Relevant bibliographies by topics / Pax3 and Pax7

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Academic literature on the topic 'Pax3 and Pax7'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Pax3 and Pax7"

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Matsunaga, Eiji, Isato Araki, and Harukazu Nakamura. "Role of Pax3/7 in the tectum regionalization." Development 128, no. 20 (October 15, 2001): 4069–77. http://dx.doi.org/10.1242/dev.128.20.4069.

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Pax3/7 is expressed in the alar plate of the mesencephalon. The optic tectum differentiates from the alar plate of the mesencephalon, and expression of Pax3/7 is well correlated to the tectum development. To explore the function of Pax3 and Pax7 in the tectum development, we misexpressed Pax3 and Pax7 in the diencephalon and ventral mesencephalon. Morphological and molecular marker gene analysis indicated that Pax3 and Pax7 misexpression caused fate change of the alar plate of the presumptive diencephalon to that of the mesencephalon, that is, a tectum and a torus semicircularis were formed ectopically. Ectopic tectum in the diencephalon appeared to be generated through sequential induction of Fgf8, En2 and Pax3/7. In ventral mesencephalon, which expresses En but does not differentiate to the tectum in normal development, Pax3 and Pax7 misexpression induced ectopic tectum. In normal development, Pax3 and Pax7 expression in the mesencephalon commences after Otx2, En and Pax2/5 expression. In addition, expression domain of Pax3 and Pax7 is well consistent with presumptive tectum region in a dorsoventral axis. Taken together with normal expression pattern of Pax3 and Pax7, results of misexpression experiments suggest that Pax3 and Pax7 define the tectum region subsequent to the function of Otx2 and En.
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Zhou, Hong-Ming, and Simon J. Conway. "Pax3 Hypomorphs Reveal Hidden Pax7 Functional Genetic Compensation in Utero." Journal of Developmental Biology 10, no. 2 (May 17, 2022): 19. http://dx.doi.org/10.3390/jdb10020019.

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Pax3 and Pax7 transcription factors are paralogs within the Pax gene family that that are expressed in early embryos in partially overlapping expression domains and have distinct functions. Significantly, mammalian development is largely unaffected by Pax7 systemic deletion but systemic Pax3 deletion results in defects in neural tube closure, neural crest emigration, cardiac outflow tract septation, muscle hypoplasia and in utero lethality by E14. However, we previously demonstrated that Pax3 hypomorphs expressing only 20% functional Pax3 protein levels exhibit normal neural tube and heart development, but myogenesis is selectively impaired. To determine why only some Pax3-expressing cell lineages are affected and to further titrate Pax3 threshold levels required for neural tube and heart development, we generated hypomorphs containing both a hypomorphic and a null Pax3 allele. This resulted in mutants only expressing 10% functional Pax3 protein with exacerbated neural tube, neural crest and muscle defects, but still a normal heart. To examine why the cardiac neural crest appears resistant to very low Pax3 levels, we examined its paralog Pax7. Significantly, Pax7 expression is both ectopically expressed in Pax3-expressing dorsal neural tube cells and is also upregulated in the Pax3-expressing lineages. To test whether this compensatory Pax7 expression is functional, we deleted Pax7 both systemically and lineage-specifically in hypomorphs expressing only 10% Pax3. Removal of one Pax7 allele resulted in partial outflow tract defects, and complete loss of Pax7 resulted in full penetrance outflow tract defects and in utero lethality. Moreover, combinatorial loss of Pax3 and Pax7 resulted in severe craniofacial defects and a total block of neural crest cell emigration from the neural tube. Pax7Cre lineage mapping revealed ectopic labeling of Pax3-derived neural crest tissues and within the outflow tract of the heart, experimentally confirming the observation of ectopic activation of Pax7 in 10% Pax3 hypomorphs. Finally, genetic cell ablation of Pax7Cre-marked cells is sufficient to cause outflow tract defects in hypomorphs expressing only 10% Pax3, confirming that ectopic and induced Pax7 can play an overlapping functional genetic compensational role in both cardiac neural crest lineage and during craniofacial development, which is normally masked by the dominant role of Pax3.
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Kumar, Deepak, Jennifer L. Shadrach, Amy J. Wagers, and Andrew B. Lassar. "Id3 Is a Direct Transcriptional Target of Pax7 in Quiescent Satellite Cells." Molecular Biology of the Cell 20, no. 14 (July 15, 2009): 3170–77. http://dx.doi.org/10.1091/mbc.e08-12-1185.

