic leucine zipper protein composed of a tissue-specific subunit, p45 NF-E2, and a smaller subunit, p18 NF-E2, that is widely expressed. In these studies, we sought to investigate the role of NF-E2 in globin expression. We show that expression of a dominant-negative mutant p18 greatly reduces the amount of functional NF-E2 complex in the cell. Reduced levels of both alpha- and beta-globin were associated with the lower levels of NF-E2 activity in this cell line. Globin expression was fully restored upon the introduction of a tethered p45-p18 heterodimer. We also examined CB3 cells, a mouse erythroleukemia (MEL) cell line that does not express endogenous p45 NF-E2, and demonstrated that the restoration of globin gene expression was dependent upon the levels of expressed tethered NF-E2 heterodimer. Results of DNase I hypersensitivity mapping and in vivo footprinting assays showed no detectable chromatin alterations in beta-LCR HS-2 due to loss of NF-E2. Finally, we examined the specificity of NF-E2 for globin gene expression in MEL cells. These experiments indicate a critical role for the amino-terminal domain of p45 NF-E2 and show that a related protein, LCRF1, is unable to restore globin gene expression in p45 NF-E2-deficient cells. From these results, we conclude that NF-E2 is specifically required for high level goblin gene expression in MEL cells.
APA, Harvard, Vancouver, ISO, and other styles
7

Jutzi, Jonas S., Ruzhica Bogeska, Gorica Nikoloski, Corina A. Schmid, Thalia S. Seeger, Frank Stegelmann, Sven Schwemmers, et al. "MPN patients harbor recurrent truncating mutations in transcription factor NF-E2." Journal of Experimental Medicine 210, no. 5 (April 15, 2013): 1003–19. http://dx.doi.org/10.1084/jem.20120521.

Full text
Abstract:
The molecular etiology of myeloproliferative neoplasms (MPNs) remains incompletely understood, despite recent advances incurred through the discovery of several different mutations in MPN patients. We have recently described overexpression of the transcription factor NF-E2 in MPN patients and shown that elevated NF-E2 levels in vivo cause an MPN phenotype and predispose to leukemic transformation in transgenic mice. We report the presence of acquired insertion and deletion mutations in the NF-E2 gene in MPN patients. These result in truncated NF-E2 proteins that enhance wild-type (WT) NF-E2 function and cause erythrocytosis and thrombocytosis in a murine model. NF-E2 mutant cells acquire a proliferative advantage, witnessed by clonal dominance over WT NF-E2 cells in MPN patients. Our data underscore the role of increased NF-E2 activity in the pathophysiology of MPNs.
APA, Harvard, Vancouver, ISO, and other styles
8

Mutschler, Manuel, Angela S. Magin, Martina Buerge, Britta Will, Ingo H. Pilz, Anna Rita Migliaccio, and Heike L. Pahl. "NF-E2 Overexpression Delays Erythroid Differentiation and Increases Erythrocyte Production." Blood 110, no. 11 (November 16, 2007): 1546. http://dx.doi.org/10.1182/blood.v110.11.1546.1546.

Full text
Abstract:
Abstract The transcription factor Nuclear-Factor-Erythroid2 (NF-E2) is overexpressed in the vast majority of patients with polycythemia vera (PV). PV affects precisely those lineages expressing NF-E2: hematopoietic precursors, erythroid, megakaryocytic and granulocytic cells. In murine models, NF-E2 overexpression increases proliferation and promotes cellular viability in the absence of EPO. EPO-independent growth is a hallmark of PV. We therefore hypothesized that NF-E2 overexpression contributes to erythrocytosis, the pathognomonic symptom of PV. Consequently, we investigated the effect of NF-E2 overexpression in healthy CD34+ cells. NF-E2 overexpression lead to a delay in erythroid differentiation, manifested by a belated appearance of GlycophorinA-positive mature erythroid cells. Differentiation delay was similarly observed in primary PV patient erythroid cultures compared to healthy controls. Protracted differentiation lead to a significant increase in the accumulated number of erythroid cells both in PV cultures and in CD34+ cells overexpressing NF-E2. Similarly, NF-E2 overexpression altered erythroid colony formation, leading to an increase in BFU-E formation. These data argue that NF-E2 overexpression delays the early phase of erythroid differentiation, resulting in an expansion of erythroid progenitors, thereby increasing the number of erythrocytes derived from one CD34+ cell. These data propose a role for NF-E2 in mediating the erythrocytosis of PV.
APA, Harvard, Vancouver, ISO, and other styles
9

