Relevant bibliographies by topics / Nkx2.2

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  2. Dissertations / Theses
  3. Book chapters
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Academic literature on the topic 'Nkx2.2'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Nkx2.2"

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Wei, Qiou, W. Keith Miskimins, and Robin Miskimins. "Stage-specific Expression of Myelin Basic Protein in Oligodendrocytes Involves Nkx2.2-mediated Repression That Is Relieved by the Sp1 Transcription Factor." Journal of Biological Chemistry 280, no. 16 (February 3, 2005): 16284–94. http://dx.doi.org/10.1074/jbc.m500491200.

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The homeodomain-containing protein Nkx2.2 is critical for the development of oligodendrocyte lineage cells, but the target genes of Nkx2.2 regulation have not been identified. In the present study, we found that the myelin basic protein gene is one of the genes that is regulated by Nkx2.2. Expression of Nkx2.2 represses the expression of myelin basic protein in oligodendrocyte progenitors. Two regulatory elements in the myelin basic protein promoter were identified and found to interact with Nkx2.2in vitro. Despite their sequence divergence, both sites were involved in the Nkx2.2-mediated repression of the myelin basic protein promoter. Binding of Nkx2.2 also blocked and disrupted the binding of the transcriptional activator Purα to the myelin basic protein promoter. Additionally Nkx2.2 recruited a histone deacetylase 1-mSin3A complex to the myelin basic protein promoter. We also found that the transcription factor Sp1 was able to compete off the binding of Nkx2.2 to its consensus binding sitein vitroand reversed the repressive effect of Nkx2.2in vivo. Our data revealed a novel role for Nkx2.2 in preventing the precocious expression of myelin basic protein in immature oligodendrocytes. Based on this study and our previous reports, a model for myelin basic protein gene control is proposed.
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Sander, M., L. Sussel, J. Conners, D. Scheel, J. Kalamaras, F. Dela Cruz, V. Schwitzgebel, A. Hayes-Jordan, and M. German. "Homeobox gene Nkx6.1 lies downstream of Nkx2.2 in the major pathway of beta-cell formation in the pancreas." Development 127, no. 24 (December 15, 2000): 5533–40. http://dx.doi.org/10.1242/dev.127.24.5533.

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Most insulin-producing beta-cells in the fetal mouse pancreas arise during the secondary transition, a wave of differentiation starting at embryonic day 13. Here, we show that disruption of homeobox gene Nkx6.1 in mice leads to loss of beta-cell precursors and blocks beta-cell neogenesis specifically during the secondary transition. In contrast, islet development in Nkx6. 1/Nkx2.2 double mutant embryos is identical to Nkx2.2 single mutant islet development: beta-cell precursors survive but fail to differentiate into beta-cells throughout development. Together, these experiments reveal two independently controlled pathways for beta-cell differentiation, and place Nkx6.1 downstream of Nkx2.2 in the major pathway of beta-cell differentiation.
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Kucenas, Sarah, Heather Snell, and Bruce Appel. "nkx2.2a promotes specification and differentiation of a myelinating subset of oligodendrocyte lineage cells in zebrafish." Neuron Glia Biology 4, no. 2 (May 2008): 71–81. http://dx.doi.org/10.1017/s1740925x09990123.

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During development, multipotent neural precursors give rise to oligodendrocyte progenitor cells (OPCs), which migrate and divide to produce additional OPCs. Near the end of embryogenesis and during postnatal stages, many OPCs stop dividing and differentiate as myelinating oligodendrocytes, whereas others persist as nonmyelinating cells. Investigations of oligodendrocyte development in mice indicated that the Nkx2.2 transcription factor both limits the number of OPCs that are formed and subsequently promotes their differentiation, raising the possibility that Nkx2.2 plays a key role in determining myelinating versus nonmyelinating fate. We used in vivo time-lapse imaging and loss-of-function experiments in zebrafish to further explore formation and differentiation of oligodendrocyte lineage cells. Our data show that newly specified OPCs are heterogeneous with respect to gene expression and fate. Whereas some OPCs express the nkx2.2a gene and differentiate as oligodendrocytes, others that do not express nkx2.2a mostly remain as nonmyelinating OPCs. Similarly to mouse, loss of nkx2.2a function results in excess OPCs and delayed oligodendrocyte differentiation. Notably, excess OPCs are formed as a consequence of prolonged OPC production from neural precursor cells. We conclude that Nkx2.2 promotes timely specification and differentiation of myelinating oligodendrocyte lineage cells from species representing different vertebrate taxa.
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Qi, Yingchuan, Jun Cai, Yuanyuan Wu, Rui Wu, Jeffrey Lee, Hui Fu, Mahendra Rao, Lori Sussel, John Rubenstein, and Mengsheng Qiu. "Control of oligodendrocyte differentiation by the Nkx2.2 homeodomain transcription factor." Development 128, no. 14 (July 15, 2001): 2723–33. http://dx.doi.org/10.1242/dev.128.14.2723.

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Oligodendrocytes are derived from glial precursors that arise from the ventral neural tube early in development. In the developing chicken CNS, oligodendrocyte progenitors selectively express Nkx2.2 homeodomain transcription factor, raising the possibility that Nkx2.2 may directly regulate oligogliogenesis. In this study, we have examined Nkx2.2 expression in rodent glial precursors and studied the effect of a loss of Nkx2.2 on oligodendrocyte and astrocyte differentiation. We show that Nkx2.2 is also expressed in mammalian oligodendrocyte progenitors and that the differentiation of MBP-positive and PLP-DM20-positive oligodendrocytes is dramatically retarded in Nkx2.2-null mutants along the entire rostrocaudal axis. In contrast, no effect is seen on astrocytic differentiation. Interestingly, absence of Nkx2.2 expression leads to a ventral expansion of the Olig1/Olig2 expression in neuroepithelial cells into the Nkx2.2 domain and a consequent increase in the production of Olig1/Olig2-positive and platelet-derived growth factor receptor α-positive oligodendrocyte progenitors. These results strongly suggest that Nkx2.2 regulates the differentiation and/or maturation, but not the initial specification, of oligodendrocyte progenitors. Consistent with this suggestion, overproduction of Nkx2.2 protein in fibroblast cells can induce gene expression from the proteolipid protein promoter.
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Wang, Yu-Cheng, Emerick Gallego-Arteche, Gioia Iezza, Xiaochen Yuan, Mary R. Matli, Su-Pin Choo, Marlene B. Zuraek, et al. "Homeodomain transcription factor NKX2.2 functions in immature cells to control enteroendocrine differentiation and is expressed in gastrointestinal neuroendocrine tumors." Endocrine-Related Cancer 16, no. 1 (March 2009): 267–79. http://dx.doi.org/10.1677/erc-08-0127.

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The homeodomain transcription factor NKX2.2 is necessary for neuroendocrine (NE) differentiation in the central nervous system and pancreas. NE tumors derived from the gut are defined by their NE phenotype, which is used for diagnosis and contributes to tumorigenicity. We hypothesized that NKX2.2 is important for NE differentiation in normal and neoplastic gut. NKX2.2 and NE marker expression was investigated in the small intestine of embryonic and adult mice using immunofluorescence (IF). To determine the role of NKX2.2 in NE differentiation of the intestine, the phenotype of Nkx2.2 (−/−) mice was examined by IF and real-time (RT)-PCR. NKX2.2 and NE marker expression in human NE tumors of the gut and normal tissues were evaluated by immunohistochemistry and qRT-PCR. NKX2.2 expression was detected in the intervillus/crypt regions of embryonic and adult mouse intestine. Co-expression of Nkx2.2 with neurogenin3 (NEUROG3) and hormones was observed in the adult intestinal crypt compartment, suggesting NKX2.2 functions in NEUROG3-positive endocrine progenitors and newly differentiated endocrine cells. In the intestine of Nkx2.2 (−/−) mice, we found a dramatic reduction in the number of cells producing numerous hormones, such as serotonin, gastrin, cholecystokinin, somatostatin, glucagon-like peptide 1 (GLP-1), and secretin, but an increase in cells producing ghrelin. NKX2.2 was expressed in most (24 of 29) human NE tumors derived from diverse primary sites. We conclude NKX2.2 functions in immature endocrine cells to control NE differentiation in normal intestine and is expressed in most NE tumors of the gut, and is therefore a novel target of diagnosis for patients with gastrointestinal NE tumors.
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Sussel, L., J. Kalamaras, D. J. Hartigan-O'Connor, J. J. Meneses, R. A. Pedersen, J. L. Rubenstein, and M. S. German. "Mice lacking the homeodomain transcription factor Nkx2.2 have diabetes due to arrested differentiation of pancreatic beta cells." Development 125, no. 12 (June 15, 1998): 2213–21. http://dx.doi.org/10.1242/dev.125.12.2213.

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The endocrine pancreas is organized into clusters of cells called islets of Langerhans comprising four well-defined cell types: alpha beta, delta and PP cells. While recent genetic studies indicate that islet development depends on the function of an integrated network of transcription factors, the specific roles of these factors in early cell-type specification and differentiation remain elusive. Nkx2.2 is a member of the mammalian NK2 homeobox transcription factor family that is expressed in the ventral CNS and the pancreas. Within the pancreas, we demonstrate that Nkx2.2 is expressed in alpha, beta and PP cells, but not in delta cells. In addition, we show that mice homozygous for a null mutation of Nkx2.2 develop severe hyperglycemia and die shortly after birth. Immunohistochemical analysis reveals that the mutant embryos lack insulin-producing beta cells and have fewer glucagon-producing alpha cells and PP cells. Remarkably, in the mutants there remains a large population of islet cells that do not produce any of the four endocrine hormones. These cells express some beta cell markers, such as islet amyloid polypeptide and Pdx1, but lack other definitive beta cell markers including glucose transporter 2 and Nkx6.1. We propose that Nkx2.2 is required for the final differentiation of pancreatic beta cells, and in its absence, beta cells are trapped in an incompletely differentiated state.
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Fu, Hui, Yingchuan Qi, Min Tan, Jun Cai, Hirohide Takebayashi, Masato Nakafuku, William Richardson, and Mengsheng Qiu. "Dual origin of spinal oligodendrocyte progenitors and evidence for the cooperative role of Olig2 and Nkx2.2 in the control of oligodendrocyte differentiation." Development 129, no. 3 (February 1, 2002): 681–93. http://dx.doi.org/10.1242/dev.129.3.681.

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In this study, we have investigated the relationship of Olig2+ and Nkx2.2+ oligodendrocyte progenitors (OLPs) by comparing the expression of Olig2 and Nkx2.2 in embryonic chicken and mouse spinal cords before and during the stages of oligodendrogenesis. At the stages of neurogenesis, Olig2 and Nkx2.2 are expressed in adjacent non-overlapping domains of ventral neuroepithelium. During oligodendrogenesis stages, these two domains generate distinct populations of OLPs. From the Olig2+ motoneuron precursor domain (pMN) arise the Olig2+/Pdgfra+ OLPs, whereas the Nkx2.2+ p3 domain give rise to Nkx2.2+ OLPs. Despite their distinct origins, both populations of OLPs eventually appear to co-express Olig2 and Nkx2.2 in the same cells. However, there is a species difference in the timing of acquiring Nkx2.2 expression by the Olig2+/Pdgfra+ OLPs. The co-expression of Nkx2.2 and Olig2 in OLPs is tightly associated with myelin gene expression in the normal and PDGFA–/– embryos, suggesting a cooperative role of these transcription factors in the control of oligodendrocyte differentiation. In support of this suggestion, inhibition of expression of these two transcription factors in culture by antisense oligonucleotides has an additive inhibitory effect on OLP differentiation and proteolipid protein (PLP) gene expression.
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Gross, Stefanie, Dina Balderes, Jing Liu, Samuel Asfaha, Guoqiang Gu, Timothy C. Wang, and Lori Sussel. "Nkx2.2 is expressed in a subset of enteroendocrine cells with expanded lineage potential." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 12 (December 15, 2015): G975—G987. http://dx.doi.org/10.1152/ajpgi.00244.2015.

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There are two major stem cell populations in the intestinal crypt region that express either Bmi1 or Lgr5; however, it has been shown that other populations in the crypt can regain stemness. In this study, we demonstrate that the transcription factor NK2 homeobox 2 (Nkx2.2) is expressed in enteroendocrine cells located in the villus and crypt of the intestinal epithelium and is coexpressed with the stem cell markers Bmi1 and Lgr5 in a subset of crypt cells. To determine whether Nkx2.2-expressing enteroendocrine cells display cellular plasticity and stem cell potential, we performed genetic lineage tracing of the Nkx2.2-expressing population using Nkx2.2Cre/+; R26RTomato mice. These studies demonstrated that Nkx2.2+ cells are able to give rise to all intestinal epithelial cell types in basal conditions. The proliferative capacity of Nkx2.2-expressing cells was also demonstrated in vitro using crypt organoid cultures. Injuring the intestine with irradiation, systemic inflammation, and colitis did not enhance the lineage potential of Nkx2.2-expressing cells. These findings demonstrate that a rare mature enteroendocrine cell subpopulation that is demarcated by Nkx2.2 expression display stem cell properties during normal intestinal epithelial homeostasis, but is not easily activated upon injury.
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Hill, Jonathon T., Christina S. Chao, Keith R. Anderson, Fernanda Kaufman, Christopher W. Johnson, and Lori Sussel. "Nkx2.2 Activates the Ghrelin Promoter in Pancreatic Islet Cells." Molecular Endocrinology 24, no. 2 (February 1, 2010): 381–90. http://dx.doi.org/10.1210/me.2009-0360.

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Abstract Nkx2.2 is an essential regulator of pancreatic endocrine differentiation. Nkx2.2-null mice are completely devoid of β-ells and have a large reduction of α- and PP cells. In the place of these islet populations, there is a corresponding increase in the ghrelin-positive ε-cells. Molecular studies have indicated that Nkx2.2 functions as an activator and repressor to regulate islet cell fate decisions. To determine whether Nkx2.2 is solely important for islet cell fate decisions or also has the capability to control ghrelin at the promoter level, we studied the transcriptional regulation of the ghrelin promoter within the pancreas, in vitro and in vivo. These studies demonstrate that both of the previously identified transcriptional start sites in the ghrelin promoter are active within the embryonic pancreas; however, the long transcript is preferentially up-regulated in the Nkx2.2-null pancreas. We also show that the promoter region between −619 and −488 bp upstream of the translational start site is necessary for repression of ghrelin in αTC1 and βTC6 cells. Surprisingly, we also show that Nkx2.2 is able to bind to and activate the ghrelin promoter in several cell lines that do or do not express endogenous ghrelin. Together, these results suggest that the up-regulation of ghrelin expression in the Nkx2.2-null mice is not due to loss of repression of the ghrelin promoter in the nonghrelin islet populations. Furthermore, Nkx2.2 may contribute to the activation of ghrelin in mature islet ε-cells.
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Mariyath, Mubeena P. M., Mehdi H. Shahi, Shirin Farheen, Mohd Tayyab, Nabeela Khanam, and Asif Ali. "Novel Homeodomain Transcription Factor Nkx2.2 in the Brain Tumor Development." Current Cancer Drug Targets 20, no. 5 (June 5, 2020): 335–40. http://dx.doi.org/10.2174/1568009618666180102111539.

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Background: Complex central nervous system (CNS) is made up of neuronal cells and glial cells. Cells of central nervous system are able to regenerate after injury and during repairing. Sonic hedgehog pathway initiated by Shh-N a glycoprotein plays vital role in CNS patterning growth, development and now tumorigenesis. Nkx2.2 homeodomain transcription factor is an effecter molecule, which is positively regulated by Shh during normal growth. Nkx2.2 is essential for V3 domain specification during neural tube patterning at embryonic stage. MBP + oligodendrocytes are differentiated from progenitor cells which express Olig2. Nx2.2 is co-expressed with Olig2 in oligodendrocytes and is essential for later stage of oligodendrocyte maturation. Objective: This review paper explores the potential role of Nkx2.2 transcription factor in glioblastoma development. Conclusion: Shh pathway plays a vital role in oligodendrocytes differentiation and Nkx2.2 transcription factor is essential for oligodendrocytes differentiation and maturation. Intriguingly, down regulation of Nkx2.2 transcription factor with aberrant Shh signaling pathway is reported in glioma samples. So here it is suggested that Nkx2.2 expression pattern could be used as a potential biomarker for the early diagnosis of glioma.
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Dissertations / Theses on the topic "Nkx2.2"

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Falha, Layal. "Implication du facteur de transcription dans Nkx2.2 gliomagenesis." Thesis, Montpellier 2, 2014. http://www.theses.fr/2014MON20065.

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Glioblastome représente la tumeur la plus courante du cerveau primaire avec une survie de moins de 2 ans. Ces tumeurs sont très infiltrantes et angiogéniques et contiennent une sous population de cellules souches cancéreuses. Nkx2.2 est un homéodomaine facteur de transcription, impliqué dans la formation d'oligodendrocytes au cours du développement. Nkx2.2 joue un rôle central dans la tumorogenèse de Ewing'sarcoma. L'utilisation de la QPCR et de la matrice du tissu de gliome, nous a permis de mettre en évidence la forte expression de Nkx2 dans le glioblastome. Nkx2.2 a également été détecté dans 3 cultures de cellules de gliomes où il est co-exprimé avec des marqueurs de cellules souches tels que CD133 et CD15. Il a été récemment proposé que la surexpression de Nkx2.2 pourrait induire à la différenciation oligodendrocytaire de la cellule du gliome tige-comme et au blocage de la formation des tumeurs dans la xénotransplantation (Cancer Res fév 2011 1; 71 (3): 1135-1145). Pour explorer cette possibilité, nous avons utilisé des rétrovirus pour surexprimer Nkx2.2 dans nos cultures cellulaires. De manière surprenante, nous avons trouvé que Nkx2.2, induit la prolifération des cellules souches du gliome et n'a en conséquent aucun effet de différenciation. Microarray analyses a confirmé que la surexpression de Nkx2.2 n'a en effet aucune influence sur la différenciation des oligodendrocytes. Cette analyse a également révélé que Nkx2.2 était capable d'induire une forte expression de YKL-40 40 dans le surnageant des cellules souches du gliome. YKL-40 est en fait, une glycoprotéine sécrétée et impliquée dans l'inflammation, l'angiogenèse et la prolifération. Elle est souvent associée à un mauvais pronostic dans plusieurs types de cancers. En outre, nous avons effectué une transplantation orthotopique afin d'explorer le rôle de Nkx2.2 dans la gliomagenèse in vivo et avons constaté que Nkx2.2 ne réduit pas l'agressivité du glioblastome.Dans l'autre partie de ma thèse, nous avons utilisé la gamme Taqman à basse densité et la validation des miRNA par la Qpcr afin de chercher ces derniers dans la culture cellulaire du glioblastome humain. Nous avons ensuite étudié le rôle des miARN dans la transcription de 3'UTR de Nkx2.2. Les résultats d'analyse de la mutagénèse dirigée (SDM) et de la double-luciférase ont montré que l'expression de Nkx2.2 est régulée par la diminution de mir-133b ainsi que celle de mir-202
Glioblastoma represent the most common primary brain tumor with an overall survival of less than 2 years. These tumors are highly infiltrative and angiogenic and contain a sub population of cancer stem cells. Nkx2.2 is a homeodomain transcription factor which is implicated in the formation of oligodendrocytes during development. Nkx2.2 is central in tumorogenesis of Ewing'sarcoma. Using QPCR and glioma tissue array, we found that Nkx2.2 is highly expressed in glioblastoma. Nkx2.2 was also detected in 3 glioma stem-like cell cultures (neurospheres) where it is co-expressed with stem cell markers such as CD133 and CD15. It was recently proposed that overexpression of Nkx2.2 could induce terminal oligodendrocytic differentiation of glioma stem-like cell and inhibit tumor formation in xenotransplantation (Cancer Res. 2011 Feb 1;71(3):1135-45).To explore this possibility further, we used retroviruses to overexpress Nkx2.2 in our cell cultures. Surprisingly, we found that Nkx2.2, induce glioma stem cell proliferation and had no oligodendrocyte differentiating effect. Microarray analyses confirmed that Nkx2.2 overexpression had no influence in oligodendrocyte differentiation. This analysis further revealed that Nkx2.2 was able to induce a strong expression of YKL40 protein in the supernatant of glioma stem cells and increase YKL-40 promoter activity. YKL-40 is a secreted glycoprotein which is involved in inflammation, angiogenesis and proliferation and which is often associated with a bad prognosis in several cancers. In addition, we performed orthotopic transplantation to explore the role of Nkx2.2 in gliomagenesis in vivo and found that Nkx2.2 did not reduce the aggressiveness of glioblastoma. In the other part of my thesis we used Taqman low-density arrays (TLDA) and individual miRNA QPCR validation to find the microRNA (miRNA) signature in human glioblastoma cell cultures. Then we investigated the role of miRNA in the 3'UTR of Nkx2.2 transcript. Site directed mutagenesis (SDM) and dual-Luciferase reporter assay results showed that the Nkx2.2 expression is downregulated by mir-133b and mir-202
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Pravemann, Jana Verfasser], and Hans-Henning [Akademischer Betreuer] [Arnold. "Die Rolle der Transkriptionsfaktoren Nkx2.2 und Nkx2.9 in der Entwicklung des Neuralrohrs: Herstellung einer Nkx2.9 Cre knock-in Mausmutante / Jana Pravemann ; Betreuer: Hans-Henning Arnold." Braunschweig : Technische Universität Braunschweig, 2014. http://d-nb.info/1175820709/34.

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Guichet, Pierre-Olivier. "Rôle de NKX2-2, NGN2 et DCX dans la prolifération, différenciation et migration des cellules tumorales de glioblastomes." Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20143.

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Les Glioblastomes (Gb) sont des tumeurs primaires du SNC les plus fréquentes et sont particulièrement agressives car résistantes à la radio/chimiothérapie. Elles présentent généralement une composante solide et infiltrante. Cette dernière étant difficile à éliminer par la chirurgie sera en partie responsable de la récurrence de la tumeur. Une des avancées majeures du domaine est la mise en évidence dans les Gb de sous populations présentant des caractéristiques de précurseurs neuraux. Ces cellules cancéreuses utilisent des réseaux de gènes spécifiques pour maintenir leur prolifération et leur état indifférencié. Une approche possible pour éliminer ces cellules cancéreuses serait de cibler les facteurs de transcription impliqués dans la prolifération ou encore de forcer leur différenciation. Dans ce but, j'ai étudié le rôle de NKX2.2 et NGN2 à partir de 3 cultures primaires multipotentes. Les résultats montrent que l'expression de NKX2.2 dans ces cultures est nécessaire pour la survie, la prolifération et la capacité à former des neurosphères. A l'inverse, la surexpression de NGN2 conduit à une apoptose massive, à un arrêt de la prolifération avec formation de neurones dont certains sont électrophysiologiquement actifs. Une approche différente consisterait à cibler une des protéines impliquées dans la migration pour limiter la composante infiltrante. Des études antérieures ont montrées un rôle clef de DCX dans la migration des jeunes neurones au cours du développement. La forte expression de DCX dans certains Gb m'a conduit à étudier la régulation et le rôle de ce gène. In vitro, les résultats obtenus montrent que DCX est exprimé par une sous population de cellules. La purification des cellules Dcx+ ainsi qu'une étude clonale a permis de montrer qu'elles se comportent comme des progéniteurs multipotents avec une capacité d'autorenouvellement restreinte. Par ailleurs, j'ai montré que les cellules Dcx+ peuvent réverter vers un état Dcx- et que le gène Dcx est régulé par les voies NOTCH et SHH
Glioblastomas (GB) are the most common primary tumors of the CNS and are particularly resistant to radio/chemotherapy. They generally have a solid and infiltrative component. The latter being difficult to remove by surgery will be partly responsible for tumor recurrence. One of the major advances in the field is highlighted in the Gb of subpopulations with features of neural precursors. Cancer cells use specific gene networks to maintain their proliferation and undifferentiated state. One approach to eliminate these cancer cells would be to target transcription factors involved in the proliferation or to force their differentiation. To this end, I studied the role of NKX2.2 and NGN2 from 3 primary multipotent cultures. The results show that NKX2.2 expression in these cultures is necessary for survival, proliferation and ability to form neurospheres. Conversely, overexpression of NGN2 led to massive apoptosis, proliferation arrest with formation of neurons, some of which are electrophysiologically active. A different approach would be to target proteins involved in migration to limit the invasive component. Previous studies have shown a key role of DCX in the migration of young neurons during development. The strong expression of DCX in some Gb led me to study the regulation and the role of this gene. In vitro, the results show that DCX is expressed by a subpopulation of cells. Purification of Dcx+ cells and clonal study has shown that they behave as multipotent progenitors with limited self-renewal capacity. I also found that Dcx+ cells can revert back to a Dcx- state and that DCX is regulated by SHH and NOTCH pathways
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岡原, 京平. "糖脂質ガラクトシルセラミドのオリゴデンドロサイト特異的な発現調節機構に関する研究." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/192153.

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Jarrar, Wassan [Verfasser], and Hans-Henning [Akademischer Betreuer] Arnold. "Genetic analysis of Nkx2.2 and Nkx2.9 transcription factors in mouse brain development: specific functions in the hindbrain / Wassan Jarrar ; Betreuer: Hans-Henning Arnold." Braunschweig : Technische Universität Braunschweig, 2014. http://d-nb.info/1175821233/34.

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Doyle, Michelle Joanne. "Multiple transcriptional activities of NKX2.2 in the embryonic and adult pancreas /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado at Denver and Health Sciences Center, 2006.
Typescript. Includes bibliographical references (leaves 137-151). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;
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Chao, Christina Seng. "The roles of Nkx2.2 in determination of mouse islet cell fates /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Cell & Developmental Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 144-158). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Hill, Katy Victoria. "Regulation of Nkx2.2 gene expression in the vertebrate neural tube : a target of graded Sonic hedgehog signalling." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444785/.

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Sonic hedgehog (Shh) is a morphogen implicated in the developmental patterning of many vertebrate tissues. One such tissue is the neural tube (NT). In ventral regions of the NT distinct neuronal subtypes emerge in precise spatial order from progenitor cells arrayed along its dorsal-ventral axis. Shh regulates this process by controlling the expression patterns of transcription factors in progenitor cells. In addition, cross- repressive interactions between pairs of transcription factors, expressed in adjacent regions, ensures the generation of defined domains. The regulation of Nkx2.2 and Nkx2.9 expression represents an example of this mechanism. The expression of these genes is restricted to a ventral (p3) domain, comprising neural progenitors dorsal to the floor plate. Induction of Nkx2.2 and Nkx2.9 requires high levels of Shh signalling. In part this appears to be because the homeodomain protein Pax6 must be repressed to allow Nkx2.2/2.9 induction. We have analysed the regulatory regions of the Nkx2 genes in order to understand the molecular mechanisms underpinning their expression pattern. The 5' flanking region of Nkx2.2 and Nkx2.9 contains a 250bp block of highly conserved DNA (CNCR) that is found in human, mouse, Fugu and zebrafish. This region includes a binding site for the transcriptional regulators of the Shh pathway: Gli (GBS). Using a BAC homologous recombination system and assays in zebrafish, we provide evidence that the CNCR is required to direct Nkx2.2a-like gene expression. Mouse in vivo reporter assays using fragments containing the CNCR of zNkx2.2a, indicate the CNCR is sufficient to direct reporter gene expression in the p3 domain of the NT. Mutational analysis indicates that the GBS is necessary but not sufficient to account for this expression profile. In vivo assays further suggest correct Nkx2.2 expression requires input from additional transcriptional activators as well as a floor plate repressor. All these factors appear to act through regulatory elements within the CNCR.
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Wankerl, Ludwig Verfasser], and Gunter [Akademischer Betreuer] [Meister. "Characterization of CAMTA1 and Nkx2.2 in the context of glioblastoma cancer stem cell biology / Ludwig Wankerl. Betreuer: Gunter Meister." Regensburg : Universitätsbibliothek Regensburg, 2016. http://d-nb.info/1083251341/34.

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Kordowich, Simon Verfasser], Ernst A. [Akademischer Betreuer] Wimmer, Ahmed [Akademischer Betreuer] Mansouri, Detlef [Akademischer Betreuer] [Doenecke, and Annette [Akademischer Betreuer] Borchers. "Funktionelle Charakterisierung der Transkriptionsfaktoren Nkx2.2 und Arx in der Entwicklung der endokrinen Zellen im murinen Pankreas / Simon Kordowich. Gutachter: Ahmed Mansouri ; Detlef Doenecke ; Annette Borchers. Betreuer: Ernst A. Wimmer." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1042641218/34.

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Book chapters on the topic "Nkx2.2"

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Akazawa, Hiroshi, and Issei Komuro. "Cardiac Homeobox Protein Csx/Nkx2.5 and its Associated Proteins." In Cardiovascular Development and Congenital Malformations, 31–36. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch8.

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Jay, Patrick Y., Charles I. Berul, Makoto Tanaka, Masao Ishii, Yoshihisa Kurachi, and Seigo Izumo. "Cardiac Conduction and Arrhythmia: Insights from Nkx2.5 Mutations in Mouse and Humans." In Novartis Foundation Symposia, 227–41. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868066.ch14.

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Ponticos, Markella. "The Role of the Homeodomain Transcription Factor Nkx2-5 in the Cardiovascular System." In Advances in Vascular Medicine, 113–30. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-637-3_7.

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Schwartz, Robert J., Jorge Sepulveda, and Narasimhaswamy S. Belaguli. "Molecular Regulation of Cardiac Myofibrillogenesis: Roles of Serum Response Factor, Nkx2-5, and GATA-4." In Myofibrillogenesis, 103–27. Boston, MA: Birkhäuser Boston, 2002. http://dx.doi.org/10.1007/978-1-4612-0199-1_7.

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Scott, Ian C. "Life Before Nkx2.5." In Current Topics in Developmental Biology, 1–31. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-387786-4.00001-4.

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Mak, Tak W., Josef Penninger, John Roder, Janet Rossant, and Mary Saunders. "Nkx2–5." In The Gene Knockout FactsBook, 802–3. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012466044-1/50442-7.

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Gazit, Avihu Z., Susan N. Foerster, and Patrick Y. Jay. "NKX2-5 and Congenital Heart Disease." In Epstein's Inborn Errors of Development, 733–39. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199934522.003.0102.

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Memon, Bushra, and Essam M. Abdelalim. "Highly Efficient Differentiation of Human Pluripotent Stem Cells into Pancreatic Progenitors Co-expressing PDX1 and NKX6.1." In Methods in Molecular Biology. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/7651_2020_323.

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Conference papers on the topic "Nkx2.2"

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Mucenski, Michael, Michael Bruno, Susan Wert, Joseph Locker, and Jeffrey Whitsett. "NKX2.8 Participates In A Regulatory Network In Submucosal Glands And Tracheal Epithelium." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5495.

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DeMaio, L., A. Banfalvi, P. Flodby, P. Minoo, ED Crandall, and Z. Borok. "Nkx2.1-Cre Reporter Mice Demonstrate Alveolar Epithelial-Mesenchymal Transition (EMT)In VivoandIn Vitro." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5291.

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Louw, Alison, Marc A. Thomas, Jennet Harvey, and Jacqueline M. Bentel. "Abstract 4075: Regulation of NKX3.1 by RMND5 proteins." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4075.

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Logan, Monica, Philip Anderson, and Sarki Abdulkadir. "Abstract 2734: Genome-wide analysis of direct Nkx3.1 target genes." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2734.

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Li, Hsin-Jung, Yu-Lueng Shih, Ming-De Yan, Pei-Ning Yu, and Ya-Wen Lin. "Abstract 575: NKX6.1 functions as a tumor suppressor in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-575.

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Li, Hsin-Jung, Pei-Ning Yu, Yu-Lueng Shih, and Ya-Wen Lin. "Abstract 4108: NKX6.1 suppresses cancer invasion and epithelial-mesenchymal transition in cervical cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4108.

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McKissic, Sydika, Meejeon Roh, and Sarki Abdulkadir. "Abstract 2401: Loss of Nkx3.1 cooperates with Myc overexpression to promote prostate tumorigenesis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2401.

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Lin, Ya-Wen, Sou-Yi Chang, Chih-Chi Kuo, Cheng-Wen Hsiao, Chih-Hsiung Hsu, Yu-Ching Chou, and Yu-Lueng Shih. "Abstract 2575: NKX6.1 hypermethylation predicts the outcome of stage II colorectal cancer patients undergoing chemotherapy." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2575.

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Anderson, Philip D., Sydika A. McKissic, Monica Logan, Meejeon Roh, Omar Franco, Jie Wang, Irina Doubinskaia, et al. "Abstract 2983: Nkx3.1 and c-Myc co-regulate shared target genes involved in prostate cancer." 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.am2012-2983.

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Decker, Josua, Garima Jain, Philip Harazim, Tina Kießling, Peter Möller, and Ralf Marienfeld. "Abstract 1667: Prostatitis related mitogenic stimuli cause loss of NKX3.1: Increased risk for prostate cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1667.

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Reports on the topic "Nkx2.2"

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Gelmann, Edward P. NKX3.1 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada415376.

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Gelmann, Edward P. NKX3.1 In Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada376365.

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Ouyang, Xuesong. Isolation of Target Genes for NKX3.1 in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada426046.

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Ouyang, Xuesong. Isolating of Target Genes for NKX3.1 in Prostate Carcinogenesis. Fort Belvoir, VA: Defense Technical Information Center, March 2005. http://dx.doi.org/10.21236/ada437384.

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Gelmann, Edward P. NKX3.1 Genotype and IGF-1 Interact in Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada488982.

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Gelmann, Edward P. NKX3.1 Genotype and IGF-1 Interact in Prostate Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada535355.

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Milbrandt, Jeffrey D. Role of Nkx3.1 Homeodomain Protein in Prostate Carcinogenesis and Differentiation. Fort Belvoir, VA: Defense Technical Information Center, February 2000. http://dx.doi.org/10.21236/ada391011.

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Muhlbradt, Erin E. Inflammatory Cytokines Induce Ubiquitination and Loss of the Prostate Suppressor Protein NKX3.1. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada518629.

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Jiao, Jing. Molecular Mechanism of Nkx3.1 Deregulation and Its Function in Murine Pten Prostate Cancer Model. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada446368.

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Jiao, Jing. Molecular Mechanism of Nkx3.1 Deregulation and its Function in Murine Pten Prostate Cancer Model. Fort Belvoir, VA: Defense Technical Information Center, September 2006. http://dx.doi.org/10.21236/ada483121.

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