Relevant bibliographies by topics / SoxB

Academic literature on the topic 'SoxB'

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

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Journal articles on the topic "SoxB"

1

Friedrich, Cornelius G., Armin Quentmeier, Frank Bardischewsky, Dagmar Rother, Regine Kraft, Susanne Kostka, and Heino Prinz. "Novel Genes Coding for Lithotrophic Sulfur Oxidation of Paracoccus pantotrophus GB17." Journal of Bacteriology 182, no. 17 (September 1, 2000): 4677–87. http://dx.doi.org/10.1128/jb.182.17.4677-4687.2000.

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ABSTRACT The gene region coding for lithotrophic sulfur oxidation ofParacoccus pantotrophus GB17 is located on a 13-kb insert of plasmid pEG12. Upstream of the previously described six open reading frames (ORFs) soxABCDEF with a partial sequence ofsoxA and soxF (C. Wodara, F. Bardischewsky, and C. G. Friedrich, J. Bacteriol. 179:5014–5023, 1997), 4,350 bp were sequenced. The sequence completed soxA, and uncovered six new ORFs upstream of soxA, designated ORF1, ORF2, and ORF3, and soxXYZ. ORF1 could encode a 275-amino-acid polypeptide of 29,332 Da with a 61 to 63% similarity to LysR transcriptional regulators. ORF2 could encode a 245-amino-acid polypeptide of 26,022 Da with the potential to form six transmembrane helices and with a 48 to 51% similarity to proteins involved in redox transport in cytochrome c biogenesis. ORF3 could encode a periplasmic polypeptide of 186 amino acids of 20,638 Da with a similarity to thioredoxin-like proteins and with a putative signal peptide of 21 amino acids. Purified SoxXA, SoxYZ, and SoxB are essential for thiosulfate or sulfite-dependent cytochrome creduction in vitro. N-terminal and internal amino acid sequences identified SoxX, SoxY, SoxZ, and SoxA to be coded by the respective genes. The molecular masses of the mature proteins determined by electrospray ionization spectroscopy (SoxX, 14,834 Da; SoxY, 11,094 Da; SoxZ, 11,717 Da; and SoxA, 30,452 Da) were identical or close to those deduced from the nucleotide sequence with differences for the covalent heme moieties. SoxXA represents a novel type of periplasmicc-type cytochromes, with SoxX as a monoheme and SoxA as a hybrid diheme cytochrome c. SoxYZ is an as-yet-unprecedented soluble protein. SoxY has a putative signal peptide with a twin arginine motif and possibly cotransports SoxZ to the periplasm. SoxYZ neither contains a metal nor a complex redox center, as proposed for proteins likely to be transported via the Tat system.
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2

Rother, Dagmar, Grazyna Orawski, Frank Bardischewsky, and Cornelius G. Friedrich. "SoxRS-mediated regulation of chemotrophic sulfur oxidation in Paracoccus pantotrophus." Microbiology 151, no. 5 (May 1, 2005): 1707–16. http://dx.doi.org/10.1099/mic.0.27724-0.

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Paracoccus pantotrophus GB17 requires thiosulfate for induction of the sulfur-oxidizing (Sox) enzyme system. The soxRS genes are divergently oriented to the soxVWXYZA–H genes. soxR predicts a transcriptional regulator of the ArsR family and soxS a periplasmic thioredoxin. The homogenote mutant GBΩS carrying a disruption of soxS by the Ω-kanamycin-resistance-encoding interposon expressed a low thiosulfate-oxidizing activity under heterotrophic and mixotrophic growth conditions. This activity was repressed by complementation with soxR, suggesting that SoxR acts as a repressor and SoxS is essential for full expression. Sequence analysis uncovered operator characteristics in the intergenic regions soxS–soxV and soxW–soxX. In each region a transcription start site was identified by primer extension analysis. Both regions were cloned into the vector pRI1 and transferred to P. pantotrophus. Strains harbouring pRI1 with soxS–soxV or soxW–soxX expressed the sox genes under heterotrophic conditions at a low rate, indicating repressor titration. Sequence analysis of SoxR suggested a helix–turn–helix (HTH) motif at position 87–108 and uncovered an invariant Cys-80 and a cysteine residue at the C-terminus. SoxR was overproduced in Escherichia coli with an N-terminal His6-tag and purified to near homogeneity. Electrophoretic gel mobility shift assays with SoxR retarded the soxS–soxV region as a single band while the soxW–soxX region revealed at least two protein–DNA complexes. These data demonstrated binding of SoxR to the relevant DNA. This is believed to be the first report of regulation of chemotrophic sulfur oxidation at the molecular level.
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3

Rother, Dagmar, Hans-Jürgen Henrich, Armin Quentmeier, Frank Bardischewsky, and Cornelius G. Friedrich. "Novel Genes of the sox Gene Cluster, Mutagenesis of the Flavoprotein SoxF, and Evidence for a General Sulfur-Oxidizing System in Paracoccus pantotrophusGB17." Journal of Bacteriology 183, no. 15 (August 1, 2001): 4499–508. http://dx.doi.org/10.1128/jb.183.15.4499-4508.2001.

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ABSTRACT The novel genes soxFGH were identified, completing the sox gene cluster of Paracoccus pantotrophus coding for enzymes involved in lithotrophic sulfur oxidation. The periplasmic SoxF, SoxG, and SoxH proteins were induced by thiosulfate and purified to homogeneity from the soluble fraction.soxF coded for a protein of 420 amino acids with a signal peptide containing a twin-arginine motif. SoxF was 37% identical to the flavoprotein FccB of flavocytochrome csulfide dehydrogenase of Allochromatium vinosum. The mature SoxF (42,832 Da) contained 0.74 mol of flavin adenine dinucleotide per mol. soxG coded for a novel protein of 303 amino acids with a signal peptide containing a twin-arginine motif. The mature SoxG (29,657 Da) contained two zinc binding motifs and 0.90 atom of zinc per subunit of the homodimer. soxH coded for a periplasmic protein of 317 amino acids with a double-arginine signal peptide. The mature SoxH (32,317 Da) contained two metal binding motifs and 0.29 atom of zinc and 0.20 atom of copper per subunit of the homodimer. SoxXA, SoxYZ, SoxB, and SoxCD (C. G. Friedrich, A. Quentmeier, F. Bardischewsky, D. Rother, R. Kraft, S. Kostka, and H. Prinz, J. Bacteriol. 182:4476–4487, 2000) reconstitute a system able to perform thiosulfate-, sulfite-, sulfur-, and hydrogen sulfide-dependent cytochrome c reduction, and this system is the first described for oxidizing different inorganic sulfur compounds. SoxF slightly inhibited the rate of hydrogen sulfide oxidation but not the rate of sulfite or thiosulfate oxidation. From use of a homogenote mutant with an in-frame deletion insoxF and complementation analysis, it was evident that the soxFGH gene products were not required for lithotrophic growth with thiosulfate.
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4

Turner, Monte E., Daniel Ely, Jeremy Prokop, and Amy Milsted. "Sry, more than testis determination?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 3 (September 2011): R561—R571. http://dx.doi.org/10.1152/ajpregu.00645.2010.

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The Sry locus on the mammalian Y chromosome is the developmental switch responsible for testis determination. Inconsistent with this important function, the Sry locus is transcribed in adult males at times and in tissues not involved with testis determination. Sry is expressed in multiple tissues of the peripheral and central nervous system. Sry is derived from Sox3 and is similar to other SOXB family loci. The SOXB loci are responsible for nervous system development. Sry has been demonstrated to modulate the catecholamine pathway, so it should have functional consequences in the central and peripheral nervous system. The nervous system expression and potential function are consistent with Sry as a SOXB family member. In mammals, Sox3 is X-linked and undergoes dosage compensation in females. The expression of Sry in adult males allows for a type of sexual differentiation independent of circulating gonadal hormones. A quantitative difference in Sox3 plus Sry expression in males vs. females could drive changes in the transcriptome of these cells, differentiating male and female cells. Sry expression and its transcriptional effects should be considered when investigating sexual dimorphic phenotypes.
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5

Haseeb, Abdul, and Véronique Lefebvre. "The SOXE transcription factors—SOX8, SOX9 and SOX10—share a bi-partite transactivation mechanism." Nucleic Acids Research 47, no. 13 (June 13, 2019): 6917–31. http://dx.doi.org/10.1093/nar/gkz523.

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Abstract SOX8, SOX9 and SOX10 compose the SOXE transcription factor group. They govern cell fate and differentiation in many lineages, and mutations impairing their activity cause severe diseases, including campomelic dysplasia (SOX9), sex determination disorders (SOX8 and SOX9) and Waardenburg-Shah syndrome (SOX10). However, incomplete knowledge of their modes of action limits disease understanding. We here uncover that the proteins share a bipartite transactivation mechanism, whereby a transactivation domain in the middle of the proteins (TAM) synergizes with a C-terminal one (TAC). TAM comprises amphipathic α-helices predicted to form a protein-binding pocket and overlapping with minimal transactivation motifs (9-aa-TAD) described in many transcription factors. One 9-aa-TAD sequence includes an evolutionarily conserved and functionally required EΦ[D/E]QYΦ motif. SOXF proteins (SOX7, SOX17 and SOX18) contain an identical motif, suggesting evolution from a common ancestor already harboring this motif, whereas TAC and other transactivating SOX proteins feature only remotely related motifs. Missense variants in this SOXE/SOXF-specific motif are rare in control individuals, but have been detected in cancers, supporting its importance in development and physiology. By deepening understanding of mechanisms underlying the central transactivation function of SOXE proteins, these findings should help further decipher molecular networks essential for development and health and dysregulated in diseases.
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6

Zhu, Chuankun, Lei Zhang, Huaiyu Ding, and Zhengjun Pan. "Transcriptome-wide identification and characterization of the Sox gene family and microsatellites for Corbicula fluminea." PeerJ 7 (October 22, 2019): e7770. http://dx.doi.org/10.7717/peerj.7770.

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The Asian clam, Corbicula fluminea, is a commonly consumed small freshwater bivalve in East Asia. However, available genetic information of this clam is still limited. In this study, the transcriptome of female C. fluminea was sequenced using the Illumina HiSeq 2500 platform. A total of 89,563 unigenes were assembled with an average length of 859 bp, and 36.7% of them were successfully annotated. Six members of Sox gene family namely SoxB1, SoxB2, SoxC, SoxD, SoxE and SoxF were identified. Based on these genes, the divergence time of C. fluminea was estimated to be around 476 million years ago. Furthermore, a total of 3,117 microsatellites were detected with a distribution density of 1:12,960 bp. Fifty of these microsatellites were randomly selected for validation, and 45 of them were successfully amplified with 31 polymorphic ones. The data obtained in this study will provide useful information for future genetic and genomic studies in C. fluminea.
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7

Ogawa, Takuro, Toshinari Furusawa, Ryohei Nomura, Daisuke Seo, Naomi Hosoya-Matsuda, Hidehiro Sakurai, and Kazuhito Inoue. "SoxAX Binding Protein, a Novel Component of the Thiosulfate-Oxidizing Multienzyme System in the Green Sulfur Bacterium Chlorobium tepidum." Journal of Bacteriology 190, no. 18 (July 18, 2008): 6097–110. http://dx.doi.org/10.1128/jb.00634-08.

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ABSTRACT From the photosynthetic green sulfur bacterium Chlorobium tepidum (pro synon. Chlorobaculum tepidum), we have purified three factors indispensable for the thiosulfate-dependent reduction of the small, monoheme cytochrome c 554. These are homologues of sulfur-oxidizing (Sox) system factors found in various thiosulfate-oxidizing bacteria. The first factor is SoxYZ that serves as the acceptor for the reaction intermediates. The second factor is monomeric SoxB that is proposed to catalyze the hydrolytic cleavage of sulfate from the SoxYZ-bound oxidized product of thiosulfate. The third factor is the trimeric cytochrome c 551, composed of the monoheme cytochrome SoxA, the monoheme cytochrome SoxX, and the product of the hypothetical open reading frame CT1020. The last three components were expressed separately in Escherichia coli cells and purified to homogeneity. In the presence of the other two Sox factors, the recombinant SoxA and SoxX showed a low but discernible thiosulfate-dependent cytochrome c 554 reduction activity. The further addition of the recombinant CT1020 protein greatly increased the activity, and the total activity was as high as that of the native SoxAX-CT1020 protein complex. The recombinant CT1020 protein participated in the formation of a tight complex with SoxA and SoxX and will be referred to as SAXB (SoxAX binding protein). Homologues of the SAXB gene are found in many strains, comprising roughly about one-third of the thiosulfate-oxidizing bacteria whose sox gene cluster sequences have been deposited so far and ranging over the Chlorobiaciae, Chromatiaceae, Hydrogenophilaceae, Oceanospirillaceae, etc. Each of the deduced SoxA and SoxX proteins of these bacteria constitute groups that are distinct from those found in bacteria that apparently lack SAXB gene homologues.
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Awad, Nemat M., A. A. Abd El-Kader, M. Attia, and A. K. Alva. "Effects of Nitrogen Fertilization and Soil Inoculation of Sulfur-Oxidizing or Nitrogen-Fixing Bacteria on Onion Plant Growth and Yield." International Journal of Agronomy 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/316856.

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A field experiment was conducted in a newly reclaimed soil at El-Saff region, El-Giza Governorate, Egypt to study the effects of different rates of nitrogen (N: 62 to 248 kg ha-1) with or without soil inoculation of sulfur- (S-) oxidizing bacteria (SoxB) and combined inoculation of SoxB and N-fixing bacteria (NFxB) on yield, quality and nutritional status of onion (Allium cepa L., “Giza 20”). Elemental S at 620 kg ha-1was applied to all treatments. Application of N at 62, 124, and 248 kg ha-1rates increased onion yield, plant height, and N uptake by 28 to 76%, 32 to 53%, and 61 to 145%, as compared to those of the plants that received no N. Inoculation of SoxB at various N rates increased onion yields by 47 to 69% and N uptake by 76 to 93%, as compared to those of the plants which received the respective rates of N but no SoxB inoculation. Inoculation with SoxB and NFxB increased onion yield by 221%, plant height by 62%, and N uptake by 629%, as compared to those of the plants grown without inoculation and no N applied.
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9

Wang, Yubin, Xiangzhong Luo, Chunjuan Qu, Tao Xu, Guiwei Zou, and Hongwei Liang. "The Important Role of Sex-Related Sox Family Genes in the Sex Reversal of the Chinese Soft-Shelled Turtle (Pelodiscus sinensis)." Biology 11, no. 1 (January 6, 2022): 83. http://dx.doi.org/10.3390/biology11010083.

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The Chinese soft-shelled turtle Pelodiscus sinensis shows obvious sexual dimorphism. The economic and nutrition value of male individuals are significantly higher than those of female individuals. Pseudo-females which are base to all-male breeding have been obtained by estrogen induction, while the gene function and molecular mechanism of sex reversal remain unclear in P. sinensis. Here, comparative transcriptome analyses of female, male, and pseudo-female gonads were performed, and 14,430 genes differentially expressed were identified in the pairwise comparison of three groups. GO and KEGG analyses were performed on the differentially expressed genes (DEGs), which mainly concentrated on steroid hormone synthesis. Furthermore, the results of gonadal transcriptome analysis revealed that 10 sex-related sox genes were differentially expressed in males vs. female, male vs. pseudo-female, and female vs. pseudo-female. Through the differential expression analysis of these 10 sox genes in mature gonads, six sox genes related to sex reversal were further screened. The molecular mechanism of the six sox genes in the embryo were analyzed during sex reversal after E2 treatment. In mature gonads, some sox family genes, such as sox9sox12, and sox30 were highly expressed in the testis, while sox1, sox3, sox6, sox11, and sox17 were lowly expressed. In the male embryos, exogenous estrogen can activate the expression of sox3 and inhibit the expression of sox8, sox9, and sox11. In summary, sox3 may have a role in the process of sex reversal from male to pseudo-female, when sox8 and sox9 are inhibited. Sox family genes affect both female and male pathways in the process of sex reversal, which provides a new insight for the all-male breeding of the Chinese soft-shelled turtle.
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Headd, Brendan, and Annette Summers Engel. "Evidence for Niche Partitioning Revealed by the Distribution of Sulfur Oxidation Genes Collected from Areas of a Terrestrial Sulfidic Spring with Differing Geochemical Conditions." Applied and Environmental Microbiology 79, no. 4 (December 7, 2012): 1171–82. http://dx.doi.org/10.1128/aem.02812-12.

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ABSTRACTThe diversity and phylogenetic significance of bacterial genes in the environment has been well studied, but comparatively little attention has been devoted to understanding the functional significance of different variations of the same metabolic gene that occur in the same environment. We analyzed the geographic distribution of 16S rRNA pyrosequences andsoxBgenes along a geochemical gradient in a terrestrial sulfidic spring to identify how different taxonomic variations of thesoxBgene were naturally distributed within the spring outflow channel and to identify possible evidence for altered SoxB enzyme function in nature. Distinct compositional differences between bacteria that utilize their SoxB enzyme in theParacoccussulfide oxidation pathway (e.g.,Bradyrhizobium,Paracoccus, andRhodovulum) and bacteria that utilize their SoxB enzyme in the branched pathway (e.g.,Chlorobium,Thiothrix,Thiobacillus,Halothiobacillus, andThiomonas) were identified. Different variations of thesoxBgenes were present at different locations within the spring outflow channel in a manner that significantly corresponded to geochemical conditions. The distribution of the differentsoxBgene sequence variations suggests that the enzymes encoded by these genes are functionally different and could be optimized to specific geochemical conditions that define niche space for bacteria capable of oxidizing reduced sulfur compounds.
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Dissertations / Theses on the topic "SoxB"

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Richardson, Nainoa. "Sox8 compense la perte de Sox9 pendant le développement testiculaire physiopathologique chez la souris présentant une perte de fonction du gène R-spondin1." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR6005.

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Chez les mammifères, le développement testiculaire des gonades XY est initié par les facteurs de transcription SRY/SOX9 qui promeuvent la différenciation des cellules de Sertoli. Chez l’embryon XX, la signalisation RSPO1/WNT/beta-catenin contrôle la différenciation des cellules de la granulosa et le développement ovarien. De fait, les souris XY n’exprimant pas Sox9 (KO) développent des ovaires et les souris XX n’exprimant pas Rspo1(KO) développent des ovotestis, constitués d’une partie testiculaire et une ovarienne. Leur formation est due à la différenciation précoce de cellules de granulosa et la reprogrammation d’une partie d’entre elles, en cellules de Sertoli. Chez les souris XX Rspo1 KO, SRY n’est pas nécessaire au développement testiculaire.De plus, les gonades des souris XX et XY présentant une double inactivation des gènes Rspo1 et Sox9 (Double Knockout/DKO) montrent une différenciation testiculaire partielle et complète respectivement, avec un développement d’ovotestis chez les individus XX DKO et un développement de testicules hypoplasiques chez les souris XY DKO. SOX9 et/ou SRY ne sont donc pas nécessaires à la différenciation testiculaire dans ce contexte, suggérant l’implication d’autres facteurs.L’objectif de ma thèse est de tester l’hypothèse selon laquelle SOX8, un facteur de transcription de la même famille que SOX9, pourrait induire le développement testiculaire chez les souris XX et XY DKO Rspo1 Sox9. Afin d’établir l’existence d’une compensation entre ces gènes SOX, nous avons analysé leur expression et le développement des gonades chez la souris DKO pour les gènes Rspo1 et Sox8 ou Sox9. Nous avons ensuite étudié les souris mutantes simultanément pour les gènes Rspo1, Sox8 et Sox9 (triple knockout/TKO). Notre hypothèse est qu’une perte d’expression des gènes Sox8 et Sox9 chez les souris TKO empêche la reprogrammation des cellules de la granulosa en Sertoli et par conséquent le développement testiculaire. Nous avons donc analysé la morphologie des gonades, les caractères sexuels secondaires, ainsi que l’organisation des gonades avec les différentes populations cellulaires qui les constituent par histologie et immuno-marquages à différents stades : à 17.5 jours de développement embryonnaire (E17.5) où la reprogrammation de cellules de granulosa en Sertoli commence dans la souris XX Rspo1 KO; chez les souris juvéniles au jour 10 (P10) où le développement somatique est achevé; et chez les souris adultes 40 jours après la naissance (P40).Nos résultats montrent que SOX8 et SOX9 sont exprimés de manière indépendante dans les gonades des souris XY and XX DKO Rspo1 Sox9 et DKO Rspo1 Sox8 à E17.5 et à P10. De plus, les souris XY et XX DKO Rspo1 Sox8 développent des testicules et des ovotestis indiquant que la perte d’un seul facteur SOX n’altère pas la formation des testicules, comme dans les souris XY et XX DKO Rspo1 Sox9. Cependant, chez les souris XX et XY TKO, la reprogrammation des granulosa en Sertoli à E17.5 et le développement testiculaire postnatal ne sont plus observés, démontrant que SOX8 peut compenser la perte de SOX9. De plus, les gonades des souris XY et XX TKO sont des ovaires atrophiques, indiquant que la différenciation ovarienne peut s’opérer.En résumé, nous avons analysé l’étiologie du développement physiopathologique des gonades chez les souris ayant une perte de fonction de RSPO1. Bien que SOX8 ne soit pas nécessaire à la différenciation testiculaire chez la souris, il peut promouvoir le développement testiculaire en l’absence de SRY et SOX9 en raison de sa redondance fonctionnelle avec SOX9. Chez l’Homme, dans les cas cliniques d’ambiguïtés sexuelles avec différenciation testiculaire, qui ne sont pas expliqués par le défaut d’expression de SRY ou SOX9, SOX8 pourrait ainsi être un facteur causatif
In humans and mice, testicular development in XY gonads involves SRY/SOX9 signaling to promote Sertoli cell differentiation and their formation as testis chords. For ovarian development in XX gonads, RSPO1/WNT/beta-catenin signaling is the main pathway for granulosa cell differentiation and their subsequent assembly into follicles. Indeed, XY Sox9 mutant mice develop ovaries, and XX Rspo1 mutant mice develop ovo-testes, a gonad containing a testicular and an ovarian part. In XX Rspo1 mutant mice, ovo-testicular development involves precocious differentiation of some granulosa cells and their and reprogramming as Sertoli cells. Thus, these single mutant studies demonstrated that SOX9 and RSPO1 are required for testicular and ovarian development respectively, and that SRY is dispensable for testicular development in XX Rspo1 mice. Interestingly, gonad development in XY and XX Rspo1 Sox9 double knockout (DKO) mice has challenged the requirement of SOX9 for testicular development. In XX Rspo1 single mutants, it was assumed that Sertoli cell differentiation was SOX9-dependent, but co-inactivation of Sox9 in DKO mice does not impair the ovo-testicular phenotype. For XY Sox9 single mutant mice developing ovaries, co-inactivation of Rspo1 in XY DKO mice rescues the sex reversal, though the testes are hypo-plastic. Thus, in XY and XX Rspo1 Sox9 DKO mice, SOX9 and/or SRY are dispensable for testicular differentiation, indicating that an alternate testis factor exists. For my research project, we hypothesized that a SOX9-related transcription factor, SOX8, acts redundantly for testicular development in XY and XX Rspo1 Sox9 DKO mice. Thus, to first establish redundancy among the SOX factors, we first analyzed their expression in Rspo1 mutant mice lacking Sox8 or Sox9, and then generated and analyzed gonad development in XY and XX Rspo1 Sox8 DKO mice. Then to test our hypothesis, we studied Rspo1 Sox8 Sox9 triple knockout (TKO) mice. We predicted that a loss of both Sox genes in TKO mice would prevent granulosa cell reprogramming as Sertoli cells and subsequent testicular development. To characterize gonad development and their effects in DKO and TKO mice, we performed analyses in embryonic day 17.5 (E17.5) mice, when granulosa-to-Sertoli cell reprogramming begins in XX Rspo1 single mutants; in juvenile post-natal day 10 (P10) mice, when gonad fate is set; and in young adult P40 mice. We examined a variety of parameters including gonad morphology and secondary sex characteristics, as well as gonad organization and cell population by histological and immunostaining analyses. We report that SOX8 and SOX9 are expressed independently in XY and XX Rspo1 Sox9 DKO and Rspo1 Sox8 DKO gonads in embryonic and juvenile mice. Next, XY and XX Rspo1 Sox8 DKO mice developed testes and ovo-testes, indicating that loss of one SOX factor does not impair testicular differentiation, as in XY and XX Rspo1 Sox9 DKO mice. In XY and XX Rspo1 Sox8 Sox9 TKO mice, granulosa-to-Sertoli cell reprogramming was impaired at E17.5 and post-natal gonads lacked testicular development. Thus, SOX8 can compensate for the loss of SOX9 in Rspo1 Sox9 DKO mice. In addition, gonads in XY and XX TKO mice developed as atrophied ovaries, indicating that ovarian fate is partially maintained.In total, we investigated the etiology of pathophysiological testicular development in RSPO1 loss-of-function mice. Remarkably, though SOX8 is dispensable for male sex determination in mice, it can promote testicular differentiation in the absence of SRY and SOX9 because of functional redundancy with SOX9. Thus, in human cases of sex reversal where testicular development cannot be explained by misexpression of SRY or SOX9, SOX8 could be a causative factor
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2