Wang, Wei, Sven Schwemmers, and Heike L. Pahl. "AML-1/RUNX-1 Is Overexpressed in Patients with Myeloproliferative Neoplasms and Mediates JAK2 V617F-Independent Overexpression of NF-E2." Blood 114, no. 22 (November 20, 2009): 3893. http://dx.doi.org/10.1182/blood.v114.22.3893.3893.

Full text
Abstract:
Abstract Abstract 3893 Poster Board III-829 The transcription factor nuclear factor erythroid-2 (NF-E2) plays an essential role in both erythropoiesis and megakaryopoiesis. In addition to erythroid, megakaryocytic and granulocytic progenitors, NF-E2 is expressed in hematopoietic stem cells and in mature granulocytes. We have previously shown that NF-E2 is overexpressed in the vast majority of patients with polycythemia vera (PV). Concomitantly, 90 – 95% of these patients carry the JAK2V617F point mutation. Even though NF-E2 levels correlated with JAK2V671F allele burden in some PV cohorts, the molecular mechanism causing aberrant NF-E2 expression in PV patients has not been described. Here we show that NF-E2 expression is also increased in patients with Essential Thrombocythemia (ET) and that this is independent of the presence of the JAK2V617F mutation. Characterization of the NF-E2 promoter revealed multiple binding sites for Acute Myeloid Leukemia-1 (AML-1/RUNX-1), which were shown to be functional by deletion analysis and site directed mutagenesis. Chromatin Immunoprecipitation (ChIP) demonstrated AML-1 binding to the NF-E2 promoter in vivo. Moreover, AML-1 binding to the NF-E2 promoter in vivo is significantly increased in primary granulocytes from PV patients compared to healthy controls. Subsequently, we demonstrated that mRNA and protein expression of AML-1 is elevated in PV and ET patients, both in the presence and absence of JAK2V617F. In addition, AML-1 and NF-E2 expression are highly correlated. RNAi-mediated suppression of AML-1 levels significantly decreased NF-E2 expression. In summary, our data identify NF-E2 as a novel AML-1 target gene and point to a role of aberrant AML-1 expression in mediating elevated NF-E2 expression in MPN patients. Disclosures: No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
10

Kashif, Muhammed, Hellwig Andrea, Herzog Stefanie, Vinnikov Ilya, Shahzad Khurrum, Nawroth Peter, and Berend Isermann. "The Transcription Factor NF-E2 Regulates Trophoblast Differentiation and Placental Vascularisation Independent of Platelets." Blood 112, no. 11 (November 16, 2008): 3927. http://dx.doi.org/10.1182/blood.v112.11.3927.3927.

