Relevant bibliographies by topics / Gata6

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Academic literature on the topic 'Gata6'

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Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Gata6"

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Capo-chichi, Callinice D., Jennifer L. Smedberg, Malgorzata Rula, Emmanuelle Nicolas, Anthony T. Yeung, Richard F. Adamo, Andrey Frolov, Andrew K. Godwin, and Xiang-Xi Xu. "Alteration of Differentiation Potentials by Modulating GATA Transcription Factors in Murine Embryonic Stem Cells." Stem Cells International 2010 (2010): 1–15. http://dx.doi.org/10.4061/2010/602068.

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Background. Mouse embryonic stem (ES) cells can be differentiated in vitro by aggregation and/or retinoic acid (RA) treatment. The principal differentiation lineage in vitro is extraembryonic primitive endoderm. Dab2, Laminin, GATA4, GATA5, and GATA6 are expressed in embryonic primitive endoderm and play critical roles in its lineage commitment.Results. We found that in the absence of GATA4 or GATA5, RA-induced primitive endoderm differentiation of ES cells was reduced. GATA4 (−/−) ES cells express higher level of GATA5, GATA6, and hepatocyte nuclear factor 4 alpha marker of visceral endoderm lineage. GATA5 (−/−) ES cells express higher level of alpha fetoprotein marker of early liver development. GATA6 (−/−) ES cells express higher level of GATA5 as well as mesoderm and cardiomyocyte markers which are collagen III alpha-1 and tropomyosin1 alpha. Thus, deletion of GATA6 precluded endoderm differentiation but promoted mesoderm lineages.Conclusions. GATA4, GATA5, and GATA6 each convey a unique gene expression pattern and influences ES cell differentiation. We showed that ES cells can be directed to avoid differentiating into primitive endoderm and to adopt unique lineages in vitro by modulating GATA factors. The finding offers a potential approach to produce desirable cell types from ES cells, useful for regenerative cell therapy.
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Yu, Min, Ulrica Wang, and Zhengxin Wang. "E2F and GATA switches turn off WD repeat domain 77 expression in differentiating cells." Biochemical Journal 473, no. 15 (July 28, 2016): 2331–43. http://dx.doi.org/10.1042/bcj20160130.

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WDR77 (WD repeat domain 77) is expressed during earlier lung development when cells are rapidly proliferating, but is absent from adult lung. It is re-activated during lung tumorigenesis and is essential for lung cancer cell proliferation. Signalling pathways/molecules that control WDR77 gene expression are unknown. Promoter mapping, gel shift assay and ChIP revealed that the WDR77 promoter contains bona fide response elements for E2F and GATA transcriptional factors as demonstrated in prostate cancer, lung cancer and erythroid cells, as well as in mouse lung tissues. The WDR77 promoter is transactivated by E2F1, E2F3, GATA1 and GATA6, but suppressed by E2F6, GATA1 and GATA3 in prostate cancer PC3 cells. WDR77 expression is associated with E2F1, E2F3, GATA2 and GATA6 occupancy on the WDR77 gene, whereas, in contrast, E2F6, GATA1 and GATA3 occupancy is associated with the loss of WDR77 expression during erythroid maturation and lung development. More importantly, the loss of WDR77 expression that results from E2F and GATA switches is required for cellular differentiation of erythroid and lung epithelial cells. In contrast, lung cancer cells avoid post-mitotic differentiation by sustaining WDR77 expression. Altogether, the present study provides a novel molecular mechanism by which WDR77 is regulated during erythroid and lung development and lung tumorigenesis.
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Engels, Manon, Paul N. Span, Rod T. Mitchell, Joop J. T. M. Heuvel, Monica A. Marijnissen-van Zanten, Antonius E. van Herwaarden, Christina A. Hulsbergen-van de Kaa, et al. "GATA transcription factors in testicular adrenal rest tumours." Endocrine Connections 6, no. 8 (November 2017): 866–75. http://dx.doi.org/10.1530/ec-17-0215.

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Testicular adrenal rest tumours (TARTs) are benign adrenal-like testicular tumours that frequently occur in male patients with congenital adrenal hyperplasia. Recently, GATA transcription factors have been linked to the development of TARTs in mice. The aim of our study was to determine GATA expression in human TARTs and other steroidogenic tissues. We determined GATA expression in TARTs (n = 16), Leydig cell tumours (LCTs; n = 7), adrenal (foetal (n = 6) + adult (n = 10)) and testis (foetal (n = 13) + adult (n = 8)). We found testis-like GATA4, and adrenal-like GATA3 and GATA6 gene expressions by qPCR in human TARTs, indicating mixed testicular and adrenal characteristics of TARTs. Currently, no marker is available to discriminate TARTs from LCTs, leading to misdiagnosis and incorrect treatment. GATA3 and GATA6 mRNAs exhibited excellent discriminative power (area under the curve of 0.908 and 0.816, respectively), while immunohistochemistry did not. GATA genes contain several CREB-binding sites and incubation with 0.1 mM dibutyryl cAMP for 4 h stimulated GATA3, GATA4 and GATA6 expressions in a human foetal testis cell line (hs181.tes). Incubation of adrenocortical cells (H295RA) with ACTH, however, did not induce GATA expression in vitro. Although ACTH did not dysregulate GATA expression in the only human ACTH-sensitive in vitro model available, our results do suggest that aberrant expression of GATA transcription factors in human TARTs might be involved in TART formation.
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Zhao, Roong, Alistair J. Watt, Jixuan Li, Jennifer Luebke-Wheeler, Edward E. Morrisey, and Stephen A. Duncan. "GATA6 Is Essential for Embryonic Development of the Liver but Dispensable for Early Heart Formation." Molecular and Cellular Biology 25, no. 7 (April 1, 2005): 2622–31. http://dx.doi.org/10.1128/mcb.25.7.2622-2631.2005.

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ABSTRACT Several lines of evidence suggest that GATA6 has an integral role in controlling development of the mammalian liver. Unfortunately, this proposal has been impossible to address directly because mouse embryos lacking GATA6 die during gastrulation. Here we show that the early embryonic deficiency associated with GATA6-knockout mice can be overcome by providing GATA6-null embryos with a wild-type extraembryonic endoderm with the use of tetraploid embryo complementation. Analysis of rescued Gata6 − / − embryos revealed that, although hepatic specification occurs normally, the specified cells fail to differentiate and the liver bud does not expand. Although GATA6 is expressed in multiple tissues that impact development of the liver, including the heart, septum transversum mesenchyme, and vasculature, all are relatively unaffected by loss of GATA6, which is consistent with a cell-autonomous requirement for GATA6 during hepatogenesis. We also demonstrate that a closely related GATA factor, GATA4, is expressed transiently in the prehepatic endoderm during hepatic specification and then lost during expansion of the hepatic primordium. Our data support the proposal that GATA4 and GATA6 are functionally redundant during hepatic specification but that GATA6 alone is available for liver bud growth and commitment of the endoderm to a hepatic cell fate.
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Sartori, Daniel J., Christopher J. Wilbur, Simon Y. Long, Matthew M. Rankin, Changhong Li, Jonathan P. Bradfield, Hakon Hakonarson, Struan F. A. Grant, William T. Pu, and Jake A. Kushner. "GATA Factors Promote ER Integrity and β-Cell Survival and Contribute to Type 1 Diabetes Risk." Molecular Endocrinology 28, no. 1 (January 1, 2014): 28–39. http://dx.doi.org/10.1210/me.2013-1265.

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Abstract Pancreatic β-cell survival remains poorly understood despite decades of research. GATA transcription factors broadly regulate embryogenesis and influence survival of several cell types, but their role in adult β-cells remains undefined. To investigate the role of GATA factors in adult β-cells, we derived β-cell-inducible Gata4- and Gata6-knockout mice, along with whole-body inducible Gata4 knockouts. β-Cell Gata4 deletion modestly increased the proportion of dying β-cells in situ with ultrastructural abnormalities suggesting endoplasmic reticulum (ER) stress. Notably, glucose homeostasis was not grossly altered in Gata4- and Gata6-knockout mice, suggesting that GATA factors do not have essential roles in β-cells. Several ER stress signals were up-regulated in Gata4 and Gata6 knockouts, most notably CHOP, a known regulator of ER stress-induced apoptosis. However, ER stress signals were not elevated to levels observed after acute thapsigargin administration, suggesting that GATA deficiency only caused mild ER stress. Simultaneous deletion of Gata4 and CHOP partially restored β-cell survival. In contrast, whole-body inducible Gata4 knockouts displayed no evidence of ER stress in other GATA4-enriched tissues, such as heart. Indeed, distinct GATA transcriptional targets were differentially expressed in islets compared with heart. Such β-cell-specific findings prompted study of a large meta-analysis dataset to investigate single nucleotide polymorphisms harbored within the human GATA4 locus, revealing several variants significantly associated with type 1 diabetes mellitus. We conclude that GATA factors have important but nonessential roles to promote ER integrity and β-cell survival in a tissue-specific manner and that GATA factors likely contribute to type 1 diabetes mellitus pathogenesis.
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Hui, Yvonne Y., and Holly A. LaVoie. "GATA4 Reduction Enhances 3′,5′-Cyclic Adenosine 5′-Monophosphate-Stimulated Steroidogenic Acute Regulatory Protein Messenger Ribonucleic Acid and Progesterone Production in Luteinized Porcine Granulosa Cells." Endocrinology 149, no. 11 (July 24, 2008): 5557–67. http://dx.doi.org/10.1210/en.2008-0484.

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Previous studies with cultured granulosa cells implicated GATA4 in gonadotropin regulation of the steroidogenic acute regulatory protein (STAR) gene. Caveats to these prior studies exist. First, GATA4 levels are reduced in granulosa-luteal cells after the LH surge when GATA6 expression is relatively high. Second, STAR mRNA expression is negligible in granulosa cells until after the LH surge. Both exogenous GATA4 and GATA6 can transactivate STAR gene promoter constructs. We used an RNA interference (RNAi) approach to determine the contributions of GATA4 and GATA6 to cAMP analog regulation of the endogenous STAR gene in luteinizing granulosa cells. STAR mRNA was stimulated by cAMP under control RNAi conditions. Surprisingly, GATA4 reduction by its respective RNAi approximately doubled the cAMP induction of STAR mRNA. At 24 h cAMP treatment, this augmentation was abolished by co-down-regulation of GATA4+GATA6. GATA6 down-regulation by itself did not alter STAR mRNA levels. GATA4+GATA6 co-down-regulation elevated basal CYP11A mRNA at 24 h treatment but did not affect its induction by cAMP. Basal levels of HSD3B mRNA were reduced by GATA4 RNAi conditions leading to a greater fold induction of its mRNA by cAMP. Fold cAMP-stimulated progesterone production was enhanced by GATA4 down-regulation but not by GATA4+GATA6 co-down-regulation. These data implicate GATA6 as the facilitator in cAMP-stimulated STAR mRNA and downstream progesterone accumulation under reduced GATA4 conditions. Data also demonstrate that basal levels of GATA4/6 are not required for cAMP induction of the STAR gene. The altered ratio of GATA4 to GATA6 after ovulation may allow GATA6 to enhance STAR mRNA accumulation.
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Sumi, Koichi, Toshiya Tanaka, Aoi Uchida, Kenta Magoori, Yasuyo Urashima, Riuko Ohashi, Hiroto Ohguchi, et al. "Cooperative Interaction between Hepatocyte Nuclear Factor 4α and GATA Transcription Factors Regulates ATP-Binding Cassette Sterol Transporters ABCG5 and ABCG8." Molecular and Cellular Biology 27, no. 12 (April 2, 2007): 4248–60. http://dx.doi.org/10.1128/mcb.01894-06.

