Relevant bibliographies by topics / Pitx2

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Academic literature on the topic 'Pitx2'

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

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Journal articles on the topic "Pitx2"

1

Kitamura, K., H. Miura, S. Miyagawa-Tomita, M. Yanazawa, Y. Katoh-Fukui, R. Suzuki, H. Ohuchi, et al. "Mouse Pitx2 deficiency leads to anomalies of the ventral body wall, heart, extra- and periocular mesoderm and right pulmonary isomerism." Development 126, no. 24 (December 15, 1999): 5749–58. http://dx.doi.org/10.1242/dev.126.24.5749.

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Pitx2, a bicoid-related homeobox gene, is involved in Rieger's syndrome and the left-right (L-R) asymmetrical pattern formation in body plan. In order to define the genomic structure and roles of Pitx2, we analyzed the genomic structure and generated Pitx2-deficient mice with the lacZ gene in the homeobox-containing exon of Pitx2. We were able to show that among three isoforms of Pitx2, Pitx2c shows asymmetrical expression whereas Pitx2a, Pitx2b and Pitx2c show symmetrical expression. In Pitx2(−)(/)(−) embryos there was an increase in mesodermal cells in the distal end of the left lateral body wall and an amnion continuous with the lateral body wall thickened in its mesodermal layer. These changes resulted in a failure of ventral body wall closure. In lung and heart in which Pitx2 is expressed asymmetrically, right pulmonary isomerism, atrioventricular canals with prominent swelling, and juxtaposition of the atrium were detected. The hearts failed to develop tricuspid and mitral valves and a common atrioventricular valve forms. Further, dysgenesis of the Pitx2(−)(/)(−) extraocular muscle and thickening of the mesothelial layer of cornea were observed in the ocular system where Pitx2 is expressed symmetrically, and these resulted in enophthalmos. The present study shows that Pitx2 expressed in various sites participates in morphogenesis through three types of actions: the involvement of asymmetric Pitx2 expression in the entire morphogenetic process of L-R asymmetric organs; the involvement of asymmetric Pitx2 expression in the regional morphogenesis of asymmetric organs; and finally the involvement of symmetric Pitx2 expression in the regional morphogenesis of symmetric organs.
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Yu, X., T. R. St Amand, S. Wang, G. Li, Y. Zhang, Y. P. Hu, L. Nguyen, M. S. Qiu, and Y. P. Chen. "Differential expression and functional analysis of Pitx2 isoforms in regulation of heart looping in the chick." Development 128, no. 6 (March 15, 2001): 1005–13. http://dx.doi.org/10.1242/dev.128.6.1005.

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Pitx2, a bicoid-related homeobox gene, plays a crucial role in the left-right axis determination and dextral looping of the vertebrate developing heart. We have examined the differential expression and function of two Pitx2 isoforms (Pitx2a and Pitx2c) that differ in the region 5′ to the homeodomain, in early chick embryogenesis. Northern blot and RT-PCR analyses indicated the existence of Pitx2a and Pitx2c but not Pitx2b in the developing chick embryos. In situ hybridization demonstrated a restricted expression of Pitx2c in the left lateral plate mesoderm (LPM), left half of heart tube and head mesoderm, but its absence in the extra-embryonic tissues where vasculogenesis occurs. RT-PCR experiments revealed that Pitx2a is absent in the left LPM, but is present in the head and extra-embryonic mesoderm. However, ectopic expression of either Pitx2c or Pitx2a via retroviral infection to the right LMP equally randomized heart looping direction. Mapping of the transcriptional activation function to the C terminus that is identical in both isoforms explained the similar results obtained by the gain-of-function approach. In contrast, elimination of Pitx2c expression from the left LMP by antisense oligonucleotide resulted in a randomization of heart looping, while treatment of embryos with antisense oligonucleotide specific to Pitx2a failed to generate similar effect. We further constructed RCAS retroviral vectors expressing dominant negative Pitx2 isoforms in which the C-terminal transcriptional activation domain was replaced by the repressor domain of the Drosophila Engrailed protein (En(r)). Ectopic expression of Pitx2c-En(r), but not Pitx2a-En(r), to the left LPM randomized the heart looping. The results thus demonstrate that Pitx2c plays a crucial role in the left-right axis determination and rightward heart looping during chick embryogenesis.
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Lamba, Pankaj, Vishal Khivansara, Ana C. D'Alessio, Michelle M. Santos, and Daniel J. Bernard. "Paired-Like Homeodomain Transcription Factors 1 and 2 Regulate Follicle-Stimulating Hormone β-Subunit Transcription through a Conserved cis-Element." Endocrinology 149, no. 6 (March 13, 2008): 3095–108. http://dx.doi.org/10.1210/en.2007-0425.

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Paired-like homeodomain transcription factors (PITX) regulate the activity of pituitary hormone-encoding genes. Here, we examined mechanisms through which the family of PITX proteins control murine FSH β-subunit (Fshb) transcription. We observed that endogenous PITX1 and PITX2 isoforms from murine LβT2 gonadotrope cells could bind a highly conserved proximal cis-element. Transfection of PITX1 or PITX2C in heterologous cells stimulated both murine and human Fshb/FSHB promoter-reporter activities, and in both cases, mutation of the critical cis-element abrogated these effects. In homologous LβT2 cells, the same mutation decreased basal reporter activity and greatly reduced activin A-stimulated transcription from murine and human promoter-reporters. Transfecting dominant-negative forms of PITX1 or PITX2C or knocking down PITX1 or -2 expression by RNA interference in LβT2 cells inhibited murine Fshb transcription, confirming roles for endogenous PITX proteins. Both PITX1 and PITX2C interacted with Smad3 (an effector of the activin signaling cascade in these cells) in coprecipitation experiments, and the PITX binding site mutation greatly inhibited Smad2/3/4-stimulated Fshb transcription. In summary, both PITX1 and PITX2C regulate murine and human Fshb/FSHB transcription through a conserved cis-element in the proximal promoter. Furthermore, the data indicate both common and distinct mechanisms of PITX1 and PITX2C action.
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Essner, J. J., W. W. Branford, J. Zhang, and H. J. Yost. "Mesendoderm and left-right brain, heart and gut development are differentially regulated by pitx2 isoforms." Development 127, no. 5 (March 1, 2000): 1081–93. http://dx.doi.org/10.1242/dev.127.5.1081.

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The pitx2 gene is a member of the bicoid-homeodomain class of transcription factors that has been implicated in the control of left-right asymmetry during organogenesis. Here we demonstrate that in zebrafish there are two pitx2 isoforms, pitx2a and pitx2c, which show distinct expression patterns and have non-overlapping functions during mesendoderm and asymmetric organ development. pitx2c is expressed symmetrically in presumptive mesendoderm during late blastula stages and in the prechordal plate during late gastrulation. pitx2a expression is first detected at bud stage in the anterior prechordal plate. The regulation of early mesendoderm pitx2c expression is dependent on one-eyed pinhead (EGF-CFC-related gene) and spadetail (tbx-transcription factor) and can be induced by ectopic goosecoid expression. Maintenance of pitx2c midline expression is dependent on cyclops (nodal) and schmalspur, but not no tail (brachyury). Ectopic expression of pitx2 isoforms results in distinct morphological and molecular phenotypes, indicating that pitx2a and pitx2c have divergent regulatory functions. Both isoforms downregulate goosecoid on the dorsal side, but in contrast to earlier reports that nodal and lefty are upstream of pitx2, ectopic pitx2c in other regions induces cyclops, lefty2 and goosecoid expression. Asymmetric isoform expression occurs in non-overlapping domains, with pitx2c in left dorsal diencephalon and developing gut and pitx2a in left heart primordium. Targeted asymmetric expression in Xenopus shows that both isoforms can alter left-right development, but pitx2a has a slightly stronger effect on heart laterality. Our results indicate that distinct genetic pathways regulate pitx2a and pitx2c isoform expression, and each isoform regulates different downstream pathways during mesendoderm and asymmetric organ development.
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Liu, Chengyu, Wei Liu, Mei-Fang Lu, Nigel A. Brown, and James F. Martin. "Regulation of left-right asymmetry by thresholds of Pitx2c activity." Development 128, no. 11 (June 1, 2001): 2039–48. http://dx.doi.org/10.1242/dev.128.11.2039.

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Although much progress has been made in understanding the molecular mechanisms regulating left-right asymmetry, the final events of asymmetric organ morphogenesis remain poorly understood. The phenotypes of human heterotaxia syndromes, in which organ morphogenesis is uncoupled, have suggested that the early and late events of left-right asymmetry are separable. The Pitx2 homeobox gene plays an important role in the final stages of asymmetry. We have used two new Pitx2 alleles that encode progressively higher levels of Pitx2c in the absence of Pitx2a and Pitx2b, to show that different organs have distinct requirements for Pitx2c dosage. The cardiac atria required low Pitx2c levels, while the duodenum and lungs used higher Pitx2c doses for normal development. As Pitx2c levels were elevated, the duodenum progressed from arrested rotation to randomization, reversal and finally normal morphogenesis. In addition, abnormal duodenal morphogenesis was correlated with bilateral expression of Pitx2c. These data reveal an organ-intrinsic mechanism, dependent upon dosage of Pitx2c, that governs asymmetric organ morphogenesis. They also provide insight into the molecular events that lead to the discordant organ morphogenesis of heterotaxia.
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Toro, Rafael, Irfan Saadi, Adisa Kuburas, Mona Nemer, and Andrew F. Russo. "Cell-specific Activation of the Atrial Natriuretic Factor Promoter by PITX2 and MEF2A." Journal of Biological Chemistry 279, no. 50 (October 1, 2004): 52087–94. http://dx.doi.org/10.1074/jbc.m404802200.

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The PITX2 homeodomain protein is mutated in patients with Axenfeld-Rieger syndrome and is involved in the development of multiple organ systems, including the heart. We have examined the interaction of PITX2 isoforms with myocyte-enhancing factor 2A (MEF2A), which is a known regulator of cardiac development. A direct interaction between PITX2a and MEF2A was demonstrated using yeast two-hybrid and GST pull-down assays. To study the functional significance of this interaction, we used the atrial natriuretic factor (ANF) promoter. Coexpression of MEF2A and PITX2a or Pitx2c resulted in a strong synergistic activation of the ANF promoter in LS8 oral epithelial cells but not in other cell lines (NIH/3T3, Chinese hamster ovary, or C2C12). The synergism was dependent on promoter context, because it required MEF2 binding sites and was not seen with two other PITX2 target promoters. DNA binding by MEF2A was required but not sufficient for synergism. Upstream activators of p38 MAP kinases, MKK3 and MKK6, increased PITX2a and Pitx2c activity to yield up to 90-fold activation of the ANF promoter in LS8 cells. Because Axenfeld-Rieger syndrome is autosomal dominant and affects development of the oral epithelium, we tested one of the known PITX2 mutants. The PITX2a-K88E mutant protein suppressed wild type PITX2a synergism with MEF2A. These results demonstrate a promoter- and cell-specific functional interaction between PITX2 and MEF2A and suggest the possibility of coordinate control by these factors in the oral epithelium.
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Suh, Hoonkyo, Philip J. Gage, Jacques Drouin, and Sally A. Camper. "Pitx2is required at multiple stages of pituitary organogenesis: pituitary primordium formation and cell specification." Development 129, no. 2 (January 15, 2002): 329–37. http://dx.doi.org/10.1242/dev.129.2.329.

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Analysis of an allelic series in mice revealed that the Pitx2 homeobox gene is required at multiple stages of pituitary development. It is necessary for initiating expansion of Rathke’s pouch and maintaining expression of the fetal-specific transcription factors Hesx1 and Prop1. At later stages Pitx2 is necessary for specification and expansion of the gonadotropes and Pit1 lineage within the ventral and caudomedial anterior pituitary. Mechanistically, this is due to the dependence of several critical lineage-specific transcription factors, Pit1, Gata2, Egr1 and Sf1, on a threshold level of PITX2. The related Pitx1 gene has a role in hormone gene transcription, and it is important late in ontogeny for the final expansion of the differentiated cell types. Pitx1 and Pitx2 have overlapping functions in the expansion of Rathke’s pouch, revealing the sensitivity of pituitary organogenesis to the dosage of the PITX family. The model developed for PITX gene function in pituitary development provides a better understanding of the etiology of Rieger syndrome and may extend to other PITX-sensitive developmental processes.
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Schweickert, Axel, Marina Campione, Herbert Steinbeisser, and Martin Blum. "Pitx2 isoforms: involvement of Pitx2c but not Pitx2a or Pitx2b in vertebrate left–right asymmetry." Mechanisms of Development 90, no. 1 (January 2000): 41–51. http://dx.doi.org/10.1016/s0925-4773(99)00227-0.

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Zhang, Min, Matthew C. Hill, Zachary A. Kadow, Ji Ho Suh, Nathan R. Tucker, Amelia W. Hall, Tien T. Tran, et al. "Long-range Pitx2c enhancer–promoter interactions prevent predisposition to atrial fibrillation." Proceedings of the National Academy of Sciences 116, no. 45 (October 21, 2019): 22692–98. http://dx.doi.org/10.1073/pnas.1907418116.

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Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia, is associated with noncoding sequence variants located in proximity to PITX2. Cardiomyocyte-specific epigenomic and comparative genomics uncovered 2 AF-associated enhancers neighboring PITX2 with varying conservation in mice. Chromosome conformation capture experiments in mice revealed that the Pitx2c promoter directly contacted the AF-associated enhancer regions. CRISPR/Cas9-mediated deletion of a 20-kb topologically engaged enhancer led to reduced Pitx2c transcription and AF predisposition. Allele-specific chromatin immunoprecipitation sequencing on hybrid heterozygous enhancer knockout mice revealed that long-range interaction of an AF-associated region with the Pitx2c promoter was required for maintenance of the Pitx2c promoter chromatin state. Long-range looping was mediated by CCCTC-binding factor (CTCF), since genetic disruption of the intronic CTCF-binding site caused reduced Pitx2c expression, AF predisposition, and diminished active chromatin marks on Pitx2. AF risk variants located at 4q25 reside in genomic regions possessing long-range transcriptional regulatory functions directed at PITX2.
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Herraiz-Martínez, Adela, Carmen Tarifa, Estefanía Lozano-Velasco, Verónica Jiménez-Sábado, Sergi Casabella, Francisco Hernández-Torres, Houria Daimi, et al. "Novel PITX2 Homeodomain-Contained Mutations from ATRIAL Fibrillation Patients Deteriorate Calcium Homeostasis." Hearts 2, no. 2 (May 5, 2021): 251–71. http://dx.doi.org/10.3390/hearts2020020.

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Atrial fibrillation (AF) is the most common cardiac arrhythmia in the human population, with an estimated incidence of 1–2% in young adults but increasing to more than 10% in 80+ years patients. Pituitary Homeobox 2, Paired Like Homeodomain 2 (PITX2c) loss-of-function in mice revealed that this homeodomain (HD)-containing transcription factor plays a pivotal role in atrial electrophysiology and calcium homeostasis and point to PITX2 as a candidate gene for AF. To address this issue, we recruited 31 AF patients for genetic analyses of both the known risk alleles and PITX2c open reading frame (ORF) re-sequencing. We found two-point mutations in the homedomain of PITX2 and three other variants in the 5’untranslated region. A 65 years old male patient without 4q25 risk variants but with recurrent AF displayed two distinct HD-mutations, NM_000325.5:c.309G>C (Gln103His) and NM_000325.5:c.370G>A (Glu124Lys), which both resulted in a change within a highly conserved amino acid position. To address the functional impact of the PITX2 HD mutations, we generated plasmid constructs with mutated version of each nucleotide variant (MD4 and MD5, respectively) as well as a dominant negative control construct in which the PITX2 HD was lacking (DN). Functional analyses demonstrated PITX2c MD4 and PITX2c MD5 decreased Nppa-luciferase transactivation by 50% and 40%, respectively, similar to the PITX2c DN (50%), while Shox2 promoter repression was also impaired. Co-transactivation with other cardiac-enriched co-factors, such as Gata4 and Nkx2.5, was similarly impaired, further supporting the pivotal role of these mutations for correct PITX2c function. Furthermore, when expressed in HL1 cardiomyocyte cultures, the PITX2 mutants impaired endogenous expression of calcium regulatory proteins and induced alterations in sarcoplasmic reticulum (SR) calcium accumulation. This favored alternating and irregular calcium transient amplitudes, causing deterioration of the beat-to-beat stability upon elevation of the stimulation frequency. Overall this data demonstrate that these novel PITX2c HD-mutations might be causative of atrial fibrillation in the carrier.
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Dissertations / Theses on the topic "Pitx2"

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Quentien, Marie-Hélène. "Différenciation des cellules du lignage antéhypophysaire somatolactotrope : un r^ole pour les facteurs de transcription Pitx1 et Pitx2." Aix-Marseille 2, 2002. http://www.theses.fr/2002AIX22080.

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Kulak, Stephen. "Mutational analysis of the homeobox transcription factor PITX2." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0021/MQ47053.pdf.

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Doerdelmann, Thomas. "Structural and Biophysical Studies of the Pitx2 Homeodomain." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1307443112.

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Fung, Khe Cheong Frederic, and 馮啟昌. "Upregulation of PITX2 transcription factor is associated with ovarian tumorigenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45988183.

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Kieusseian, Aurélie. "Etude du rôle du facteur de transcription Pitx2 dans la régulation de l'hématopoïèse." Paris 7, 2005. http://www.theses.fr/2005PA077147.

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Yu, Wenjie. "A Pitx2-Irx1 regulatory network controls dental epithelial stem cell differentiation during tooth development." Diss., University of Iowa, 2017. https://ir.uiowa.edu/etd/6020.

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Tooth development is precisely controlled by epithelium-mesenchyme interactions, coordinated signaling pathways and associated transcription factors. Although the processes involved in tooth development are well established, details of the cellular and molecular mechanisms that control tooth development are not fully understood. One of the primary unknown mechanisms is the regulation of dental epithelial stem cells (DESCs), including DESC specification, proliferation and differentiation. In this dissertation, I have addressed this gap in knowledge by studying the role of Pituitary homeobox 2 (Pitx2) and Iroquois 1 (Irx1) in teeth at the cellular and molecular level in mice. PITX2 contains mutations of which are associated for Axenfeld-Rieger syndrome (ARS) in humans and is also required for early tooth development. All the background knowledge is included in Chapter I. In Chapter II, I describe the conditional ablation of Pitx2 in the dental epithelium using a Krt14Cre driver line (Pitx2cKO mice). Knocking out Pitx2 in teeth led to delayed epithelial invagination at bud stage and disruption of tooth morphogenesis at cap stage. At the cellular level, Pitx2 mediates DESC differentiation, daughter cell proliferation in bud stage tooth and regulates enamel knot formation in cap stage tooth. At the molecular level, Pitx2 acts as an upstream regulator of the sonic hedgehog (Shh) signaling pathway by regulating the expression of Shh in the dental epithelial signaling center during early tooth development. In addition, I demonstrated that Pitx2 directly controls the transcription of Irx1. In Chapter III, I determined the cellular and molecular mechanisms of Irx1 in mice. Irx1 general knockout mice were generated by replacing the entire Irx1 gene body with a LacZ reporter gene. Irx1 null mice are neonatal lethal and this lethality is due to pulmonary immaturity with defective surfactant protein secretion. In teeth, Irx1 is expressed in the outer enamel epithelium (OEE) and stratum reticulum (SR) and mediates DESC to OEE and SR differentiation through regulation of Forkhead box protein J1 (Foxj1) and Sex determining region Y-box9 (Sox9). In summary, I identified a Pitx2-Irx1 regulatory network that controls DESC differentiation in teeth, which provided the field with a better understanding of tooth development and tooth regeneration.
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Kendall, Jed. "Targeting ß-catenin in MPNSTs." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin149155952770148.