Full text
Abstract:
Abstract Embryonic growth restriction is associated with increased perinatal morbidity and mortality. We previously established that the embryonic lack of the transcription factor NF-E2 results in intrauterine growth restriction (IUGR) associated with a reduced placental vascularisation. The mechanism underlying the reduced placental vascularisation in embryos lacking NF-E2 remains unknown. The transcription factor NF-E2 is expressed in cells of the erythrocyte and megakaryocyte lineage. Absence of NF-E2 impairs thrombocytopoiesis secondary to a megakaryocyte defect, resulting in severe thrombocytopenia. The mechanisms underlying the IUGR and reduced placental vascularisation, in particular the role of thrombocytopenia, remains unknown. Analysis of placental vascularisation and embryonic growth revealed a reduction of vascularisation in NF-E2−/− placenta as early as day 14.5 p.c., while the growth retardation of NF-E2−/− embryos was only observed at day 17.5 p.c. Therefore, the placental phenotype precedes embryonic growth retardation, consistent with a primary defect within the placenta. RT-PCR and in situ hybridization detected expression of NF-E2 in the labyrinthine layer and the junctional zone of the E 14.5 placenta as well as in murine trophoblast stem cells in vitro. To determine whether platelet deficiency or a trophoblast specific defect impairs placental vascularisation various in vivo experiments were conducted. Restoring platelet generation in NF-E2 knock out embryos using tetraploid aggregation or via in utero megakaryocyte transplantation does not rescue the vascularisation defect. Consistently, platelet depletion in NF-E2 expressing embryos is not sufficient to reduce placental vascularisation. Therefore, the impaired vascularisation in NF-E2 deficient placenta is independent of the platelet deficiency and results from NF-E2-deficieny in trophoblast cells. Expression analysis (RT-PCR, in situ hybridisation) showed up regulation of syncytiotrophoblast marker Gcm1 and down regulation of labyrinthine layer marker Esx1 in NF-E2−/− placentae. Using electron microscopy we detected thickening of labyrinth trophoblast layers (syncytiotrophoblast layer II and III). To further delineate the mechanisms gene-expression analyses was performed. A number of genes known to be relevant for placental development were less expressed in the absence of NF-E2. Among these genes Fra-1, a member of the AP-1 dimeric transcription factor family with an established role for placental labyrinthine formation, was markedly reduced. Using EMSA we detected a marked reduction of AP-1 binding activity in placental extracts of NF-E2 deficient embryos. These data establish that NF-E2 and Fra-1 interact directly, as has been previously established, or indirectly, through NF-E2 dependent regulation of Fra-1 expression in trophoblast cells, to regulate placental vascularisation. These experiments identify a role of the transcription factor NF-E2 in non-hematopoetic cells. NF-E2 regulates expression of genes relevant for placental development, including the transcription factor Fra-1. The absence of NF-E2 results in impaired placental vascularisation and enhanced syncytium formation independent of platelets through a trophoblast specific defect. These studies therefore identify a new NF-E2 dependent mechanism underlying IUGR.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "NF-E2"

1

Bogeska, Ruzhica [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Biological effects of NF-E2 overexpression in hematopoietic stem cells = Biologische Effekte der NF-E2 Überexpression in hämatopoietischen Stammzellen." Freiburg : Universität, 2012. http://d-nb.info/1114669725/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Gothwal, Monika [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Characterization of a mouse model overexpressing transcription factor NF-E2 = Characterisierung eines Maus Modell mit einer Überexpression von NF-E2." Freiburg : Universität, 2012. http://d-nb.info/1123471118/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Fock, Ee-Ling Clinical School St George Hospital Faculty of Medicine UNSW. "Molecular regulation and enhancement of megakaryopoiesis and thrombopoiesis by the p45 subunit of NF-E2." Publisher:University of New South Wales. Clinical School - St George Hospital, 2008. http://handle.unsw.edu.au/1959.4/42885.

Full text
Abstract:
Megakaryocytes (MKs) are a rare population of haematopoietic cells, which produce platelets. Platelet production is a complex process that is tightly regulated at the transcriptional level by lineage specific transcription factors such as p45 NF-E2. Understanding how transcriptional regulators operate is imperative to advance our knowledge of disease pathophysiology and to propose novel treatment options. Therefore, the aims of this study were to: i) study the effects of p45 NF-E2 overexpression on various stages of megakaryopoiesis; (ii) elucidate the nuclear transport mechanisms of p45 NF-E2; and iii) determine the impact of a p45 NF-E2 modification called SUMOylation on thrombopoiesis. Exogenous p45 NF-E2 was overexpressed in haematopoietic cells in culture and various aspects of megakaryopoiesis were examined. Overexpression of p45 NF-E2 enhanced multiple stages of MK differentiation such as colony forming unit (CFU)-MK formation and terminal MK maturation. Most importantly, p45 NF-E2 overexpression resulted in significant increases in proplatelet and functional platelet production in vitro. This latter result was confirmed in vivo using lethally irradiated mice transplanted with cells that overexpressed p45 NF-E2. Unexpectedly, the enhancement of MK differentiation was at the expense of myeloid development and, for the first time, identified p45 NF-E2 as a negative regulator of myeloid differentiation. Secondly, we determined the nuclear localisation signal of p45-NF-E2 and the pathway responsible for nuclear import. We also investigated the importance of p45 NF-E2 nuclear import in thrombopoiesis. Finally, we showed that p45 NF-E2 is modified mainly by SUMO-2/3 in bone marrow cells and this process is involved in the transcriptional activation of MK-specific genes and platelet release. Taken together, these results suggest that enforced expression of p45 NF-E2 selectively enhances many aspects of MK differentiation including early and terminal MK maturation, proplatelet formation and platelet release. Equally important, this thesis also indicates that white blood cell differentiation may be inhibited by p45 overexpression, while molecular processes such as the nuclear import and SUMOylation of p45 NF-E2 are vital for thrombopoiesis. These observations will facilitate subsequent studies into the feasibility of manipulating p45 NF-E2 protein levels for the treatment of conditions such as thrombocytopaenia and other platelet disorders.
APA, Harvard, Vancouver, ISO, and other styles
4