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ABSTRACT Cholesterol homeostasis is maintained by coordinate regulation of cholesterol synthesis and its conversion to bile acids in the liver. The excretion of cholesterol from liver and intestine is regulated by ATP-binding cassette half-transporters ABCG5 and ABCG8. The genes for these two proteins are closely linked and divergently transcribed from a common intergenic promoter region. Here, we identified a binding site for hepatocyte nuclear factor 4α (HNF4α) in the ABCG5/ABCG8 intergenic promoter, through which HNF4α strongly activated the expression of a reporter gene in both directions. The HNF4α-responsive element is flanked by two conserved GATA boxes that were also required for stimulation by HNF4α. GATA4 and GATA6 bind to the GATA boxes, coexpression of GATA4 and HNF4α leads to a striking synergistic activation of both the ABCG5 and the ABCG8 promoters, and binding sites for HNF4α and GATA were essential for maximal synergism. We also show that HNF4α, GATA4, and GATA6 colocalize in the nuclei of HepG2 cells and that a physical interaction between HNF4α and GATA4 is critical for the synergistic response. This is the first demonstration that HNF4α acts synergistically with GATA factors to activate gene expression in a bidirectional fashion.
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Rath, Nibedita, Zhishan Wang, Min Min Lu, and Edward E. Morrisey. "LMCD1/Dyxin Is a Novel Transcriptional Cofactor That Restricts GATA6 Function by Inhibiting DNA Binding." Molecular and Cellular Biology 25, no. 20 (October 15, 2005): 8864–73. http://dx.doi.org/10.1128/mcb.25.20.8864-8873.2005.

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ABSTRACT The activity of GATA factors is regulated, in part, at the level of protein-protein interactions. LIM domain proteins, first defined by the zinc finger motifs found in the Lin11, Isl-1, and Mec-3 proteins, act as coactivators of GATA function in both hematopoietic and cardiovascular tissues. We have identified a novel GATA-LIM interaction between GATA6 and LMCD1/dyxin. The LIM domains and cysteine-rich domains in LMCD1/dyxin and the carboxy-terminal zinc finger of GATA6 mediate this interaction. Expression of LMCD1/dyxin is remarkably similar to that of GATA6, with high-level expression observed in distal airway epithelium of the lung, vascular smooth muscle, and myocardium. In contrast to other GATA-LIM protein interactions, LMCD1/dyxin represses GATA6 activation of both lung and cardiac tissue-specific promoters. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that LMCD1/dyxin represses GATA6 function by inhibiting GATA6 DNA binding. These data reveal an interaction between GATA6 and LMCD1/dyxin and demonstrate a novel mechanism through which LIM proteins can assert their role as transcriptional cofactors of GATA proteins.
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Laforest, Brigitte, and Mona Nemer. "GATA5 interacts with GATA4 and GATA6 in outflow tract development." Developmental Biology 358, no. 2 (October 2011): 368–78. http://dx.doi.org/10.1016/j.ydbio.2011.07.037.

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Yang, Honghua, Min Min Lu, Lili Zhang, Jeffrey A. Whitsett, and Edward E. Morrisey. "GATA6 regulates differentiation of distal lung epithelium." Development 129, no. 9 (May 1, 2002): 2233–46. http://dx.doi.org/10.1242/dev.129.9.2233.

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GATA6 is a member of the GATA family of zinc-finger transcriptional regulators and is the only known GATA factor expressed in the distal epithelium of the lung during development. To define the role that GATA6 plays during lung epithelial cell development, we expressed a GATA6-Engrailed dominant-negative fusion protein in the distal lung epithelium of transgenic mice. Transgenic embryos lacked detectable alveolar epithelial type 1 cells in the distal airway epithelium. These embryos also exhibited increased Foxp2 gene expression, suggesting a disruption in late alveolar epithelial differentiation. Alveolar epithelial type 2 cells, which are progenitors of alveolar epithelial type 1 cells, were correctly specified as shown by normal thyroid transcription factor 1 and surfactant protein A gene expression. However, attenuated endogenous surfactant protein C expression indicated that alveolar epithelial type 2 cell differentiation was perturbed in transgenic embryos. The number of proximal airway tubules is also reduced in these embryos, suggesting a role for GATA6 in regulating distal-proximal airway development. Finally, a functional role for GATA factor function in alveolar epithelial type 1 cell gene regulation is supported by the ability of GATA6 to trans-activate the mouse aquaporin-5 promoter. Together, these data implicate GATA6 as an important regulator of distal epithelial cell differentiation and proximal airway development in the mouse.
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Dissertations / Theses on the topic "Gata6"

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Decker, Kimberly Jean. "Gata6 regulates pancreatic branching morphogenesis and endocrine differentiation /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 160-175). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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Liljeström, E. (Emmi). "Transcription factor GATA6 in ductal metaplasia of hepatocytes." Bachelor's thesis, University of Oulu, 2019. http://jultika.oulu.fi/Record/nbnfioulu-201902051147.

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Abstract. GATA6 is evolutionary highly conserved transcription factor and a newish indicator and possible causer of ductal metaplasia in biliary atresia (BA). BA is a rare neonatal cholestatic liver disease caused by fibroinflammatory obstruction of bile ducts. BA causes proliferation of bile ducts which is also called ductal metaplasia. In ductal metaplasia hepatocytes phenotype starts resembling more cholangiocytes. When bile gathers inside the liver it (liver) starts to create new bile ducts. This reaction is called ductal reaction what is a consequence of ductal metaplasia. In this thesis work we, study the role of GATA6 in ductal metaplasia. We have two different kinds of mice: control mouse (ctrl) and knock out mouse (cKO). Both mice were operated with bile duct ligation (BDL) to resemble the BA-like condition. Our control (Ctrl) mouse only went over BDL and cKO mouse’s GATA6 gene was silenced in addition of the BDL. Missing of GATA6 has shown histology changes in liver tissue — there is no clear bile duct structure like in normal BA-like tissue. Post-mortem tells also a bad condition of the liver of cKO mouse. Similarly, gene expression studies supports hypothesis that ductal reaction hardly ever happens when GATA6 is missing.
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Patil, Shilpa [Verfasser]. "EZH2-GATA6 axis in Pancreatic ductal adenocarcinoma / Shilpa Patil." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2020. http://d-nb.info/1218780746/34.

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Rodrigues, Patricia. "Regulation of lipid metabolism by GATA6 : an integrated 'omics' approach." Thesis, Cardiff University, 2019. http://orca.cf.ac.uk/120173/.

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The transcription factor GATA6 was recently recognised as a master regulator of the phenotype and function of peritoneal resident macrophages (pResMf), whose deficiency results in dysregulated proliferative renewal during homeostasis and altered inflammatory responses, associated with delays in resolution. Herein, I show using microarray analysis that mice with a myeloid deficiency of Gata6 (Gata6-KOmye mice) have significant changes in genes associated with lipid metabolism, in particular sphingolipids (SL). Three of the most notable alterations were the downregulation of genes responsible for the degradation of glucosylceramides (GlcCer) and sphingomyelins (SM) (Gba2 and Smpd1), as well as a gene involved in the regulation of lysosomal pH, and consequently, lysosomal function. To characterise the metabolic defect, I compared the lipidome of Gata6-KOmye and wild-type (WT) pResMf using a high-resolution LC-MS based global lipidomics approach and replicated my findings using targeted LC-MS/MS. SL showed a high percentage of changes (25% of all lipids levels were altered significantly) with a marked increase in Gata6-KOmye pResMf. SL are important constituents of the plasma membrane in eukaryotes and, as second messengers, modulate apoptosis, cell proliferation and differentiation. Targeted lipidomics by LC-MS/MS showed that the most significantly-increased molecular species were long chain GlcCer and SM. This linked with downregulation of Gba2, Ctse and Smpd1, observed during the microarray analysis, and was confirmed by supressing these pathways, in RAW 264.7 cells, using knockdown (shRNA) approaches. Accumulation of SL metabolites in tissues is implicated in a plethora of patho-physiological complications such as development of neurological dysfunctions, atherosclerosis, diabetes, and heart failure, whilst in cells it correlates with defects in cell migration, cholesterol traffic and efflux, lipid transport, cell activation, proliferation and apoptosis. Overall, I concluded that GATA6 regulates lipid metabolism in pResMf, on both a transcriptional and metabolic level, with particular focus on SL levels. Furthermore,there is indication that this regulation may at least in part control phenotype and function in pResMf through altering SL signalling. Thus, my studies propose GATA6 as a new lipid-regulating transcription factor and highlight the importance of lipid regulation in pResMf biology.
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Gharibeh, Lara. "Gata6 Haploinsufficiency Leads to Aortic Valve, Conduction System and Limbs Defects." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37584.

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Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. Congenital heart disease (CHD) is a risk factor for premature cardiovascular complications. Great advances have occurred in the past years leading to the identification of several genes essential for proper cardiac formation such as GATA4/5/6 mutated in some individuals with CHD. GATA6 is a zinc finger transcription factor whose presence is crucial for early embryonic development. GATA6 is expressed in many cell types of the heart including myocardial, endocardial, neural crest, and vascular smooth muscle. In human, mutations in GATA6 result in variable cardiac phenotypes. The objective of this thesis was to determine the roles that GATA6 play in the different cell types of the heart and to elucidate the molecular basis of the cardiac defects associated with Gata6 haploinsufficiency. For this, a combination of cell and molecular techniques were used in vitro and in vivo. First, we show that Gata6 heterozygozity leads to RL-type bicuspid aortic valve (BAV)- the most common CHD affecting 2% of the population. GATA6-dependent BAV is the result of disruption of valve remodeling and extracellular matrix composition in Gata6 haploinsufficient mice. Cell-specific inactivation of one Gata6 allele from Isl-1 positive cells, but not from endothelial or neural crest cells, recapitulates the phenotype of Gata6 heterozygous mice revealing an essential role for GATA6 in secondary heart field myocytes during valvulogenesis. We further uncovered a role for GATA6 as an important regulator of the cardiac conduction system and revealed that GATA6 expression regulates the activity of the cardiac pacemaker. GATA6 exerts its role via regulation of the cross-talk among the different cell types of the SAN. Lastly, some CHDs are characterized by abnormalities of both the limbs and the heart such as the Holt Oram syndrome (caused by mutation in TBX5 transcription factor). The molecular basis for limb-heart defects remain poorly understood. In the course of this work, we discovered that Gata6 haploinsufficiency resulted in a partially penetrant polysyndactyly (extra digits fused together) phenotype. Together, the data provide novel molecular and cellular insight into GATA6 role in normal and pathologic heat development. Our results also suggest that GATA6 should be added to the list of genes whose mutations are potentially associated with heart and limb abnormalities. Better knowledge of the molecular basis of CHD is a prerequisite for the development of diagnostic and therapeutic strategies to improve care of individuals with congenital heart disease.
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Chia, Crystal Ying. "The role of transcription factor GATA6 in the development of the human pancreas." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271836.

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While there has been an opulence of data and studies surrounding the study of the developing pancreas in mammals and other vertebrates, the focus has largely been in mice. The paucity of research in the development of the human pancreas has led to diminished knowledge in the area, compared to other species. Recent discoveries provide growing evidence for discrepancies between mouse and human pancreatic development and diseases and highlight the fact that developmental studies of the pancreas in humans are imperative. The need to develop therapies for diabetes, a growing and one of the leading health problems worldwide, further compels more exploration in this area to deepen our understanding in the different aspects of diabetes in humans and its underlying causes. Research involving modelling human diseases in vitro enables the investigation of the cellular and molecular mechanisms underlying these diseases as well as the development of therapies for treating them. The availability of hPSCs brings with it the advantage of overcoming the limitations of animal models for certain disorders such as pancreatic agenesis, the focus of my project. The use of site-specific nucleases such as TALENs for such a purpose represents a paradigm shift in disease modelling, where TALENs are capable of directly correcting disease-causing mutations, therefore permanently eliminating the symptoms with precise genome modifications. Alternatively, TALENs can also be used to inactivate specific genes by inducing site-specific mutations. Using these tools, I found that GATA6 is required for the formation of the definitive endoderm (DE) and pancreas in humans; hPSCs harbouring homozygous GATA6 mutations fail to form the definitive endoderm, and consequently the pancreas, whereas hPSCs harbouring heterozygous GATA6 mutations exhibited impairment in definitive endoderm development, although it remains unclear if this is a protocol dependent defect. At the pancreatic stage, heterozygous GATA6 mutations consistently compromised pancreas formation regardless of protocol used. I also found that GATA6 transcriptionally activates the development of the definitive endoderm and pancreatic endoderm, and possibly represses the development of mesoderm. Furthermore, I also established that GATA6 directly interacts with key definitive endoderm markers CXCR4 and SOX17, and pancreatic marker PDX1. Taken together, the work herein demonstrates the successful use of hPSCs coupled with the TALEN genome editing technology as a unique in vitro system for disease modelling. These findings also establish two developmental windows, the DE and pancreatic progenitor stages, where GATA6 haploinsufficiency can result in the impairment of pancreatic development leading to pancreatic hypoplasia observed in human GATA6 heterozygous patients. Lastly, my work also provides the molecular mechanism by which GATA6 regulates pancreatic development. Overall, this study provided new insights in the role of GATA6 during development of the human pancreas. These results will be important in developing new methods of differentiation for hPSCs and understanding the interconnection between early organogenesis and late onset of diabetes.
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Montagni, Elisa 1984. "Transcription factor GATA6 and ISC gene SMOC2 in the regulation of BMP pathway in intestinal adenoma." Doctoral thesis, Universitat Pompeu Fabra, 2015. http://hdl.handle.net/10803/523489.

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The first chapter identifies the transcription factor GATA6 as negative regulator of a transcriptional circuit dedicated to prevent the expansion of Adenoma Stem Cells (AdSCs) during the onset of colorectal cancer (CRC). In particular, we show that GATA6 directly activates the expression of the WNT pathway component LGR5 and represses BMP levels in adenoma by competing with the β-catenin/TCF4 complex for the binding to BMP4 enhancer regions. As a result of this mechanism, two compartments are established within an adenoma: a BMP positive differentiated cell zone and a BMP negative undifferentiated cell zone, where AdSCs reside. Genetic deletion of Gata6 increases BMP levels in the AdSC compartment, inhibiting self-renewal and intestinal tumorigenesis. These findings represent a key contribution to understand the mechanisms that regulate tumor hierarchy and reveal for the first time the existence of a niche that protects AdSCs from BMP signals. The second chapter focuses on the functional characterization of Smoc2, a novel Intestinal Stem Cell (ISC) gene. We generated genetic mouse models in order to overexpress or ablate Smoc2 in the intestine. We found that SMOC2 acts as a BMP inhibitor in the intestine and that it is not only restricted to epithelial Stem Cells (SCs) but it is also expressed by the stroma. Although it is dispensable for normal ISC maintenance and intestinal homeostasis, high levels of SMOC2 are required for tumorigenesis. Indeed, Smoc2 overexpression leads to spontaneous development of hamartomas and enhances adenoma formation in mice with an Apc mutant background; inversely, Smoc2 deficiency decreases tumorigenesis and prolongs survival of Apc mutant mice. In particular, we observed that SMOC2-mediated BMP inhibition positively affects Insulin-like Growth Factor (Igf1) expression in adenoma endothelial cells (ECs). Our data suggest that SMOC2 could enhance tumor-associated inflammation through BMP-mediated Igf1 regulation in the stroma.
El primer capítulo describe la identificación del factor de transcripción GATA6 como regulador negativo de un circuito transcripcional fisiológico dedicado a reprimir la expansión de las células madre de los adenomas (Adenoma Stem Cells o AdSCs) en el inicio de la tumorogénesis colorrectal. De manera específica, mostramos como el factor GATA6 activa directamente la expresión del componente de la ruta de WNT, LGR5, y también directamente reprime niveles de hormona BMP (Bone Morphogenetic Protein) a través de la competición directa con el complejo beta-catenina-TCF4 por la unión a regiones enhancer del gen BMP4. Como resultado de este circuito transcripcional que hemos descubierto, en los adenomas se generan dos compartimentos, una zona positiva para la señalización mediada por BMP que contiene las células diferenciadas de los adenomas, y un área negativa para BMP, donde residen y se expanden las AdSCs. La ablación genética de Gata6 incrementa los niveles de BMPs en el compartimento de las AdSCs, inhibiendo la autorenovación de las mismas y por ende la tumorogénesis. Este descubrimiento representa una aportación clave para entender los mecanismos que regulan la jerarquía tumoral y revelan por primera vez la existencia de un nicho que protege las AdSCs de las señales de BMP. El segundo capítulo describe la caracterización funcional de Smoc2, uno de los genes identificados en el laboratorio dentro del programa genético específico de las células madre del intestino (Intestinal Stem Cells o ISCs). Durante el transcurso de la tesis
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Fletcher, Georgina Clare. "A role for GATA6 in mediating anterior mesendoderm migration in the Xenopus laevis gastrula." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416041.

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Whissell, Gavin 1978. "WNT signaling, hypoxia and GATA6 : their role in colorectal cancer, stem cells and disease progression." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/295581.

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The recent discovery that intestinal adenomas are built on a stem cell hierarchy has raised great interest in understanding the signals that maintain tumor stem cells. We unveiled the existence of a transcriptional circuit dedicated to prevent the expansion of adenoma stem cells during the onset of CRC. This circuit was found to be controlled by the transcription factor GATA6, which directly activated the expression of the WNT pathway component LGR5 and repressed BMP levels in adenomas. As a result of this mechanism, two cell compartments were established in adenomas: a BMP positive zone that comprises differentiated tumor cells and a BMP negative niche that hosts adenoma stem cells. Genetic deletion of Gata6 elevated BMP levels in tumors, which in turn inhibited adenoma stem cell self-renewal and intestinal tumorigenesis. These findings represent a key contribution to understand the mechanisms that regulate the tumor stem cell hierarchy and reveal for first time the existence of a niche that protects AdSCs from BMP signals. In subsequent studies, we further explore the role of GATA factors in EMT both in Drosophila and mammalian models. During the formation of the Drosophila endoderm relatively static epithelial cells have to convert to highly migratory cells to form a large part of the intestinal tract. We showed that the Drosophila GATA factor Srp is necessary to induce EMT, which resulted in relocalization of E-cadherin protein without altering its expression. Mammalian GATA4 and GATA6 also induced an EMT when ectopically expressed in culture. GATA factor Srp and GATA6 both transcriptionally inhibited Crumbs orthologues, delocalized E-cadherin and activated mesenchymal genes. This work has uncovered a novel evolutionarily conserved alternative route to EMT that is Snail independent. This discovery could have important clinical implications in pathogenesis, namely in cancer progression. Further studies aimed to characterize WNT signaling during CRC progression. WNT signaling is required for the maintenance of colorectal cancer stem cells (CRC-SCs) but paradoxically low levels of WNT genes associate with a higher risk of disease relapse. We identified a core expression program driven by beta-catenin/TCF in CRC-SCs, which was shown to be a strict indicator of the dependency on WNT signaling for growth. We showed that during disease progression, a subset of WNT genes is downregulated as a consequence of tumor hypoxia. This response characterized a group of patients displaying very high risk of cancer recurrence after therapy. Hypoxia-induced genes were prominently expressed at invasion fronts coinciding with lower expression of the WNT program. Therefore, hypoxia refines the WNT program in CRC-SCs during the acquisition of a malignant phenotype. This finding has important implications in CRC progression, as it explains how some CRC-SC genes (like EPHB2) are shut down during the progression of the disease and directly challenges recent high impact work in the field that points to methylation as the mechanism responsible for the refinement of WNT signaling. Moreover it identifies hypoxia as a culprit in this invasive cell phenotype. These findings may have important clinical implications in treatment of CRC.
El reciente descubrimiento de que los adenomas intestinales mantienen una jerarquía similar a la del epitelio intestinal normal, ha despertado gran interés por entender las señales que especifican y mantienen a las células madre tumorales. En este trabajo, damos a conocer la existencia de un circuito transcripcional dedicado a prevenir la expansión de células madre de adenoma durante el inicio del cáncer colorectal (CCR). Este circuito está controlado por el factor de transcripción GATA6, el cual activa directamente el componente de la vía de señalización WNT LGR5, y reprime los niveles de BMP en adenomas. Como resultado de este mecanismo, se establecen dos compartimentos celulares en los adenomas: una zona BMP positiva que contiene células tumorales diferenciadas y un nicho BMP negativo que aloja células madre de adenoma. La deleción genética de Gata6 eleva los niveles de BMP en tumores, lo que a su vez inhibe la auto-renovación de células madre de adenoma y la tumorigénesis intestinal. Estos hallazgos representan una contribución fundamental para comprender los mecanismos que regulan la jerarquía de las células madre tumorales y revelan por primera vez la existencia de un nicho que protege a las células madre de adenoma de señales BMP. En estudios posteriores, continuamos explorando el rol de los factores GATA en la transición epitelio-mesénquima tanto en modelos de Drosophila como de mamífero. Durante el desarrollo del endodermo en Drosophila, células epiteliales relativamente estáticas se convierten en células migratorias para formar una gran parte del tracto intestinal a través del proceso de transición epitelio-mesénquima. Hemos demostrado que el factor GATA -en Drosophila denominado Srp- es necesario para inducir una transición epitelio-mesénquima que da lugar a la relocalización de la proteína E-cadherina sin alterar su expresión. Los factores GATA4 y GATA6 de mamífero también inducen transición epitelio-mesénquima cuando son expresados de forma ectópica en cultivos celulares. Tanto el factor GATA Srp como GATA6 inhiben la transcripción de ortólogos de Crumbs, deslocalizan la E-cadherina y activan genes mesenquimales. Nuestro trabajo ha dado a conocer una nueva ruta alternativa para la transición epitelio-mesénquima que se encuentra conservada evolutivamente y que es independiente de Snail. Este descubrimiento podría tener importantes implicaciones clínicas en patogenia, y más específicamente en la progresión del cáncer. Un tercer aspecto del trabajo presentado se centra en la caracterización de la vía de señalización WNT durante la progresión del CCR. La señalización WNT es necesaria para el mantenimiento de las células madre de cáncer colorectal (CM-CCR), aunque paradójicamente, bajos niveles de genes WNT se asocian con un mayor riesgo de recaída de la enfermedad. Hemos identificado un programa básico de expresión impulsado por beta-catenina/TCF en CM-CCR, que se ha demostrado ser un indicador estricto de la dependencia de señalización WNT para el crecimiento. Hemos demostrado que durante la progresión de la enfermedad, se suprime la expresión de un subconjunto de genes WNT como consecuencia de hipoxia tumoral. Esta respuesta caracteriza a un grupo de pacientes con un muy alto riesgo de reincidencia del cáncer después de la terapia. Los genes inducidos por hipoxia se expresan de manera prominente en frentes de invasión coincidiendo con una menor actividad de la vía del programa WNT. Por lo tanto, la hipoxia refina el programa WNT en CM-CCR durante la adquisición de un fenotipo maligno. Este hallazgo tiene implicaciones importantes para la progresión del CCR, porque explica cómo algunos genes de CM-CCR (como receptores EPHB2) se apagan durante la progresión de la enfermedad y directamente desafía trabajos de alto impacto recientemente reportados en el área, que apuestan por la metilación como mecanismo responsable del refinamiento del programa WNT. Por otra parte, identifica a la hipoxia como un culpable de este fenotipo de células invasivas. Estos hallazgos podrían tener importantes implicaciones clínicas en el tratamiento del cáncer colorectal.
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Bessonnard, Sylvain. "Régulations génétiques contrôlant l'engagement cellulaire au cours du développement murin : différenciation de l'épiblaste versus l'endoderme primitif." Thesis, Clermont-Ferrand 1, 2012. http://www.theses.fr/2012CLF1MM06.

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A 3.5 jours de développement (J3.5), l'embryon de souris est constitué d'un épithélium externe, le trophectoderme, et d'une masse cellulaire interne (MCI). La MCI est hétérogène, constituée des précurseurs de l'épiblaste (Epi) et de l'endoderme primitif (EPr), représentée par l'expression exclusive de Nanog et de Gata6 respectivement. Lors de l'implantation à E4.5, l'EPr forme un épithélium à la surface de la MCI, en regard de la cavité blastocoelique. L'Epi donnera tous les tissus du nouveau-né. L'EPr permet les premiers échanges nutritionnels entre l'embryon et la mère. Je m'intéresse au rôle de Nanog et de Gata6 dans la détermination et la différenciation de l'Epi et de l'EPr. De plus, je m'intéresse à l'implication de la signalisation RTK dans l'expression de ces deux gènes. Enfin, je cherche à comprendre les interrelations entre Gata6 et Nanog. A l'aide des modèles de souris KO, des modèles in vitro ainsi que des techniques innovantes développées au sein du laboratoire, nous avons mis en évidence que la modulation de l'expression de Nanog, Gata6, Fgf4 et Fgfr2 semble suffisante pour l'engagement des cellules vers un devenir Epi ou EPr. De plus, ces résultats permettent de proposer un nouveau modèle expliquant le rôle de Gata6 et de Nanog dans la spécification des cellules Epi et EPr
At 3.5 days of development (E3.5), the mouse embryo consists of an outer epithelium, the trophectoderm, and an inner cell mass (ICM). The ICM is heterogeneous, composed of the precursors of the epiblast (Epi) and the primitive endoderm (PrE), expressing either Nanog or Gata6 respectively. Upon implantation at E4.5 the EPr forms an epithelium on the surface of the ICM, facing the blastocoelic cavity. The Epi give rise all tissues of the newborn. The PrE allows the first nutritional exchanges between the embryo and the mother. I focus on the role of Nanog and Gata6 in the determination and differentiation of Epi and PrE. In addition I am interested in the involvement of RTK signaling in the expression of both genes. Finally, I seek to understand the relationships between Gata6 and Nanog. Using the transgenic mouse models, in vitro models as well as innovative techniques developed in the laboratory, we have demonstrated that modulating the expression of Nanog, Gata6, FGF4 and FGFR2 seems sufficient for commitment of cells to become an Epi or EPr. Furthermore, these results allow proposing a new model explaining the role of Gata6 and Nanog in the determination and differentiation of Epi and PrE cells
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Books on the topic "Gata6"

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Gatan goton gatan goton. Tōkyō: Fukuinkan Shoten, 1987.

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Marklund, Liza. Lyckliga gatan. Stockholm: Piratförlaget, 2013.

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Calvillo, Ignacio Flores. Las Gatas. México: Colibrí, 2000.

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Pál, Jón. Gatan: Ljóðsaga. Reykjavík: Höfundaútgáfan, 2013.

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Calvillo, Ignacio Flores. Las gatas. México, D.F: Leega, 1995.

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Nakashima, Toshiaki. C-gata kan'en B-gata kan'en. Tōkyō: Shufu No Tomosha, 2007.

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Díaz, Rosa. Gata mamá. Madrid: Hiperión Ediciones, 2003.

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Lawal, Nafisa Muda. Allah gatan kowa. Nigeria?: s.n., 2002.

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Năzirli, Shămistan. Goridăn ġălăn gatar. Bakı: Azärbaycan Dövlät Näşriyyatı, 1993.

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Nogueira, Hermelindo Castro. Las salinas de Cabo de Gata: Ecología y dinámica anual de las poblaciones de aves en las salinas de Cabo de Gata (Almería). Almería: Instituto de Estudios Almerienses, 1993.

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Book chapters on the topic "Gata6"

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Moriguchi, Takashi, Mikiko Suzuki, James Douglas Engel, and Masayuki Yamamoto. "GATA1 and GATA2 Function in Hematopoietic Differentiation." In Hematopoietic Stem Cell Biology, 117–42. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-347-3_5.