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Pax7 is a key regulator of skeletal muscle stem cells and is required along with Pax3 to generate skeletal muscle precursors. We have identified a collection of genes induced by either Pax3 or Pax7 in C2C12 muscle cells. Two notable Pax3/7 targets are the inhibitory helix-loop-helix (HLH) proteins inhibitor of DNA binding (Id) 2 and Id3, both of which are coordinately expressed with Pax7 in quiescent satellite cells and are induced in quiescent C2C12 myogenic cells after ectopic expression of either Pax3 or Pax7. Ectopic Pax7 activates expression of a luciferase reporter driven by the Id3 promoter, and maximal induction of this reporter requires a conserved Pax7 binding site located upstream of the Id3 gene. Chromatin immunoprecipitation indicated that Pax7 is bound upstream of the Id3 promoter in quiescent satellite cells. In addition, short hairpin RNA-mediated knockdown of Pax7 expression in cultured satellite cells coordinately decreased both Id2 and Id3 expression. Together, these findings indicate that Id3 is a direct transcriptional target for Pax7 in quiescent satellite cells, and they suggest that Pax7 acts to block premature differentiation of quiescent satellite cells by inducing the expression of Id2 and Id3, which in turn may act to block either the precocious induction of myogenic basic (b)HLH proteins, the activity of myogenic bHLH proteins, or both.
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Kelly, K. M., R. B. Womer, P. H. Sorensen, Q. B. Xiong, and F. G. Barr. "Common and variant gene fusions predict distinct clinical phenotypes in rhabdomyosarcoma." Journal of Clinical Oncology 15, no. 5 (May 1997): 1831–36. http://dx.doi.org/10.1200/jco.1997.15.5.1831.

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PURPOSE We evaluated the clinical features of the common PAX3-FKHR and variant PAX7-FKHR gene fusions observed in rhabdomyosarcoma. PATIENTS AND METHODS Reverse-transcriptase polymerase chain reaction (RT-PCR) assays were used to detect the gene fusions in 34 cases of rhabdomyosarcoma. Clinical data were obtained retrospectively and compared with the molecular results. RESULTS The PAX3-FKHR and PAX7-FKHR gene fusions were present in tumors from 18 and 16 patients, respectively. The group with a PAX7-FKHR fusion was younger (P = .01) and presented more often with an extremity lesion (82% v 22%; P = .001). PAX7-FKHR tumors were more often localized than PAX3-FKHR tumors (P = .03). In patients with metastatic disease at diagnosis, the patterns were different: PAX7-FKHR patients had metastatic disease that involved only bone (n = 2) and distant nodes (n = 2), while the PAX3-FKHR group had multiple sites involved, including bone (n = 7), marrow (n = 7), lungs (n = 3), distant nodes (n = 2), skin (n = 1), and brain (n = 1). No significant difference in relapse rate was observed. A trend toward improved overall survival in the PAX7-FKHR group was noted (P = .09). Event-free survival for this PAX7-FKHR group was significantly longer (P = .04). CONCLUSION Our results suggest that the common PAX3-FKHR and the variant PAX7-FKHR fusions are associated with distinct clinical phenotypes. Identification of fusion gene status may be a useful diagnostic tool in rhabdomyosarcoma.
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Kirkpatrick, Lisa J., Zipora Yablonka-Reuveni, and Benjamin W. C. Rosser. "Retention of Pax3 Expression in Satellite Cells of Muscle Spindles." Journal of Histochemistry & Cytochemistry 58, no. 4 (December 21, 2009): 317–27. http://dx.doi.org/10.1369/jhc.2009.954792.

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Intrafusal fibers within muscle spindles retain features characteristic of immaturity, unlike the larger and more numerous extrafusal fibers constituting the bulk of skeletal muscle. Satellite cells (SCs), myogenic progenitors, are detected on the surfaces of both intrafusal and extrafusal fibers, but little is known of spindle SCs. We have recently demonstrated that, like their extrafusal counterparts, SCs in muscle spindles of posthatch chickens express paired box transcription factor 7 (Pax7) protein. During vertebrate embryogenesis, myogenic progenitors express both Pax7 and Pax3 proteins. In postnatal mice, Pax3 appears in rare SC subsets, whereas Pax7 is expressed by all SCs within extrafusal fibers. Here we test the hypothesis that Pax3 protein maintains localized expression within SCs of muscle spindles. Immunohistochemical techniques were used to identify SCs by their Pax7 expression within anterior latissimus dorsi muscle excised from posthatch chickens of various ages. A greater percentage of SCs express Pax3 within intrafusal than extrafusal fibers at each age, and the proportion of SCs expressing Pax3 declines with aging. This is the first study to localize Pax3 expression in posthatch avian muscle and within SCs of muscle spindles. We suggest that Pax3-positive SCs are involved in fiber maintenance.
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Relaix, Frédéric, Didier Montarras, Stéphane Zaffran, Barbara Gayraud-Morel, Didier Rocancourt, Shahragim Tajbakhsh, Ahmed Mansouri, Ana Cumano, and Margaret Buckingham. "Pax3 and Pax7 have distinct and overlapping functions in adult muscle progenitor cells." Journal of Cell Biology 172, no. 1 (December 27, 2005): 91–102. http://dx.doi.org/10.1083/jcb.200508044.

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The growth and repair of skeletal muscle after birth depends on satellite cells that are characterized by the expression of Pax7. We show that Pax3, the paralogue of Pax7, is also present in both quiescent and activated satellite cells in many skeletal muscles. Dominant-negative forms of both Pax3 and -7 repress MyoD, but do not interfere with the expression of the other myogenic determination factor, Myf5, which, together with Pax3/7, regulates the myogenic differentiation of these cells. In Pax7 mutants, satellite cells are progressively lost in both Pax3-expressing and -nonexpressing muscles. We show that this is caused by satellite cell death, with effects on the cell cycle. Manipulation of the dominant-negative forms of these factors in satellite cell cultures demonstrates that Pax3 cannot replace the antiapoptotic function of Pax7. These findings underline the importance of cell survival in controlling the stem cell populations of adult tissues and demonstrate a role for upstream factors in this context.
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Sorensen, Poul H. B., James C. Lynch, Stephen J. Qualman, Roberto Tirabosco, Jerian F. Lim, Harold M. Maurer, Julia A. Bridge, William M. Crist, Timothy J. Triche, and Frederic G. Barr. "PAX3-FKHR and PAX7-FKHR Gene Fusions Are Prognostic Indicators in Alveolar Rhabdomyosarcoma: A Report From the Children’s Oncology Group." Journal of Clinical Oncology 20, no. 11 (June 1, 2002): 2672–79. http://dx.doi.org/10.1200/jco.2002.03.137.

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PURPOSE: Alveolar rhabdomyosarcoma (ARMS) is an aggressive soft tissue malignancy of children and adolescents. Most ARMS patients express PAX3-FKHR or PAX7-FKHR gene fusions resulting from t(2;13) or t(1;13) translocations, respectively. We wished to confirm the diagnostic specificity of gene fusion detection in a large cohort of RMS patients and to evaluate whether these alterations influence clinical outcome in ARMS. PATIENTS AND METHODS: We determined PAX3-FKHR or PAX7-FKHR fusion status in 171 childhood rhabdomyosarcoma (RMS) patients entered onto the Intergroup Rhabdomyosarcoma Study IV, including 78 ARMS patients, using established reverse transcriptase polymerase chain reaction assays. All patients received central pathologic review and were treated using uniform protocols, allowing for meaningful outcome analysis. We examined the relationship between gene fusion status and clinical outcome in the ARMS cohort. RESULTS: PAX3-FKHR and PAX7-FKHR fusion transcripts were detected in 55% and 22% of ARMS patients, respectively; 23% were fusion-negative. All other RMS patients lacked transcripts, confirming the specificity of these alterations for ARMS. Fusion status was not associated with outcome differences in patients with locoregional ARMS. However, in patients presenting with metastatic disease, there was a striking difference in outcome between PAX7-FKHR and PAX3-FKHR patient groups (estimated 4-year overall survival rate of 75% for PAX7-FKHR v 8% for PAX3-FKHR; P = .0015). Multivariate analysis demonstrated a significantly increased risk of failure (P = .025) and death (P = .019) in patients with metastatic disease if their tumors expressed PAX3-FKHR. Among metastatic ARMS, bone marrow involvement was significantly higher in PAX3-FKHR–positive patients. CONCLUSION: Not only are PAX-FKHR fusion transcripts specific for ARMS, but expression of PAX3-FKHR and PAX7-FKHR identifies a very high-risk subgroup and a favorable outcome subgroup, respectively, among patients presenting with metastatic ARMS.
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Kuang, Shihuan, Sophie B. Chargé, Patrick Seale, Michael Huh, and Michael A. Rudnicki. "Distinct roles for Pax7 and Pax3 in adult regenerative myogenesis." Journal of Cell Biology 172, no. 1 (January 2, 2006): 103–13. http://dx.doi.org/10.1083/jcb.200508001.

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We assessed viable Pax7−/− mice in 129Sv/J background and observed reduced growth and marked muscle wasting together with a complete absence of functional satellite cells. Acute injury resulted in an extreme deficit in muscle regeneration. However, a small number of regenerated myofibers were detected, suggesting the presence of residual myogenic cells in Pax7-deficient muscle. Rare Pax3+/MyoD+ myoblasts were recovered from Pax7−/− muscle homogenates and cultures of myofiber bundles but not from single myofibers free of interstitial tissues. Finally, we identified Pax3+ cells in the muscle interstitial environment and demonstrated that they coexpressed MyoD during regeneration. Sublaminar satellite cells in hind limb muscle did not express detectable levels of Pax3 protein or messenger RNA. Therefore, we conclude that interstitial Pax3+ cells represent a novel myogenic population that is distinct from the sublaminar satellite cell lineage and that Pax7 is essential for the formation of functional myogenic progenitors from sublaminar satellite cells.
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Hangul, Ceren, Esin Guvenir Celik, Hacer Kaya, Onur Eroglu, Hilmi Uysal, and Sibel Berker Karauzum. "Estradiol differentially regulates DUX4, β-catenin and PAX3/PAX7 in primary myoblasts of facioscapulohumeral muscular dystrophy patients." Turkish Journal of Biochemistry 46, no. 4 (January 5, 2021): 435–44. http://dx.doi.org/10.1515/tjb-2020-0351.

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Abstract Objectives There is a clinical variability and heterogeneity among Facioscapulohumeral Muscular Dystrophy (FSHD) patients. Escalation after menopause in women, early onset in men suggests that estrogen might be a protective factor on the course of FSHD. In spite of few molecular studies supporting the protective role of estrogen in FSHD in vitro, there is no study revealing the effect of estradiol on the protein levels of DUX4, β-catenin and PAX3/PAX7. In present study, we investigated the effect of estradiol treatment on the expressions of DUX4, β-catenin and PAX3/PAX7 protein levels. Materials and Methods Primary myoblasts of 63 and 71 years old (63yM/71yM) males; 47 years old (47yF) female FSHD patients were used. Cells were processed under these conditions; (i) untreated, (ii) 10 nM-30 min estradiol and (iii) 10 nM-4 h estradiol treated. The expression of DUX4, PAX3/PAX7 and β-catenin were examined by western-blotting. Results Expression of DUX4 significantly downregulated after 4 h treatment of estradiol while PAX3/PAX7 56 kDa variant expression upregulated in 71yM cells. β-catenin and PAX3 expression was variable among the samples. Conclusion Our results suggest that estrogen might be a palliative treatment option via downregulation of DUX4 protein in DUX4 expressing FSHD patients.
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Kelly, Kara M., Richard B. Womer, and Frederic G. Barr. "PAX3-FKHR and PAX7-FKHR." Journal of Pediatric Hematology/Oncology 20, no. 5 (September 1998): 517. http://dx.doi.org/10.1097/00043426-199809000-00027.

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Dissertations / Theses on the topic "Pax3 and Pax7"

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Hammond, Christina Lindsey. "Pax3 and Pax7 in the zebrafish somite." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427989.

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Zalc, Antoine. "Study of Pax3 and Pax7 functions during the development of the mouse embryo." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066220.

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Mon travail de thèse a porté sur l'étude des mécanismes contrôlant la progression du cycle cellulaire et le devenir des cellules progénitrices dans différents tissus. Sortie du cycle cellulaire et différenciation cellulaire pendant la formation du muscle du membre Nous avons montré que la sortie du cycle cellulaire, régulée par les inhibiteurs de kinases cycline-dépendantes (CDKI) et la différentiation musculaire contrôlée par les facteurs myogéniques (MRF), peuvent être découplées génétiquement pendant la formation du muscle. Nous avons identifié une séquence régulant l'expression de CDKI, spécifique au muscle, activée par les MRF dans les myoblastes et réprimée par la voie Notch dans les progéniteurs, permettant de contrôler la balance entre amplification des progéniteurs et établissement du muscle squelettique. Contrôle de la croissance des dérivés de crête neurale craniale Bien que Pax3 et Pax7 soient essentiels pour la formation de la crête neurale, leurs rôles durant le développement craniofacial restent inconnus. À l'aide de mutants murins pour Pax3/7 présentant des fentes faciales, nous avons montré que ces défauts sont liés à la surexpression de la voie de signalisation régulée par le récepteur Aryl hydrocarbon (AhR, récepteur à la dioxine). L'augmentation de l'activité d'AhR pousse les cellules mésenchymateuses faciales hors du cycle cellulaire alors que son inhibition restaure la prolifération de ces cellules, permettant la fermeture de la face des mutants Pax3/7 et démontrant qu'une interaction entre une voie de signalisation impliquée dans la réponse au stress environnemental et les gènes régulés par Pax3/7 est nécessaire pendant le développement craniofacia
This thesis aims to decipher how Pax3 and Pax7 transcription factors control cell cycle progression of progenitor cells in different tissues.Cell cycle regulation of Pax3+ myogenic progenitors during limb muscle developmentWe showed that cell cycle exit, mediated by the cyclin-dependent kinases inhibitors (CDKI), and muscle differentiation, controlled by the myogenic regulatory factors (MRF), can be genetically uncoupled during development. We dissected a functional interplay between Notch signalling and both MRF and CDKI activities, for maintaining the cycling status of the progenitor cells. Further, we identified a CDKI, muscle-specific DNA regulatory element, activated by the MRF in myoblasts but repressed by Notch signalling in progenitor cells, controlling the equilibrium between amplification of the progenitor pool and the establishment of functional muscle.Control of Pax3+ neural crest derivatives growth, and maintenance during craniofacial developmentAlthough studies showed Pax3 and Pax7 to be essential during early neural crest development, their role during craniofacial formation is unknown. Using Pax3/7 mutant mice displaying facial clefts, we uncovered that these defects are associated with an up-regulation of the Aryl hydrocarbon Receptor (AhR, the receptor to dioxin) signalling pathway. In Pax3/7 mutants, increased AhR activity drives facial mesenchymal cells out of the cell cycle, while inhibiting AhR rescues the cycling status of these cells and the facial closure of Pax3/7 mutants. Our results identify a molecular link between an environmental stress response pathway and a Pax3/7 downstream gene regulatory network during normal craniofacial development
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Wang, Wei Zhi. "The study of PAX3 and PAX7 genes and their potential roles in neuroblastoma." Thesis, Manchester Metropolitan University, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263958.

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Zalc, Antoine. "Study of Pax3 and Pax7 functions during the development of the mouse embryo." Electronic Thesis or Diss., Paris 6, 2014. http://www.theses.fr/2014PA066220.

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Mon travail de thèse a porté sur l'étude des mécanismes contrôlant la progression du cycle cellulaire et le devenir des cellules progénitrices dans différents tissus. Sortie du cycle cellulaire et différenciation cellulaire pendant la formation du muscle du membre Nous avons montré que la sortie du cycle cellulaire, régulée par les inhibiteurs de kinases cycline-dépendantes (CDKI) et la différentiation musculaire contrôlée par les facteurs myogéniques (MRF), peuvent être découplées génétiquement pendant la formation du muscle. Nous avons identifié une séquence régulant l'expression de CDKI, spécifique au muscle, activée par les MRF dans les myoblastes et réprimée par la voie Notch dans les progéniteurs, permettant de contrôler la balance entre amplification des progéniteurs et établissement du muscle squelettique. Contrôle de la croissance des dérivés de crête neurale craniale Bien que Pax3 et Pax7 soient essentiels pour la formation de la crête neurale, leurs rôles durant le développement craniofacial restent inconnus. À l'aide de mutants murins pour Pax3/7 présentant des fentes faciales, nous avons montré que ces défauts sont liés à la surexpression de la voie de signalisation régulée par le récepteur Aryl hydrocarbon (AhR, récepteur à la dioxine). L'augmentation de l'activité d'AhR pousse les cellules mésenchymateuses faciales hors du cycle cellulaire alors que son inhibition restaure la prolifération de ces cellules, permettant la fermeture de la face des mutants Pax3/7 et démontrant qu'une interaction entre une voie de signalisation impliquée dans la réponse au stress environnemental et les gènes régulés par Pax3/7 est nécessaire pendant le développement craniofacia
This thesis aims to decipher how Pax3 and Pax7 transcription factors control cell cycle progression of progenitor cells in different tissues.Cell cycle regulation of Pax3+ myogenic progenitors during limb muscle developmentWe showed that cell cycle exit, mediated by the cyclin-dependent kinases inhibitors (CDKI), and muscle differentiation, controlled by the myogenic regulatory factors (MRF), can be genetically uncoupled during development. We dissected a functional interplay between Notch signalling and both MRF and CDKI activities, for maintaining the cycling status of the progenitor cells. Further, we identified a CDKI, muscle-specific DNA regulatory element, activated by the MRF in myoblasts but repressed by Notch signalling in progenitor cells, controlling the equilibrium between amplification of the progenitor pool and the establishment of functional muscle.Control of Pax3+ neural crest derivatives growth, and maintenance during craniofacial developmentAlthough studies showed Pax3 and Pax7 to be essential during early neural crest development, their role during craniofacial formation is unknown. Using Pax3/7 mutant mice displaying facial clefts, we uncovered that these defects are associated with an up-regulation of the Aryl hydrocarbon Receptor (AhR, the receptor to dioxin) signalling pathway. In Pax3/7 mutants, increased AhR activity drives facial mesenchymal cells out of the cell cycle, while inhibiting AhR rescues the cycling status of these cells and the facial closure of Pax3/7 mutants. Our results identify a molecular link between an environmental stress response pathway and a Pax3/7 downstream gene regulatory network during normal craniofacial development
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Charytonowicz, Elizabeth. "The role of PAX3/PAX7-FKHR in mesenchymal stem cell myogenic differentiation and rhabdomyosarcomagenesis." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2011. https://ro.ecu.edu.au/theses/381.

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Rhabdomyosarcomas are soft tissue sarcomas (STS) that, while extremely rare in adults, are one of the most common neoplasms in children and adolescents. Rhabdomyosarcomas are presumed to be associated with the skeletal muscle lineage, although surprisingly, those tumors can be present in organs histologically lacking skeletal muscle, like prostate, urinary bladder or gallbladder. Pathologically, rhabdomyosarcomas are very heterogeneous tumors and can be divided into three major groups: alveolar rhabdomyosarcomas (ARMS), embryonal rhabdomyosarcomas (ERMS), which includes the botryoid subtype, and pleomorphic rhabdomyosarcomas. Besides clinicopathological differences, these tumors also differ at the molecular level. As in many other sarcoma types, ARMS are characterized by specific chromosomal translocations and almost 75% of cases show t(2;13) or t(1;13) translocations, involving PAX3-FKHR and PAX7-FKHR fusion genes respectively. These genetic events result in a molecular gain of function of the fusion protein, which is proposed to perturb the differentiation of muscle progenitor cells. Since PAX3/7-FKHR fusions result in rearrangements of PAX3/7 and FKHR genes, such that the PAX C-terminal domain is replaced by the potent FKHR transactivation domain, we sought to investigate the implications of this translocation on function and expression of wild type PAX3 and PAX7 Cterminal isoforms. This research identified functional differences between Pax3 and Pax7 Cterminal isoforms during myogenesis, and suggests that both Pax3 and Pax7 transcripts are required for commitment of cells to the myogenic lineage. More specifically, the Pax3c isoform may be required for terminal myogenic differentiation whereas the Pax3d isoform may be involved in undifferentiated cell maintenance and/or proliferation. Therefore, different levels of individual C-terminal isoforms of Pax3 and Pax7 in normal cells v may shift the balance between the undifferentiated and differentiated phenotype during muscle cell differentiation. In ARMS, this „balance‟ appears to be further disrupted and may lead to a block in terminal differentiation.
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Zalc, Antoine [Verfasser]. "Study of Pax3 and Pax7 functions during the development of the mouse embryo / Antoine Zalc." Berlin : Freie Universität Berlin, 2019. http://d-nb.info/1181097932/34.

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Mimault, Benoît. "Modifications géniques des cellules du tube neural : implication dans le développement myogénique des somites." Nantes, 2010. http://www.theses.fr/2010NANT2074.

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Dans l’embryogenèse la myogenèse se déroule dans les somites suite à l’activation des FRM et dépend pour un déroulement correct de toutes les structures qui ceinturent le somite. Hormis les FRM les facteurs de transcription Pax3 et Pax7 qui appartiennent à la même sous famille et sont exprimés dans le TN et les somites, sont impliqués dans la myogenèse. Leur influence sur les somites depuis le compartiment neural est peu documentée. Nous montrons que la suractivation neurale de Pax3 conduit à l’inactivation de l’expression des gènes de détermination moléculaire MyoD et Myf5 ainsi que du gène Wnt11 dans les somites. Celle de Pax7 induit uniquement la dérégulation de Wnt11 à laquelle s’ajoute celle de Sim1. La sous expression neurale de Pax3 n’a aucun effet concluant sur les somites, en revanche dans le cas d’inhibition neurale totale, Myf5 n’est plus activé dans le somite. La sous expression neurale de Pax7 n’a pas cet effet par contre là encore Sim1 et Wnt11 sont dérégulés. Il semblerait que les effets de Pax3 neural s’opèrent sur le somite épaxial (via Myf5, MyoD, Wnt11) ceux de Pax7 se situent à la fois dans le somite épaxial et hypaxial (via Wnt11 et Sim1). Nos résultats doivent faire admettre que Pax3 et Pax7 interfèrent depuis le TN sur la myogenèse somitique. Par ailleurs, nous induisons dans les cellules neurales l’expression ectopique de gènes impliqués dans la myogenèse épaxiale (MyoD, Wnt11) et hypaxiale (Sim1). A partir de l’ensemble de nos résultats nous proposons un nouveau schéma récapitulant les interactions moléculaires TN/somites
In embryogenesis the skeletal myogenesis takes place in somites after the myogenic regulatory factor (MRF) activation. This process depends on environmental cues. Out of MRF, the transcription factors Pax3 and Pax7 which belong to the same factor family are also involved in myogenesis. They are both expressed in somites and neural tube. Their somitic influence from the neural tube is poorly documented. We demonstrate that the neural Pax3 upregulation leads to inactivation of the MRF MyoD and Myf5, and of the Wnt11 gene in the somites. The neural Pax7 upregulation only leads to Wnt11 and Sim1 misregulation. The neural downregulation of Pax3 has no effects about somites. When Pax3 is totally absent in neural tube through Pax3 deletion, Myf5 is no more activated in somites. The neural downregulation of Pax7 leads to the misregulation of Sim1 and Wnt11. It seems that the neural Pax3 acts on epaxial somite (via Myf5, MyoD, and Wnt11) and Pax7 on epaxial and hypaxial somite(via Wnt11 and Sim1). Our results must do accept that Pax3 and Pax7 influence somitic myogenesis from the neural tube. Otherwise we can induce in neural cells the ectopic expression of myogenic genes (MyoD, Wnt11, and Sim1). Consequently we propose a new scheme about the neural tube/somite interactions
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Maderer, Carmen [Verfasser], and Markus [Gutachter] Metzler. "Etablierung einer routinetauglichen PCR-Methode zur Charakterisierung genomischer PAX3/FKHR bzw. PAX7/FKHR Bruchpunkte bei Patienten mit alveolärem Rhabdomyosarkom / Carmen Maderer ; Gutachter: Markus Metzler." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2017. http://d-nb.info/1148105158/34.

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Torban, Elena. "Functions of PAX2 and PAX8 genes during kidney development." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36844.

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The 9 PAX genes constitute a family of developmental transcriptional regulators characterized by a highly conserved "paired-box" domain. Mutations in 6 of the 9 PAX genes result in autosomal dominant congenital malformations in mice and in humans. PAX2 transcripts are detected in the CNS, throughout the genitourinary tract, eye and ear. In humans, mutations of PAX2 cause Renal-Coloboma Syndrome (RCS), a constellation of renal anomalies, eye defects and, less frequently, hearing loss and mild CNS manifestations. Homozygous PAX2 mutations in mice cause complete renal agenesis and perinatal death. PAX8 transcripts are found in the CNS, kidney and thyroid glands. PAX8 mutations cause congenital thyroid hypoplasia. No renal defects have been detected either in human or murine PAX8 mutants.
In spite of considerable information about PAX2 and PAX8 genes, their precise functions in development are poorly understood. This project was aimed at elucidating the functions of PAX2 and PAX8 in nephrogenesis and is subdivided into two parts: mutational screening of the PAX8 gene (Chapter 4) and delineation of the role of PAX2 in developing kidney (Chapters 5--7). The latter evolved into the major portion of this work.
Familial juvenile nephronophthisis (NPH1) is a rare disease characterized by multiple small cysts at the cortico-medullary junction and end-stage renal failure in pediatric populations. Because of its proximity to the disease locus, we considered PAX8 a candidate gene for NPH1. During analysis of PAX8 exons from patients, we identified a rare non-conservative polymorphic amino acid change, but found no causative mutations. Subsequently, other groups isolated the novel NPH1 gene. Following reports that PAX8 knockout mice have no obvious renal anomaly, we considered the possibility that PAX8 mutations might, nevertheless, affect proximal tubule function. In patients with thyroid hypoplasia and proven PAX8 mutations we found no aminoaciduria, indicating that haploinsufficiency for PAX8 does not alter tubular transport function.
In order to define PAX2 function in the two primordial cell lineages of developing kidney (induced metanephric mesenchyme and ureteric epithelium), we used both a cell culture approach and an in vivo PAX2 mutant mouse model (1Neu). We demonstrated that PAX2 plays a dual role. In mesenchymally-derived HEK293 cells expressing regulatable exogenous PAX2, we showed that PAX2 is responsible for expression of genes involved in differentiation of mesenchyme. Contrary to one published hypothesis, we found that PAX2 does not affect cell division. In ureteric epithelium, however, PAX2 plays a different role, serving as a survival factor, critical for sustaining the ureteric bud stem cell population. Attenuation of PAX2 dosage (1Neu mouse mutants or collecting duct cells transfected with an antisense PAX2 vector) results in increased apoptosis. We demonstrate that the primary renal defect in RCS is reduced nephron number associated with excessive apoptosis and simplified branching of the ureteric bud. We hypothesize that arborization of the uretric bud requires accumulation of sufficient stem cell mass to allow the next round of branching---possibly by lifting the branch point beyond a putative local inhibitory field.
In summary, we establish that inactivation of PAX8 gene expression does not disturb normal kidney development and function. Conversely, PAX2 plays a crucial dual role in the two primordial kidney cell lineages: being a differentiating factor in mesenchyme and a survival factor in ureteric epithelium.
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Zhang, Hong. "Regulation of Skeletal Muscle Development And Differentiation by Ski." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1226938149.

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Books on the topic "Pax3 and Pax7"

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Cheung, Albert. Pax3 and PAX3/FKHR induces cell aggregation and morphogenic mesenchymal-epithelial transition. Ottawa: National Library of Canada, 2002.

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Kovak, Mathilda. Paxa praja. Belo Horizonte, MG: Ed. Le, 1996.

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Faust, Eberhard. Pax Christi et Pax Caesaris. Göttingen: Vandenhoeck & Ruprecht, 1993. http://dx.doi.org/10.13109/9783666539268.

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Marroquin, Lorenzo. Pax. Bogota: Editorial La Oveja Negra Ltda., 1986.

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Renner, Paulo Roberto. Pax. Porto Alegre: [s.n.], 1989.

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Rivas Groot, José Maria, 1863-1923, ed. Pax. Bogotá, Colombia: Oveja Negra, 1986.

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Marroquín, Lorenzo. Pax. Bogotá: Círculo de Lectores, 1986.

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Guénane. Pax. Theix: Amers, 2002.

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Korsell, Ingela. Pax: Zaraza. Poznań, Poland: Media Rodzina, 2017.

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Elisha, Ron. Pax Americana. Montmorency, Vic: Yackandandah Playscripts, 1990.

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Book chapters on the topic "Pax3 and Pax7"

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Zhou, Xunlei, and Peter Gruss. "Pax4 and Pax6 in Islet Differentiation." In Molecular Basis of Pancreas Development and Function, 239–54. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1669-9_14.

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Welch, Sharon. "Pax Americana, Pax Humana." In Theological Perspectives for Life, Liberty, and the Pursuit of Happiness, 23–33. New York: Palgrave Macmillan US, 2013. http://dx.doi.org/10.1057/9781137372215_3.

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Adebajo, Adekeye. "Conclusion: Pax Nigeriana, Pax South Africana, and Pax Africana." In The Eagle and the Springbok, 258–64. London: Routledge, 2023. http://dx.doi.org/10.4324/9781003412502-19.

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McCloskey, Donald N. "Pax Cliometrica." In Econometric History, 77–84. London: Macmillan Education UK, 1987. http://dx.doi.org/10.1007/978-1-349-03174-0_5.

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Pugh, Martin. "Pax Britannica." In Britain Since 1789, 83–90. London: Macmillan Education UK, 1999. http://dx.doi.org/10.1007/978-1-349-27402-4_10.

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Young, Paul. "Pax Britannica." In Globalization and the Great Exhibition, 145–97. London: Palgrave Macmillan UK, 2009. http://dx.doi.org/10.1057/9780230594319_5.

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Dutta, Shayeari. "Pax Americana!" In Literature and the War on Terror, 77–90. London: Routledge India, 2023. http://dx.doi.org/10.4324/9781003362999-8.

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Semenza, Gregg L. "PAX Proteins." In Transcription Factors and Huinan Disease, 169–98. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195112399.003.0007.

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Abstract As in the case of the HOX proteins (described in Chapter 9), the PAX proteins represent a family of transcription factors whose members ap pear to play key roles in the development of both invertebrates and vertebrates (reviewed by Chalepakis et al., 1993; Strachan and Read, 1994; Stuart and Gruss, 1995). Nine PAX genes have been identified to date in mice and humans (Fig. 7.1). Unlike the HOX genes, which are clustered at four loci in the human and mouse genomes, mapping of the PAX genes revealed no clustering even though several of the genes have similar genomic structure and coding sequences. The proteins encoded by these genes have in common a unique 128- amino-acid DNA-binding domain, the paired domain. Although the paired domain contains three regions that are predicted to form a heli ces, there is no sequence similarity to the helix-turn-helix motif present in homeodomains. In addition to the paired domain, which is present in all nine PAX proteins, four of the proteins (PAX3, PAX4, PAX6, and PAX7) also contain a homeodomain that contributes to the affinity and specificity of DNA binding by these proteins. Curiously, three PAX proteins (PAX2, PAXS, and PAX8) contain truncated homeodomains of un known function. PAX 1 and PAX9 lack homeodomain-related sequences altogether and must therefore rely entirely on the paired domain for DNA-binding activity.
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Barr, F. G. "PAX3-FOXO1 and PAX7-FOXO1 Gene Fusions in Rhabdomyosarcoma☆." In Reference Module in Biomedical Sciences. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-801238-3.98746-4.

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Barr, Frederic G. "PAX3–FKHR and PAX7–FKHR Gene Fusions in Alveolar Rhabdomyosarcoma." In Encyclopedia of Cancer, 403–8. Elsevier, 2002. http://dx.doi.org/10.1016/b0-12-227555-1/00177-5.

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Conference papers on the topic "Pax3 and Pax7"

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Soofi, Abdulsalam, Yali Zahi, Kathleen Cho, and Greg Dressler. "Abstract PR04: Analyses of Pax2 and Pax8 in maintaining oviduct epithelial homeostasis and fertility." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-pr04.

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Dietz, Kevin N., Patrick J. Miller, and Andrew D. Hollenbach. "Abstract A62: Phosphorylation of Ser205 by the protein kinase CK2 persists on Pax3‐FOXO1, but not Pax3, throughout myogenic differentiation." 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-a62.

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Maria da Costa e Silva, Lúcia. "Programa Pax-Vóbis." In 7th International Congress of the Brazilian Geophysical Society. European Association of Geoscientists & Engineers, 2001. http://dx.doi.org/10.3997/2214-4609-pdb.217.070.

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Liu, Lingling, and Taosheng Chen. "Abstract 2482:Carnitine palmitoyltransferase 1A(CPT1A): a transcriptional target of PAX3-FKHR and mediates PAX3-FKHR-dependent motility in alveolar rhabdomyosarcoma cells." 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.am2012-2482.

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Lenisa, P. "PAX: Polarized Antiproton eXperiments." In DEEP INELASTIC SCATTERING: 13th International Workshop on Deep Inelastic Scattering; DIS 2005. AIP, 2005. http://dx.doi.org/10.1063/1.2122212.

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Muir, Shannon, Jason Nathanson, Melissa Wilbert, Gene Yeo, Frank Furnari, Karen Arden, and Webster Cavenee. "Abstract 3558: The role of miRNA in PAX3-FKHR positive rhabdomyosarcoma." 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.am2014-3558.

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Hanna, Jason A., Matthew R. Garcia, Jonathan C. Go, David Finkelstein, Kiran Kodali, Vishwajeeth Pagala, Eric N. Olson, Junmin Peng, and Mark E. Hatley. "Abstract B05: MicroRNA-206 drives rhabdomyosarcoma differentiation through downregulation of PAX7." In Abstracts: AACR Special Conference on Noncoding RNAs and Cancer: Mechanisms to Medicines; December 4-7, 2015; Boston, MA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.nonrna15-b05.

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Contalbrigo, M. "$\mathcal {PAX}$: POLARIZED ANTIPROTON EXPERIMENTS." In Transversity 2005. WORLD SCIENTIFIC, 2006. http://dx.doi.org/10.1142/9789812773272_0013.

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Gary, M., and A. Ørgaard. "Low-Emission Ro/Pax Ferry." In International Conference on the Design, Construction and Operation of Passenger Ships 2013. RINA, 2013. http://dx.doi.org/10.3940/rina.pass.2013.09.

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Nekipelov, M. "DOUBLE POLARISATION OBSERVABLES AT PAX." In Proceedings of the Second Workshop on Transverse Polarization Phenomena in Hard Processes. WORLD SCIENTIFIC, 2009. http://dx.doi.org/10.1142/9789814277785_0019.

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Reports on the topic "Pax3 and Pax7"

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Millen, Raymond A. PAX NATO: The Opportunities of Enlargement. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada405936.

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Sutherland, John R., and III. Pax Americana: America's Bid Perpetual Peace and Hegemony. Fort Belvoir, VA: Defense Technical Information Center, May 1999. http://dx.doi.org/10.21236/ada370354.

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Harris, Joel. Thermal Conductivity of Pax 2A Explosive by DSC. Fort Belvoir, VA: Defense Technical Information Center, December 1993. http://dx.doi.org/10.21236/ada274721.

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WHITE, W. F. PFP Public Automatic Exchange (PAX) Commercial Grade Item (CGI) Critical Characteristics. Office of Scientific and Technical Information (OSTI), April 2000. http://dx.doi.org/10.2172/802993.

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Brown, William, Richard C. Burdekin, and Marc Weidenmier. Volatility in an Era of Reduced Uncertainty: Lessons from Pax Britannica. Cambridge, MA: National Bureau of Economic Research, May 2005. http://dx.doi.org/10.3386/w11319.

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Stone, John E. Clash of Strategies: Pax Americana and the Nuclear Ambitions of North Korea. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada424212.

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Hui, Liang, Liu Jie, Huang Hui, Zhao Kun, Wei Yuan, Xiao Jie, and Fu Min. Evaluation of PAX1 Methylation Triage as the Primary Screening Method in the Application of Early Diagnosis for Cervical Cancer. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2019. http://dx.doi.org/10.7546/crabs.2019.06.17.

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