Devidal, Audrey. "Mécanismes et fonctions du ciblage centrométrique de NF-E2p18/MafK, sous-unité du facteur transcriptionnel érythroide NF-E2." Paris 7, 2005. http://www.theses.fr/2005PA077133.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Jutzi, Jonas Samuel [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Mutationen im Transkriptionsfaktor NF-E2 und deren Rolle in der Entwicklung myeloproliferativer Neoplasien." Freiburg : Universität, 2013. http://d-nb.info/1123478228/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Hadlich, Tobias [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Der Transkriptionsfaktor NF-E2 und seine Rolle in der Pathogenese myeloproliferativer Erkrankungen in vivo." Freiburg : Universität, 2012. http://d-nb.info/1123473684/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Chan, Kaimin, and 陳繼明. "Isolation and characterization of NRF2: a member of the NF-E2 family of transcription factors." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31235566.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Chan, Kaimin. "Isolation and characterization of NRF2 : a member of the NF-E2 family of transcription factors /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19739989.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

DEVEAUX, SOPHIE. "Regulation des genes specifiques des megacaryocytes : role des facteurs de transcription gata, ets et nf-e2." Paris 6, 1998. http://www.theses.fr/1998PA066462.

Full text
Abstract:
Notre equipe travaille sur la regulation de genes exprimes dans la lignee hematopoietique qui produit les megacaryocytes, precurseurs des plaquettes sanguines. Nous nous sommes attaches a l'etude de l'expression specifique du gene mpl dans la lignee megacaryocytaire. Ce gene code le recepteur a la thrombopoietine, qui intervient dans la proliferation et dans la differenciation des megacaryocytes, et qui est egalement capable de stimuler la proliferation des progeniteurs precoces hematopoietiques. Nous avons montre qu'il est regule par le facteur de transcription gata-1 et des membres de la famille ets. D'autres facteurs pourraient intervenir dans l'expression du gene mpl et notamment des facteurs qui se fixent sur une region intronique qui est une region activatrice quand elle est integree dans la chromatine. Nous nous sommes egalement interesses au facteur de transcription nf-e2 qui agit dans les dernieres etapes de la megacaryopoiese. En effet, des souris depourvues de cette proteine presentent une absence totale de plaquettes. Aucun gene megacaryocytaire cible de cette proteine n'etant connu, nous avons utilise une technique d'immunoprecipitation in vivo, et identifie l'un de ces genes. Il code pour la thromboxane synthetase (txs), qui intervient dans le processus d'agregation des plaquettes. Nous avons montre que le facteur nf-e2 est crucial pour l'expression du gene de la txs dans les megacaryocytes in vivo. La mutation d'un site de fixation pour le facteur nf-e2 dans le promoteur diminue fortement l'activite de ce gene, ce qui confirme que son expression est directement regulee par nf-e2. Notre travail a donc permis d'identifier le premier gene cible du facteur de transcription nf-e2 dans les megacaryocytes.
APA, Harvard, Vancouver, ISO, and other styles
10

Kaufmann, Kai Björn [Verfasser], and Heike L. [Akademischer Betreuer] Pahl. "Überexpression des Transkriptionsfaktors NF-E2 in vivo, Etablierung eines neuen Modells zur Untersuchung und Therapie myeloproliferativer Neoplasien." Freiburg : Universität, 2012. http://d-nb.info/112346992X/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "NF-E2"