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Asa, Sylvia L. "GATA2." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-28845-1_5035-1.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "GATA-3 (GATA Binding Protein 3)." In Encyclopedia of Signaling Molecules, 760–69. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_29.

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Ray, Anuradha, Anupriya Khare, Nandini Krishnamoorthy, and Prabir Ray. "GATA-3." In Encyclopedia of Signaling Molecules, 2027–40. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_29.

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Ray, Anuradha, Anupriya Khare, Nandini Krishnamoorthy, and Prabir Ray. "GATA-3." In Encyclopedia of Signaling Molecules, 1–14. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_29-1.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "GATA-Binding Protein 3." In Encyclopedia of Signaling Molecules, 769. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100525.

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Ray, Anuradha, and Prabir Ray. "GATA-3: A Th2-Selective Target." In New Drugs for Asthma, Allergy and COPD, 222–25. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062174.

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Chen, Bohao. "GATA Transcription Factors and Cardiovascular Disease." In Translational Bioinformatics, 127–51. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1429-2_5.

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Hoene, Victoria, and Christof Dame. "Neuroblastoma: Role of GATA Transcription Factors." In Pediatric Cancer, 151–59. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2418-1_14.

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Vannucchi, Alessandro M., Silvia Linari, and Anna Rita Migliaccio. "Expression Of Distal gatal Transcripts in Erythroid Cells." In Molecular Biology of Hematopoiesis 6, 249–55. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4797-6_31.

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Conference papers on the topic "Gata6"

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Singh, Indrabahadur, Aditi Mehta, Nihan Öztürk, Julio Cordero, Adriana Contreras, Diya Hasan, Claudia Cosentino, et al. "HMGA2 mediated epigenetic regulation of Gata6 controls epithelial WNT signaling during lung development." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa3228.

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Al-Jaber, Hend Sultan, Layla Jadea Al-Mansoori, and Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.

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Background: Impaired adipogenesis plays an important role in the development of obesityassociated insulin resistance and type 2 diabetes. Adipose tissue inflammation is a crucial mediator of this process. In hyperglycemia, immune system is activated partially through upregulation of GATA3, causing exacerbation of the inflammatory state associated with obesity. GATA3 also plays a role as a gatekeeper of terminal adipocyte differentiation. Here we are examining the impact of GATA3 inhibition in adipose tissue on restoring adipogenesis, reversing insulin resistance and potentially lowering the risk of type 2 diabetes. Results: GATA-3 expression was higher in insulin resistant obese individuals compared to their insulin sensitive counterparts. Targeting GATA-3 with GATA-3 specific inhibitors reversed impaired adipogenesis and induced changes in the expression of a number insulin signaling-related genes, including up-regulation of insulin sensitivity-related gene and down-regulation of insulin resistance-related genes. Conclusion: GATA3 expression is higher in differentiating adipocytes from obese insulin resistant. Inhibiting GATA3 improves adipocytes differentiation and rescues insulin sensitivity in insulin resistant cells
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Rogerson, C., E. Britton, Y. Ang, and A. Sharrocks. "PO-305 Chromatin accessibility profiling identifies an underlying HNF4A-GATA6 regulatory module in oesophageal adenocarcinoma." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.335.

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Tang, Haoyu, Anup Sharma, Ilke Nalbantoglu, Nesrin Hasan, Andre Levchenko, and Nita Ahuja. "Abstract C54: GATA6 level is a prognostic biomarker for pancreatic cancer in African American patients." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-c54.

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Ichihara, A., T. Toyama, T. Kudryashova, S. Lenna, A. Looney, Y. Shen, T. Avolio, et al. "Endothelial GATA6 Coordinates Cross-Talk Between BMP and Oxidative Stress Axis in Pulmonary Arterial Hypertension." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6363.

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Barreto, Guillermo, Aditi Mehta, Julio Cordero, Stephanie Dobersch, Addi J. Romero-Olmedo, Rajkumar Savai, Johannes Bodner, et al. "Non-invasive lung cancer diagnosis by detection of GATA6 and NKX2-1 isoforms in exhaled breath condensate." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2033.

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Grant, Robert C., Kai Duan, Richard Jackson, William Greenhalf, Eithne Costello-Goldring, Paula Ghaneh, Christopher Halloran, et al. "Abstract PO-005: GATA6 expression is prognostic after surgical resection of pancreatic cancer: results from the ESPAC trials." In Abstracts: AACR Virtual Special Conference on Pancreatic Cancer; September 29-30, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.panca20-po-005.

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Cao, Yuxia, Tyler Longmire, Tiffany Vo, Meenakshi Lakshminarayanan, Di Zhou, Darrell Kotton, and Maria I. Ramirez. "H3K27me3 Demethylases Jmjd3 And/Or UTX Contribute To Activating Expression Of Endoderm And Early Lung Developmental Transcription Factors Foxa2 And Gata6." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3483.

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Akiyama, Yoshimitsu, Hiromi Nagasali, Ayako Kawamoto, James G. Herman, Stephen B. Baylin, and Yasuhito Yuasa. "Abstract 200: Methylation of GATA4 and GATA5 transcription factor genes in gastric cancers." 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.am10-200.

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Grant, Robert C., Kai Duan, Richard Jackson, William Greenhalf, Eithne Costello-Goldring, Paula Ghaneh, Christopher Halloran, et al. "Abstract 1193: Digital quantification of GATA6 expression from immunohistochemistry is associated with overall survival after surgery for pancreatic cancer in the ESPAC trials." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1193.

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Reports on the topic "Gata6"

1

Aksay, Ilhan A., Nan Yao, and Daniel M. Dabbs. Acquisition of the Gatan Image Filter System and an Environmental Cell for an Existing Phillips CM-200 FEG-TEM. Fort Belvoir, VA: Defense Technical Information Center, February 2001. http://dx.doi.org/10.21236/ada387368.

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