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Schmidt, Jennifer Verfasser], Wolfgang Arthur [Akademischer Betreuer] [Schulz, and Vlada B. [Akademischer Betreuer] Urlacher. "Funktionelle Charakterisierung von PITX2 im Prostatakarzinom / Jennifer Schmidt. Gutachter: Wolfgang A. Schulz ; Vlada B. Urlacher." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2015. http://d-nb.info/1065375433/34.

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Schmidt, Jennifer [Verfasser], Wolfgang Arthur [Akademischer Betreuer] Schulz, and Vlada B. [Akademischer Betreuer] Urlacher. "Funktionelle Charakterisierung von PITX2 im Prostatakarzinom / Jennifer Schmidt. Gutachter: Wolfgang A. Schulz ; Vlada B. Urlacher." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2015. http://d-nb.info/1065375433/34.

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Li, Xiao. "The molecular mechanisms of PITX2 in tooth development and enamel defects in Axenfeld-Rieger Syndrome." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/5014.

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Patients with Axenfeld-Rieger Syndrome (ARS) present various dental abnormalities. ARS is genetically associated with mutations in the PITX2 gene, which encodes one of the earliest transcription factors to initiate tooth development. Thus, Pitx2 has long been considered as an upstream regulator of the transcriptional hierarchy in tooth development. However, it is unclear how its mutant forms cause ARS dental anomalies. In this report, we outline the transcriptional mechanism that is defective in ARS. We demonstrate that during normal tooth development Pitx2 activates Amelogenin (Amel) expression, whose product is required for enamel formation, and that this regulation is perturbed by missense PITX2 mutations found in ARS patients. We further show that Pitx2-mediated Amel activation is enhanced and controlled by co-factors and target genes of Pitx2. These co-factors include cooperative transcription factors such as Dlx2 and FoxJ1; chromatin-associated remodeler factor Hmgn2; and Wnt signaling components such as Lef-1, β-catenin and Dact2. We also unveil a novel Pitx2 target gene Irx1 that functions in dental epithelium differentiation. Consistent with a physiological significance to these modulations, we show that FoxJ1, Dact2, Irx1 knockout mice and K14-Hmgn2 transgenic mice display various types of amelogenesis defects including enamel hypoplasia - consistent with the human ARS phenotype. Collectively, these findings define transcriptional mechanisms and multi-level regulations involved in normal tooth development and shed light on the molecular underpinnings of the enamel defect observed in ARS patients who carry PITX2 mutations. Moreover, our findings validate the etiology of the enamel defect in novel mouse models of enamel hypoplasia. The impact of this study on current understanding of the dental epithelium development and the translational value lie in the gene network we identified. By manipulating components of the network, pluripotent dental cells can be reprogrammed and serve as new source for tooth regeneration. Our findings brought insights of novel gene therapy approach that can alleviate the dental problems of patients with ARS and other developmental anomalies.
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Books on the topic "Pitx2"

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Campione, Marina, Amelia Aranega, and Diego Franco. Cardiac looping and laterality. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0014.

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Dextral looping is a complex process which progresses concomitantly with cardiac chamber differentiation and ultimately leads to the final alignment of the cardiac regions. Generation of cardiac asymmetry is crucial to ensure the proper form and consequent function of the heart and thus is a highly regulated process. Molecular signals originate long before morphological asymmetry and therefore can direct it; a complex regulatory network has been characterized which invariably converges on the Tgf-β‎ signalling molecule Nodal and its downstream target, the homeobox transcription factor Pitx2. We review current data regarding the cellular and molecular bases of cardiac looping and laterality, and describe current understaning of the role of Nodal and Pitx2. The morphogenetic role of the Pitx2 gene and its modulation of transcription and function, which have recently linked laterality to atrial fibrillation, are emphasized.
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Book chapters on the topic "Pitx2"

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Franco, Diego, and Amelia Aranega. "PITX2 (Pituitary Homeobox Gene 2)." In Encyclopedia of Signaling Molecules, 4024–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101670.

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Franco, Diego, and Amelia Aranega. "PITX2 (Pituitary Homeobox Gene 2)." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101670-1.

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Brown, Nigel A., Louisa M. Jones, Oliver A. T. Lyons, Chengyu Liu, Wei Liu, Jennifer Palie, Mei Fang Lu, and James F. Martin. "Pleiotropic Effects of Pitx2 Isoform C on Morphogenesis in the Mammalian Heart." In Cardiovascular Development and Congenital Malformations, 14–16. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch4.

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Smits, S. M., and M. P. Smidt. "The role of Pitx3 in survival of midbrain dopaminergic neurons." In Parkinson’s Disease and Related Disorders, 57–60. Vienna: Springer Vienna, 2006. http://dx.doi.org/10.1007/978-3-211-45295-0_10.

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Bell, Michael A., Kaitlyn E. Ellis, and Howard I. Sirotkin. "Pelvic Skeleton Reduction and Pitx1 Expression in Threespine Stickleback Populations." In Tinkering: The Microevolution of Development, 225–44. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470319390.ch15.

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Sadikot, Abbas F., Kelvin C. Luk, Pepijn van den Munckhof, Vladimir V. Rymar, Kenneth Leung, Rina Gandhi, and Jacques Drouin. "Pitx3 is Necessary for Survival of Midbrain Dopaminergic Neuron Subsets Relevant to Parkinson’s Disease." In The Basal Ganglia VIII, 265–74. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28066-9_24.

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Semina, Elena V. "PITX2 and PITX3 and the Axenfeld–Rieger Syndrome, Peters Anomaly, Anterior Segment Ocular Dysgenesis, Ring Dermoid of the Cornea, Posterior Polar Congenital Cataract (CPP4), and Microphthalmia with Neurologic Impairment." In Inborn Errors Of Development, 757–67. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0080.

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Abstract PITX2 and PITX3 represent members of the PITX family of homeobox-containing transcription factor genes that was shown to play an important role in embryonic development in different species. Humans with mutations in the PITX2 or PITX3 genes were found to exhibit a variety of ocular phenotypes such as glaucoma, cataracts, corneal anomalies, and microphthalmia that in many cases are accompanied by other developmental defects. In animal models, Pitx2 gene was shown to be essential to normal development of multiple organs such as eyes, teeth, brain, heart, lungs, liver, and body wall. Pitx3 gene was found to be involved in the development of lens and the mesencephalic dopaminergic system. Therefore, these PITX genes represent key components of the network of genes directing development of multiple organs in various species. Studies of the PITX roles in embryogenesis and cell fate decisions will lead to further exploration of the disorders associated with alterations in these genes. This will provide new insight into mechanisms of normal embryonic development, allow identification of other disease genes, and inevitably lead to the better diagnosis and treatment of the associated conditions.
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Murray, Jeffrey C., and Elena V. Semina. "PITX2 gene in development." In Genotype to Phenotype, 246–57. Garland Science, 2003. http://dx.doi.org/10.4324/9780203450420-13.

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Martin, James F., Brad A. Amendt, and Nigel A. Brown. "Pitx2 in Cardiac Left–Right Asymmetry and Human Disease." In Heart Development and Regeneration, 307–22. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-381332-9.00015-3.

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Quentien, Marie-Helene, Jean-Paul Herman, Philip J. Gage, Jean-Pierre Gautron, and Thierry Brue. "In VivoStudy of Pitx2 in the Development of Hypothalamic GnRH Neurons." In BASIC/TRANSLATIONAL - Reproduction & Neuroendocrinology, P1–258—P1–258. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.p12.p1-258.

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Conference papers on the topic "Pitx2"

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Bai, Jieyun, Yaosheng Lu, Andy C.Y. Lo, and Jichao Zhao. "PITX2 Overexpression Leads to Atrial Electrical Remodeling Linked to Atrial Fibrillation." In 2019 Computing in Cardiology Conference. Computing in Cardiology, 2019. http://dx.doi.org/10.22489/cinc.2019.002.

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Huang, Yue, and Guozhang Zhu. "Abstract 3101: Pituitary homeobox 2 (PITX2) promotes thyroid carcinogenesis by activation of cyclin D2." 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.am10-3101.

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Kiechle, Marion, Gabriele Schricker, Rudolf Napieralski, Michaela Aubele, Gert Auer, Kurt Ulm, Jonathan Perkins, Stefan Paepke, Moritz Hamann, and Olaf G. Wilhelm. "Abstract P3-08-65: PITX2 DNA methylation: A prognostic/predictive biomarker for anthracycline-based chemotherapy." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-08-65.

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Sofyanti, Ervina, Trelia Boel, Tiar Pratamawati, and Elza Ibrahim Auerkari. "Prediction of Regulatory Networks of PITX2 Gene Expression in Mandibular Asymmetry Related to Oral Muscle Function." In International Dental Conference of Sumatera Utara 2017 (IDCSU 2017). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/idcsu-17.2018.24.

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Pillai, Sreeraj G., Nupur Dasgupta, Timothy P. Fleming, Mark A. Watson, and Rebecca Aft. "Abstract 432: Expression of PITX2 is correlated with invasiveness in breast cancer cells and its downregulation reduces invasive potential." 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.am10-432.

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Bai, Jieyun, Yijie Zhu, Andy Lo, Yaosheng Lu, and Jichao Zhao. "In Silico Assessment of Genetic Variation in PITX2 Reveals the Molecular Mechanisms of Calcium-Mediated Cellular Triggered Activity in Atrial Fibrillation*." In 2020 42nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC) in conjunction with the 43rd Annual Conference of the Canadian Medical and Biological Engineering Society. IEEE, 2020. http://dx.doi.org/10.1109/embc44109.2020.9175466.

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Paepke, S., OG Wilhelm, M. Schmitt, A. Noske, G. Schricker, R. Napieralski, M. Vetter, et al. "PITX2 DNA-Methylierung: Erster klinisch validierter prädiktiver Marker zur Vorhersage des Ansprechens auf anthrazyklin-basierte Chemotherapie bei Brustkrebspatientinnen mit hohem Rezidivrisiko." In 92. Kongress BGGF 2018. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1655534.

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Kiechle, M., O. Wilhelm, S. Paepke, M. Schmitt, A. Noske, G. Schricker, R. Napieralski, et al. "PITX2 DNA-Methlyierung als klinisch validierter prädiktiver Marker zur Vorhersage des Ansprechens auf Anthrazyklin-haltige Chemotherapie bei Brustkrebspatientinnen mit hohem Rezidivrisiko." In 38. Jahrestagung der Deutschen Gesellschaft für Senologie. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1651738.

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Paepke, S., P. Fasching, M. Beckmann, M. Hamann, M. Braun, A. Schnelzer, O. Wilhelm, et al. "Prospektive Studie zur Vorhersage der Rezidivwahrscheinlichkeit nach neo-adjuvanter, Anthrazyklin-basierter Chemotherapie durch PITX2 bei Patientinnen mit Östrogenrezeptor-positivem Brustkrebs (P4-Studie)." In 39. Jahrestagung der Deutschen Gesellschaft für Senologie. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688035.

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Bahnassy, Abeer A., Abdel-Rahman N. zekri, Salem E. Salem, Hala Aziz, Abeer E. Moustafa, and Rabab M. Gaafar. "Abstract 2384: Assessment of PITX2, BMP4, FGF4, ERalpha, ERbeta promoter methylation in the circulating tumor cells (CTCs) can predict metastasis and survival in primary invasive duct carcinoma (PIDC) patients." 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.am2012-2384.

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