1

Horstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot, et al. "Nrf2 (NF-E2-Related Factor2)." In Encyclopedia of Signaling Molecules, 1262–68. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_540.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Horstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot, et al. "NF-E2-Related Factor 2." In Encyclopedia of Signaling Molecules, 1215. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100920.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Kim, Sang Geon, Woo Hyung Lee, and Young Woo Kim. "Nrf2 (NF-E2-Related Factor2)." In Encyclopedia of Signaling Molecules, 3585–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_540.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Park, Gyu Hwan, and Jung-Hee Jang. "Potentiation of Cellular Defense Capacity by Phytochemicals Activating NF-E2-Related Factor 2 for the Prevention and/or Treatment of Alzheimer’s Disease." In Aging Mechanisms, 357–93. Tokyo: Springer Japan, 2015. http://dx.doi.org/10.1007/978-4-431-55763-0_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

"NF-E2." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1343. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_11385.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "p18 NF-E2." In The Gene Knockout FactsBook, 839–40. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50462-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "p45 NF-E2." In The Gene Knockout FactsBook, 842–43. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50464-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

"NF-E2-Related Factor 2." In Encyclopedia of Signaling Molecules, 3466. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102562.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Bloom, David, Saravanakumar Dhakshinamoorthy, Wei Wang, Claudia M. Celli, and Anil K. Jaiswal. "Chapter 17 Role of NF-E2 related factors in oxidative stress." In Cell and Molecular Response to Stress, 229–38. Elsevier, 2001. http://dx.doi.org/10.1016/s1568-1254(01)80019-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Sherratt, Philip J., H. C. Huang, Truyen Nguyen, and Cecil B. Pickett. "Role of Protein Phosphorylation in the Regulation of NF-E2–Related Factor 2 Activity." In Quinones and Quinone Enzymes, Part A, 286–301. Elsevier, 2004. http://dx.doi.org/10.1016/s0076-6879(04)78022-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "NF-E2"

1

Thekkeveedu, Renjithkumart Kalikkot, Xanthi Couroucli, Chun Chu, and Bhagavatula Moorthy. "Mechanistic Role of nf-e2 Related Factor (nrf2) Pathway in Hyperoxic Lung Injury: Implications for Bronchopulmonary Dysplasia." In Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.537.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Chevillard, Grégory, Zaynab Nouhi, Anna Derjuga, Marilene Paquet, and Volker Blank. "Abstract B33: Dissecting the role of Nrf3 (NF-E2-related factor 3) in chemical carcinogenesis using knock-out mice." In Abstracts: First AACR International Conference on Frontiers in Basic Cancer Research--Oct 8–11, 2009; Boston MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.fbcr09-b33.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Thekkeveedu, Renjithkumar Kalikkot, Chun Chu, Sudeepta K. Basu, and Bhagavatula Moorthy. "Role of NF-E2 Related Factor (Nrf2) in Hyperoxic Lung Injury: Implications for Bronchopulmonary Dysplasia and Acute Respiratory Distress Syndrome." In Selection of Abstracts From NCE 2015. American Academy of Pediatrics, 2017. http://dx.doi.org/10.1542/peds.140.1_meetingabstract.53.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Guillot, X., N. Tordi, C. Laheurte, L. Pazart, C. Prati, P. Saas, and D. Wendling. "AB0083 Local ice cryotherapy decreases prostaglandin-e2, nf-kb and il-6 synovial levels in arthritic knees compared to contralateral non-treated joints." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5056.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Renaudin, F., L. Campillo-Gimenez, C. Combes, M. Gosset, M. Cohen-Solal, F. Lioté, and H.-K. Ea. "THU0046 Calcium pyrophosphate and monosodium urate crystal-induced prostaglandin E2 production involves NF-κB activation and ros production, independently of INTERLEUKIN-1BETA axis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5505.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Park, Jong-Min, Do-Hee Kim, Hye-Kyung Na, and Young-Joon Surh. "Abstract 5664: Methylseleninic acid induces NAD(P)H: quinone oxidoreductase-1 expression through activation of NF-E2-related factor 2 in Chang liver cells." 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.am10-5664.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kumar, V., and P. Bhatt. "73 Antiarthritic effect of crocetin against adjuvant induced autoinnume disease via suppression the nf-Κb expression and activating of hem oxygenase (ho)-1/nuclear factor-e2-related factor signalling pathway." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.73.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'NF-E2' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography