Relevant bibliographies by topics / Sox9b

Academic literature on the topic 'Sox9b'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Sox9b"

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Raghuveer, Kavarthapu, and Balasubramanian Senthilkumaran. "Isolation of sox9 duplicates in catfish: localization, differential expression pattern during gonadal development and recrudescence, and hCG-induced up-regulation of sox9 in testicular slices." REPRODUCTION 140, no. 3 (September 2010): 477–87. http://dx.doi.org/10.1530/rep-10-0200.

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In vertebrates, sox9 is a transcription factor that plays a crucial role in testicular development and chondrogenesis. Here, we report cloning of isoforms of sox9 (sox9a and sox9b) from air-breathing catfish Clarias gariepinus, which undergoes an annual reproductive cycle. Tissue distribution pattern showed differential expression of sox9 duplicates, wherein both forms were highly expressed in brain and gonads. Furthermore, we observed a dimorphic expression pattern of sox9a and sox9b in both adult and developing gonads using RT-PCR, indicating that sox9a retained its function in testis while sox9b might have a new role to play in ovary. Changes in sox9 mRNA levels using real-time quantitative PCR (qRT-PCR) during the seasonal reproductive cycle revealed that sox9a transcript in testis was abundant during testicular recrudescence (during spermatogenesis), and its expression significantly decreased during spawning and post-spawning phases. Furthermore, treatments of human chorionic gonadotropin and 11-ketotestosterone in vitro up-regulated sox9a mRNA levels in the testicular slices at 12 and 24 h time points, suggesting that gonadotropins might stimulate sox9 expression. These results suggest that sox9 might have a plausible role in the entrainment of the testicular cycle. In contrast, during the ovarian cycle, sox9b mRNA levels gradually declined from preparatory to post-spawning phases. Immunohistochemical (IHC) data showed that, in testis, sox9 is detectable in Sertoli and spermatogonial cell types except spermatid/spermatozoa. In the ovary, it is localized in the ooplasm of primary and pre-vitellogenic oocytes. These results were further confirmed by whole-mount IHC and qRT-PCR.
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Steeman, Tomás J., Juan A. Rubiolo, Laura E. Sánchez, Nora B. Calcaterra, and Andrea M. J. Weiner. "Conservation of Zebrafish MicroRNA-145 and Its Role during Neural Crest Cell Development." Genes 12, no. 7 (June 30, 2021): 1023. http://dx.doi.org/10.3390/genes12071023.

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The neural crest is a multipotent cell population that develops from the dorsal neural fold of vertebrate embryos in order to migrate extensively and differentiate into a variety of tissues. A number of gene regulatory networks coordinating neural crest cell specification and differentiation have been extensively studied to date. Although several publications suggest a common role for microRNA-145 (miR-145) in molecular reprogramming for cell cycle regulation and/or cellular differentiation, little is known about its role during in vivo cranial neural crest development. By modifying miR-145 levels in zebrafish embryos, abnormal craniofacial development and aberrant pigmentation phenotypes were detected. By whole-mount in situ hybridization, changes in expression patterns of col2a1a and Sry-related HMG box (Sox) transcription factors sox9a and sox9b were observed in overexpressed miR-145 embryos. In agreement, zebrafish sox9b expression was downregulated by miR-145 overexpression. In silico and in vivo analysis of the sox9b 3′UTR revealed a conserved potential miR-145 binding site likely involved in its post-transcriptional regulation. Based on these findings, we speculate that miR-145 participates in the gene regulatory network governing zebrafish chondrocyte differentiation by controlling sox9b expression.
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Russell, Jacquelyn O., Sungjin Ko, Satdarshan P. Monga, and Donghun Shin. "Notch Inhibition Promotes Differentiation of Liver Progenitor Cells into Hepatocytes via sox9b Repression in Zebrafish." Stem Cells International 2019 (March 12, 2019): 1–11. http://dx.doi.org/10.1155/2019/8451282.

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Liver regeneration after most forms of injury is mediated through the proliferation of hepatocytes. However, when hepatocyte proliferation is impaired, such as during chronic liver disease, liver progenitor cells (LPCs) arising from the biliary epithelial cell (BEC) compartment can give rise to hepatocytes to mediate hepatic repair. Promotion of LPC-to-hepatocyte differentiation in patients with chronic liver disease could serve as a potentially new therapeutic option, but first requires the identification of the molecular mechanisms driving this process. Notch signaling has been identified as an important signaling pathway promoting the BEC fate during development and has also been implicated in regulating LPC differentiation during regeneration. SRY-related HMG box transcription factor 9 (Sox9) is a direct target of Notch signaling in the liver, and Sox9 has also been shown to promote the BEC fate during development. We have recently shown in a zebrafish model of LPC-driven liver regeneration that inhibition of Hdac1 activity through MS-275 treatment enhances sox9b expression in LPCs and impairs LPC-to-hepatocyte differentiation. Therefore, we hypothesized that inhibition of Notch signaling would promote LPC-to-hepatocyte differentiation by repressing sox9b expression in zebrafish. We ablated the hepatocytes of Tg(fabp10a:CFP-NTR) larvae and blocked Notch activation during liver regeneration through treatment with γ-secretase inhibitor LY411575 and demonstrated enhanced induction of Hnf4a in LPCs. Alternatively, enhancing Notch signaling via Notch3 intracellular domain (N3ICD) overexpression impaired Hnf4a induction. Hepatocyte ablation in sox9b heterozygous mutant embryos enhanced Hnf4a induction, while BEC-specific Sox9b overexpression impaired LPC-to-hepatocyte differentiation. Our results establish the Notch-Sox9b signaling axis as inhibitory to LPC-to-hepatocyte differentiation in a well-established in vivo LPC-driven liver regeneration model.
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Burns, Felipe R., Kevin A. Lanham, Kong M. Xiong, Alex J. Gooding, Richard E. Peterson, and Warren Heideman. "Analysis of the zebrafish sox9b promoter: Identification of elements that recapitulate organ-specific expression of sox9b." Gene 578, no. 2 (March 2016): 281–89. http://dx.doi.org/10.1016/j.gene.2015.12.041.

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Gao, Ce, Weidong Huang, Yuqi Gao, Li Jan Lo, Lingfei Luo, Honghui Huang, Jun Chen, and Jinrong Peng. "Zebrafish hhex-null mutant develops an intrahepatic intestinal tube due to de-repression of cdx1b and pdx1." Journal of Molecular Cell Biology 11, no. 6 (November 14, 2018): 448–62. http://dx.doi.org/10.1093/jmcb/mjy068.

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Abstract The hepatopancreatic duct (HPD) system links the liver and pancreas to the intestinal tube and is composed of the extrahepatic biliary duct, gallbladder, and pancreatic duct. Haematopoietically expressed-homeobox (Hhex) protein plays an essential role in the establishment of HPD; however, the molecular mechanism remains elusive. Here, we show that zebrafish hhex-null mutants fail to develop the HPD system characterized by lacking the biliary marker Annexin A4 and the HPD marker sox9b. The hepatobiliary duct part of the mutant HPD system is replaced by an intrahepatic intestinal tube characterized by expressing the intestinal marker fatty acid-binding protein 2a (fabp2a). Cell lineage analysis showed that this intrahepatic intestinal tube is not originated from hepatocytes or cholangiocytes. Further analysis revealed that cdx1b and pdx1 are expressed ectopically in the intrahepatic intestinal tube and knockdown of cdx1b and pdx1 could restore the expression of sox9b in the mutant. Chromatin-immunoprecipitation analysis showed that Hhex binds to the promoters of pdx1 and cdx1b genes to repress their expression. We therefore propose that Hhex, Cdx1b, Pdx1, and Sox9b form a genetic network governing the patterning and morphogenesis of the HPD and digestive tract systems in zebrafish.
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Li, Ming, Chengtian Zhao, Ying Wang, Zhixing Zhao, and Anming Meng. "Zebrafish sox9b is an early neural crest marker." Development Genes and Evolution 212, no. 4 (April 18, 2002): 203–6. http://dx.doi.org/10.1007/s00427-002-0235-2.

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Guo, Huiping, Xinlu Du, Ying Zhang, Jiacheng Wu, Chenghui Wang, Mingyou Li, Xianxin Hua, Xin A. Zhang, and Jizhou Yan. "Specific miRNA-G Protein-Coupled Receptor Networks Regulate Sox9a/Sox9b Activities to Promote Gonadal Rejuvenation in Zebrafish." STEM CELLS 37, no. 9 (July 8, 2019): 1189–99. http://dx.doi.org/10.1002/stem.3040.

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Plavicki, Jessica S., Tracie R. Baker, Felipe R. Burns, Kong M. Xiong, Alex J. Gooding, Peter Hofsteen, Richard E. Peterson, and Warren Heideman. "Construction and characterization of a sox9b transgenic reporter line." International Journal of Developmental Biology 58, no. 9 (2014): 693–99. http://dx.doi.org/10.1387/ijdb.140288jp.

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Rodríguez-Marí, Adriana, Yi-Lin Yan, Ruth A. BreMiller, Catherine Wilson, Cristian Cañestro, and John H. Postlethwait. "Characterization and expression pattern of zebrafish anti-Müllerian hormone (amh) relative to sox9a, sox9b, and cyp19a1a, during gonad development." Gene Expression Patterns 5, no. 5 (June 2005): 655–67. http://dx.doi.org/10.1016/j.modgep.2005.02.008.

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Delous, Marion, Chunyue Yin, Donghun Shin, Nikolay Ninov, Juliana Debrito Carten, Luyuan Pan, Taylur P. Ma, Steven A. Farber, Cecilia B. Moens, and Didier Y. R. Stainier. "sox9b Is a Key Regulator of Pancreaticobiliary Ductal System Development." PLoS Genetics 8, no. 6 (June 14, 2012): e1002754. http://dx.doi.org/10.1371/journal.pgen.1002754.

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Dissertations / Theses on the topic "Sox9b"

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Heß, Isabell. "Zum regulatorischen Code Chorda-spezifischer Enhancer Analyse des E1-Enhancers von sox9a und sox9b im Zebrafisch /." [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-43665.

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Farhat, Andalib. "Implication de la voie Prostaglandine D synthase/PGD2/SOX9 dans l'ovaire normal et pathologique et régulation par la signalisation estrogénique." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20206.

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L'ovaire représente à la fois un organe cible et le principal organe producteur d'estrogènes et de progestérone qui maintiennent le développement des caractères sexuels féminins et une fonction de reproduction normale. Cette production hormonale est contrôlée par les gonadotropines FSH et LH produites dans l'hypophyse, responsables dans l'ovaire de la croissance folliculaire et de l'ovulation, respectivement. Mon travail de thèse a identifié la signalisation prostaglandine D2 (PGD2), comme un nouvel élément-clé dans la signalisation des gonadotropines, contribuant à l'activation de l'expression des récepteurs FshR et LhR et des enzymes de la stéroïdogenèse SCC et StAR. La PGD2, produite dans plusieurs tissus par deux enzymes de synthèse, les prostaglandines synthases H et L-PGDS, est impliquée dans de nombreuses fonctions physiologiques et pathologiques. Comme dans l'ovaire pathologique, nous avons montré que la PGD2 avait aussi un rôle anti-prolifératif dans la cellule de granulosa de l'ovaire normal. Le cancer de l'ovaire représente la 4ème cause de mortalité par cancer chez la femme. Les mécanismes moléculaires impliqués dans le développement de ces tumeurs sont encore peu connus, bien que l'implication des estrogènes et de la Prostaglandine E2 (PGE2) dans la progression des tumeurs ovariennes épithéliales soit bien établie. D'autre part, les ovaires des souris invalidées pour les gènes codant les récepteurs aux estrogènes ou l'aromatase, possèdent des structures tubulaires contenant des cellules de Leydig et des cellules de Sertoli re-différenciées exprimant le facteur de détermination sexuelle mâle SOX9, alors qu'il n'est pas exprimé dans l'ovaire sain. Mon travail a montré que les estrogènes inhibent la transcription des gènes Sox9 et L-Pgds dans les lignées ovariennes tumorales BG1 et COV434 et que cette régulation est la résultante d'une inhibition, via le récepteur ERa et d'une activation via le récepteur ERß. Ces résultats sont en accord avec les études sur les effets prolifératifs d'ERa et le rôle anti-prolifératif d'ERß et suggèrent donc un rôle anti-prolifératif de la PGD2 dans l'ovaire tumoral et une régulation négative directe ou indirecte de l'expression de Sox9 et des Pgds par les estrogènes
The prostaglandin D2 (PGD2) pathway is involved in numerous biological processes and while it has been identified as a partner of the embryonic sex determining male cascade, the roles it plays in ovarian function remain largely unknown. PGD2 is secreted by two prostaglandin D synthases (Pgds); the male-specific lipocalin (L)-Pgds and the hematopoietic (H)-Pgds. Here, we report the localization of H-Pgds mRNA in the granulosa cells from the primary to pre-ovulatory follicles. We used adult female mice treated with HQL-79, a specific inhibitor of H-Pgds enzymatic activity, to provide evidence of an interaction between H-Pgds-produced PGD2 signaling and FSH signaling. This leads to the activation of steroidogenic Scc and StAR gene expression through increased FshR and LhR receptor expression leading to progesterone secretion. We also identify a role whereby H-Pgds-produced PGD2 is involved in the regulation of follicular growth through inhibition of granulosa cell proliferation in the growing follicles. Indeed, we report an altered H-Pgds expression in human ovarian tumors alongside a partial or complete absence of H-Pgds protein in granulosa cell tumors, suggesting a potential association between decreased levels of H-Pgds expression and a tumoral phenotype. Together, these results show PGD2 signaling to be essential for FSH action within granulosa cells, thus identifying an important and unappreciated role for PGD2 signaling in controlling the balance of proliferation, differentiation and steroidogenic activity of these cells
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Zhao, Li. "The role of Sox9 in osteogenesis." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486259.

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Bone fOlmation is an exquisitely coordinated process involving both chondrogenic and osteogenic differentiation. SOX9 is the best-known master regulator for chondrocyte differentiation and cartilage formation. Herein we demonstrate that SOX9 also participates in osteogenic differentiation;bone formation, and the action is interlocked with cAMPIPKA signaling at multilevel. Together with osteogenic markers such as Runx2, ColI a I and osteopontin, SOX9 was up-regulated in the early osteogenic stage of primary MSCs as well as in BMP-2-indued osteoblast differentiation ofC3HlOTl/2 and C2C12 cells. Overexpression of wild-type SOX9 in the progenitor cells efficiently propelled expression of multiple osteogenic marker genes such as ALP activity, type I collagen and osteocalcin expression. The promoter of the type I collagen gene was activated by SOX9. However, pathogenic mutants showed impaired osteogenesis. Furthermore, SOX9 knockdown in the bone progenitor cells inhibited osteogenic differentiation. In vivo, SOX9 overexpression in C3HIOTl12 cells slightly increased bone formation quantity, while SOX9 knockdown significantly blocked development of bone. During signaling investigation, we found the removal of PKA-phosphorylation sites of SOX9 deprived it of stimulatory effect. Chemicals specifically activating or inhibiting PKA signaling and the cognate inhibitor of PKA, PKIy, distinctly affected the SOX9 action. Fmihennore, we provide evidence that through i,ts carboxyl tenninal domain, SOX9 physically and functionally interacts with CREB, the prototypical PKA-downstream transcription factor. Thus, these results suggest that in addition to the predominate role in driving chondrogenesis, SOX9 also plays a novel role by promoting osteogenesis, which is, at both the nuclear and cytoplasmic levels, orchestrated with the PKA pathway during bone formation.
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Savov, Vasil. "The Role of SOX9 in Medulloblastoma." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-274630.

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Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Overall survival is about 70% and in cases where current treatment fails, the disease recurs and most often is fatal. At the molecular level, MB can be divided into four defined subgroups: WNT, SHH, Group 3 and Group 4. Amplification of MYC family genes is common in MB and correlates with poor prognosis and tumor relapse. In this thesis we showed how MYCN initiates brain tumors when transduced in neural stem cells (NSCs). Prior to transduction, NSCs were isolated from different brain regions and at various time points. While overexpression of wild-type MYCN did not generate any tumors, orthotopic transplantation of MYCNT58A-expressing forebrain, brain stem and cerebellar NSCs induced diffuse malignant glioma, PNET-like tumors and MB, respectively. Interestingly, MYCNT58A-expressing cerebellar NSCs induced SHH-dependent MB from embryonic cells but SHH-independent MB from postnatal cells. We further showed that cerebellar NSCs transduced with both MYCNT58A and transcription factor SOX9 developed tumors faster and promoted distant migration into the forebrain. The function and regulation of SOX9 in MB cells is poorly understood. We identified SOX9 protein as target of FBW7 ubiquitin ligase and demonstrated the effects of SOX9 on MB cells migration, metastasis and drug resistance. We further blocked PI3K pathway to destabilize SOX9 which sensitized cells to cytostatic treatment. We used a (TetOFF) transgenic mouse model of MYCN-induced MB (GTML) and crossed it with a (TetON) transgene which allowed us to specifically target rare SOX9-positive cells in the tumor. In this system, MB develops spontaneously and SOX9-negative tumor cells can be killed off by doxycycline. The few remaining SOX9-positive cancer cells were able to promote distant MB recurrences. Such a pattern of relapse was recently shown for Group 3 and 4 human MB where about 90% of the recurrences were distant. In summary, this thesis demonstrates that MYCN can generate various types of brain tumors depending on the timing and location of its expression. It further defines the existence of a rare population of SOX9-expressing MB cells that are involved in causing distant MB recurrences. Finally, it describes how SOX9 is stabilized in MB cells and increases MB migration and therapy resistance.
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Hargus, Gunnar. "Die Funktion des Transkriptionsfaktors Sox9 während der Knorpelzelldifferenzierung Analyse Sox9-defizienter embryonaler Stammzellen der Maus in vitro /." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=976144824.

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Geng, Yuhong, and 耿雨紅. "Functional studies of SOX9 in mouse development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243071.

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Abdel-Samad, Rana. "SOX9 et MiniSOX9 dans la tumorigenèse intestinale." Thesis, Montpellier 2, 2010. http://www.theses.fr/2010MON20068.

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SOX9 est un facteur de transcription à domaine HMG. Il est impliqué dans de multiples processus biologiques au cours du développement et de la vie adulte. En particulier, SOX9 joue un rôle important dans l'homéostasie de l'épithélium intestinal. Nous avons montré que SOX9, cible positive de la voie de signalisation oncogénique Wnt/(beta)-caténine, réprime l'expression de PKC(alpha). Cette répression implique un nouveau mécanisme d'action qui ne nécessite ni la fixation du domaine HMG à l'ADN ni le domaine de transactivation de SOX9. Nous avons également identifié MiniSOX9, un nouveau variant d'épissage de SOX9, résultant de la rétention du second intron. MiniSOX9 est fortement exprimé dans les tumeurs coliques. Il agit en tant que dominant négatif de SOX9, inhibiteur de l'expression du suppresseur de tumeurs PKC(alpha) et activateur de la voie de signalisation oncogénique Wnt/(beta)-caténine. Nos données suggèrent ainsi un rôle primordial de MiniSOX9 dans la tumorigenèse intestinale. Enfin, notre étude protéomique des partenaires de SOX9 et de MiniSOX9 permet d'ouvrir de nouvelles perspectives quant aux rôles de ces deux protéines dans l'homéostasie et la tumorigenèse intestinale
SOX9 is an HMG transcription factor involved in numerous biological processes during development and adult life. It plays an important role especially in the intestinal epithelium homeostasis. In the present study, we demonstrate that SOX9, a positive target of the oncogenic signaling pathway Wnt/(beta)-catenin, represses PKC(alpha) expression. This repression involves a new mechanism of action requiring neither HMG domain binding to DNA nor the transactivation domain of SOX9. We also report the discovery of MiniSOX9, a new SOX9 splice variant, resulting from the second intron retention. MiniSOX9 is highly expressed in colon tumors. It acts as a SOX9 dominant negative, as a repressor of the expression of the tumor suppressor PKC(alpha), and as an activator of the oncogenic signaling pathway Wnt/(beta)-catenin. Our data suggest a crucial role of MiniSOX9 in intestinal tumorigenesis. Finally, a proteomic analysis allowed us to identify potential new SOX9 and MiniSOX9 partners which will be useful to decipher the roles of these two proteins in intestinal homeostasis and tumorigenesis
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Scull, Brooks Lund P. Kay. "Intestinal regeneration after irradiation stem cells and Sox9 /." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2852.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree Master of Science in the Department of Cell and Molecular Physiology." Discipline: Cell and Molecular Physiology; Department/School: Medicine.
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Nunn, A. C. "The role of SOX9 in neural progenitor identity." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1372652/.

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Recent evidence has shown that SOX9 is required for the proliferation and multipotentiality of neural progenitors in the developing CNS. Notably, these findings suggest that in contrast to previous studies, SOX9 is important for differentiation along the neuronal lineage, both in the adult and embryonic CNS. Here, a phenotypic analysis of the CNS-specific Sox9-null forebrain, including detailed analysis of cortical lamination, shows that neurons of the appropriate layer-identity are born and migrate to their destined layers. All other parameters in this analysis were normal, with the exception of the formation of glia from the ventral and dorsal telencephalons, and midline glial structures, which were absent in the mutant. Since Sox9 is expressed long before the onset of gliogenesis in these brain regions, the possibility that Sox9 may ‘prime’ the progenitors of the ventricular zone to respond to a gliogenic signal arose. To investigate this, populations of Sox9-deficient and wild-type dorsal telencephalon cells were enriched for progenitors and subjected to transcriptional profiling. Bioinformatic analysis revealed that ‘vascular endothelial growth factor’ receptors, which are important for gliogenesis, were down-regulated, in addition to two transcription factors. Previously, Sox9-deficient neural progenitors have been shown to generate neurospheres poorly, and so the dataset of potential targets was used to identify candidates that might mediate this reduced neurosphere-forming ability. Thirteen down-regulated targets were confirmed by qPCR, six of which were expressed in the same distribution as Sox9 in the embryonic telencephalon; three were also expressed in neurosphere cultures. Of these, one encoded a K+ channel (Kir4.1), and the other a modulator of the GABAA channel (DBI). In order to show that reduced expression of one of these might contribute to the Sox9-deficient neurosphere phenotype, pharmacological modulators were used and showed that blockade of Kir4.1 or enhancement of GABAA channels mimicked the effect of Sox9 loss, leaving open the possibility that Kir4.1 or DBI expression might mediate this effect.
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Roberts, Neil Alistair. "The role of SOX9 during human pancreas development." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-sox9-during-human-pancreas-development(dab5d8da-4c02-4592-b05e-471984461dcc).html.

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The work presented in this thesis is a study of human pancreas development. The principle goal of this work is to provide information that can be used in the development of treatments for Type 1 Diabetes and in pancreas regeneration methodologies. The transcription factor (TF) sex determining region Y homeobox gene 9 (SOX9) has been identified as a key factor in human pancreas development but its role has not been well characterized. The expression of SOX9 during early pancreas development was analyzed by immunostaining of fixed embryonic and fetal sections in the context of other developmentally important TFs. Modulators of SOX9 function, downstream targets and upstream regulatory pathways were investigated in human cell lines using coimmunoprecipitation, small interfering RNA (siRNA) knockdown, quantitative polymerase chain reaction (qPCR), luciferase assays and small molecule signaling pathway inhibitors. SOX9 was expressed in epithelial progenitors from initial human pancreas specification, but became excluded from the periphery of the epithelium and developing islet cells as differentiation proceeded. It was co-expressed with important endocrine and exocrine differentiation factors during the early stages of development. Some factors, such as Nirenberg and Kim 2, homeobox family member, drosophila, homolog of, 2 (NKX2.2) showed differing expression profile compared to murine development, while the widespread expression of endocrine factors before expression of the pro-endocrine gene neurogenin 3 (NGN3) suggested that these factors play an important role in initiating endocrine specification. Two transcription factors, GATA-binding protein 4 (GATA4) and neurogenic differentiation 1 (NEUROD1), were found to interact with SOX9 in potentially developmentally relevant complexes. This prompted the search for downstream targets of these transcriptional complexes by in silico analysis, which identified an array of novel potential downstream targets. Luciferase assay analysis of a subset of these genes showed SOX9 to activate a regulatory region of NGN3, and inhibit the regulatory regions of carboxy peptidase A6 (CPA6), v-ets avian erythroblastosis virus E26 oncogene homolog1 (ETS1) and SPONDIN1. An additional target of SOX9, osteopontin (OPN), was identified from a microarray of Sox9 knockout mouse pancreata. Investigation of SOX9 and OPN regulation by the Hedgehog signalling pathway (HH) identified both factors to be regulated by the pathway, suggesting SOX9 may act as a mediator of HH signalling. This is the first study to identify a range of SOX9 targets relevant to human pancreas development. While further characterization is required this work has provided essential clues to the function of SOX9, and provides a detailed framework of SOX9 expression and targets for future pancreatic studies to build upon.
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Book chapters on the topic "Sox9b"

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Koopman, Peter. "Sry, Sox9 and mammalian sex determination." In Experientia Supplementum, 25–56. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-7781-7_3.

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Guo, Jian-Kan, Annette Hammes, Marie-Christine Chaboissier, Valerie Vidal, Yiming Xing, Frances Wong, and Andreas Schedl. "Early Gonadal Development: Exploring Wt1 and Sox9 Function." In The Genetics and Biology of Sex Determination, 23–34. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868732.ch3.

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Harley, Vincent R. "The Molecular Action of Testis-Determining Factors SRY and SOX9." In The Genetics and Biology of Sex Determination, 57–67. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868732.ch6.

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Yokoi, Hayato, and John H. Postlethwait. "Genome Duplication and Subfunction Partitioning: Sox9 in Medaka and Other Vertebrates." In Medaka, 323–37. Tokyo: Springer Japan, 2011. http://dx.doi.org/10.1007/978-4-431-92691-7_21.

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Liao, Junyi, Ning Hu, Nian Zhou, Chen Zhao, Xi Liang, Hong Chen, Wei Xu, Cheng Chen, Qiang Cheng, and Wei Huang. "Sox9 Potentiates BMP2-Induced Chondrogenic Differentiation and Inhibits BMP2-Induced Osteogenic Differentiation." In Regenerative Medicine and Plastic Surgery, 263–80. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19962-3_19.

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Camaj, P., I. Ischenko, H. Seeliger, A. Renner, S. Krebs, G. J. Arnold, M. K. Angele, K. W. Jauch, and C. J. Bruns. "Sox9-assozierte Überexpression des IFIT3 Gens unterstützt Pankreastumorprogression durch Aktivierung »Pseudoentzündlicher« Signaltransduktionwege." In Chirurgisches Forum und DGAV Forum 2010, 59–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12192-0_22.

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Suzuki, Yuji, Tokio Sasaki, Keisuke Kakisaka, Hiroaki Abe, and Yasuhiro Takikawa. "Evaluation of SOX9-Positive Hepatocytes in Human Liver Specimens and Mature Mouse Hepatocytes." In Methods in Molecular Biology, 217–25. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2557-6_16.

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Gordon, Christopher T., Sabina Benko, Jeanne Amiel, and Stanislas Lyonnet. "Cis-Regulatory Disruption at the SOX9 Locus as a Cause of Pierre Robin Sequence." In Gene Regulatory Sequences and Human Disease, 123–36. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1683-8_7.

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Liao, Junyi, Ning Hu, Nian Zhou, Chen Zhao, Xi Liang, Hong Chen, Wei Xu, Cheng Chen, Qiang Cheng, and Wei Huang. "Correction to: Sox9 Potentiates BMP2-Induced Chondrogenic Differentiation and Inhibits BMP2-Induced Osteogenic Differentiation." In Regenerative Medicine and Plastic Surgery, C1—C8. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-19962-3_32.

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Qiu, Boning, Ruben J. de Vries, and Massimiliano Caiazzo. "Direct Cell Reprogramming of Mouse Fibroblasts into Functional Astrocytes Using Lentiviral Overexpression of the Transcription Factors NFIA, NFIB, and SOX9." In Methods in Molecular Biology, 31–43. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_3.

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Conference papers on the topic "Sox9b"

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Лебедева, Елена, Анатолий Щастный, and Андрей Бабенко. "Токсическое поражение печени стимулирует дифференцировку СК19+/SOX9+ клеток внутрипеченочных желчных протоков и проточков в холангиоциты и гепатоциты." In Международная научная и методическая конференция, посвященная году фундаментальных наук: "Современные аспекты морфологии, патоморфологии и онкопатологии организма человека". ФГБОУ ВО КГМУ Минздрава России, 2022. http://dx.doi.org/10.21626/cb.22.humanmorphology/14.

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В настоящее временя клеточно-молекулярные механизмы регенерации и резервные возможности печени при ее токсическом поражении до конца не изучены. Цель работы – выяснить роль СК19+ и SOX9+ клеток на разных стадиях токсического поражения печени.
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SUZUKI, TAKASHI, DAISUKE SAKAI, NORIKO OSUMI, and YOSHIO WAKAMATSU. "EXPRESSION OF Sox9-INTERACTING PROTEIN SC35/Sfrs2 IN AVIAN EMBRYOS." In Proceedings of the Final Symposium of the Tohoku University 21st Century Center of Excellence Program. IMPERIAL COLLEGE PRESS, 2006. http://dx.doi.org/10.1142/9781860948800_0022.

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Campos, Ligia Ribeiro de, Maria Luiza Lyczacovski Riesemberg, Maria Victória Ferreira Piccoli, and Milene Krefer Machado. "MECANISMOS GÊNICOS RELACIONADOS ÀS ETAPAS DO PROCESSO EMBRIONÁRIO DE DIFERENCIAÇÃO SEXUAL." In I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3218.

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Introdução: A diferenciação sexual ocorre em torno da sétima semana após a fertilização, que estabelece o sexo cromossômico. Esse processo é mediado por genes, os quais, expressos ou não, geram uma cascata de fatores e hormônios que diferenciam morfológica e funcionalmente estruturas primitivas do embrião resultando na manifestação sexual fenotípica. Objetivos: Destacar a implicação dos genes SRY, DAX 1 e SOX9, bem como fatores e hormônios decorrentes da expressão ou não desses no fenômeno de diferenciação sexual. Assim como diferenças entre esses processos conforme o sexo cromossômico. Metodologia: Este estudo consistiu em uma revisão literária de artigos escritos em inglês e português publicados nas bases de dados “Pubmed”, “Scielo”, no período entre 2000 e 2021. Resultados: Com base na análise literária, destaca-se o processo de diferenciação gonadal no período embrionário, através das características e importância de cada gene. A princípio, o fator determinante testicular (TDF) é responsável por ativar o gene SOX9, que tem sua expressão evidenciada nas células de Sertoli e ausente no tecido ovariano. Tal fator - codificado pelo gene SRY e expresso pelas células somáticas dos cordões sexuais masculinos - auxilia na diferenciação primeiramente de células de Sertoli e secundariamente em células de Leydig, que em conjunto formam os testículos. Ademais, os ductos paramesonéfricos regridem devido à secreção do hormônio antimulleriano (MIF) e os mesonéfricos mantêm-se, em seguida com o auxílio da di-hidrotestosterona, diferenciam-se em genitália externa masculina. Enquanto em indivíduos do sexo feminino, que não expressam o gene SRY e o TDF mas sim o DAX-1, há a inibição da formação testicular. Bem como, os fatores Wnt4 e Rspo1 estimulam a diferenciação de células foliculares em ovogônias e, por fim, a formação dos ovários. Ocorre também a não regressão dos ductos paramesonéfricos devido à ausência de MIF, permitindo o desenvolvimento das estruturas da genitália interna feminina. Conclusão: Evidencia-se, então, o destaque da atuação gênica bem como o desencadeamento de fatores e hormônios relacionados a ela quanto o fenômeno embriogênico da diferenciação sexual.
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Dong, Shiwu, Bo Yang, Dajun Ying, and Zhao Xie. "Chondrogenic Differentiation of MSCs Induced via Cbfa1 Driven by SOX9 Promoter." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5517448.

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Pinho, Andreia V., Adrien Grimont, Mark J. Cowley, Cecile Augereau, Amanda Mawson, Marc Giry-Laterriere, Geraldine Van den Steen, et al. "Abstract LB-73: SOX9 regulates EGFR/ERBB signaling in pancreatic cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-73.

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Deng, Wentao, and J. Michael Ruppert. "Abstract 4029: Sox9 functions downstream of Hedgehog-Gli1 in epithelial transformation." 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.am10-4029.

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Merkes, Chris, Timothy K. Turkalo, Nicole Wilder, Hyewon Park, and Mizuki Azuma. "Abstract 73: Ewing's sarcoma Ewsa protein regulates Sox9 during skeletogenesis in zebrafish." 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.am2014-73.

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Gajjala, P. R., D. Soundararajan, R. K. Kasam, D. Sinner, S. K. Huang, A. Jegga, and S. K. Madala. "SOX9 Is a Positive Regulator of Fibroblast Activation in Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4406.

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Laid, Lina, Sokratia Georgaka, Alexandra Njegic, Kara Simpson, Nigel Hammond, Min Zi, Elliot Jokl, Elizabeth Cartwright, and Karen Piper Hanley. "BS23 Spatial transcriptomics provides a mechanistic insight into SOX9 mediated cardiac fibrosis." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.203.

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Zuo, Wei, Ting Zhang, and Tao Ren. "Regeneration of functional lung by adult human SOX9+ airway basal cell transplantation." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa589.

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Reports on the topic "Sox9b"

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Yuan, Xin. SOX9 Is a Progressive Factor in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada593774.

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Plymate, Stephen R. Superoxide Dismutase and Transcription Factor sox9 as Mediators of Tumor Suppression by mac25 (IGFBP-rp1) in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2006. http://dx.doi.org/10.21236/ada463476.

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