Sandberg, Magnus. "Sox proteins and neurogenesis." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-873-0/.

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3

Rammah-Bouazza, Cyrine. "Implication de SOX9 et de MiniSOX9 dans la tumorigenèse colorectale." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON1T020.

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SOX9 est un facteur de transcription, appartenant à la famille des protéines à domaine HMG, et connu pour réguler la transcription grâce à la liaison de ce domaine à l'ADN. Au laboratoire, il a été montré que SOX9 possédait des propriétés anti-oncogéniques, cependant, de façon paradoxale, SOX9 est surexprimé dans les tumeurs colorectales. Nous avons mis en évidence l'existence d'un nouveau variant d'épissage de SOX9, MiniSOX9, qui possède un effet dominant négatif vis-à-vis de l'activité transcriptionnelle de SOX9. MiniSOX9 est fortement exprimé dans les tumeurs en comparaison avec le tissu sain adjacent à la tumeur. Nous avons émis l'hypothèse que MiniSOX9 pourrait donc avoir, dans les tumeurs, un effet antagoniste à SOX9 et s'opposer à ses propriétés anti-oncogéniques. Grâce à la mise en place de modèles cellulaires tumoraux de surexpression de SOX9 et MiniSOX9, inductibles à la doxycycline, nous avons mis en évidence que SOX9 réduit la prolifération, la migration et l'invasion cellulaire. De manière surprenante, MiniSOX9 ne possède aucun effet sur la prolifération cellulaire, suggérant que les effets de SOX9 pourraient être dus à son activité transcriptionnelle. En revanche, SOX9 ainsi que MiniSOX9 réduisent la capacité clonale des cellules et leur capacité à former des tumorosphères. Dans ce cas, il serait probable que SOX9 et MiniSOX9 modulent l'activité de protéines partenaires
SOX9 is an HMG transcription factor known to regulate transcription by binding of its HMG domain to DNA. We previously demonstrated that SOX9 has anti-oncogenic-properties but SOX9 is overexpressed in colon tumors when compared to adjacent healthy tissu. This overexpression appears paradoxical, unless its anti-oncogenic activity cannot be exert. In this study, we report the discovery of MiniSOX9, a new SOX9 splice variant, which is highly expressed in colon tumors. MiniSOX9 acts as a SOX9 dominant negative isoform. Our hypothesis was that MiniSOX9 antagonizes the SOX9 anti-oncogenic activity in tumors.Using tumors cells lines inducible for SOX9 and MiniSOX9 overexpression, we showed that SOX9 reduces cell proliferation, migration and invasion. Surprisingly, MiniSOX9 has no effect on cell proliferation, suggesting that SOX9 effects could be du to his transcriptionnal activity. However, SOX9 and MiniSOX9 decrease cell clonal ability and tumorosphere formation. In this case, it is likely that SOX9 and MiniSOX9 modulate the activity of proteins partners
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4

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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5

Agustí, Benito Cristina. "Mecanisme d'activació de fibronectina i LEF1 per Snail1 durant la transició epili-mesènquima." Doctoral thesis, Universitat Pompeu Fabra, 2007. http://hdl.handle.net/10803/7107.

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La transició Epiteli-Mesènquima es dóna durant el desenvolupament embrionari i en els estadis tardans de la progressió tumoral permetent que es produeixi la metàstasi. Aquestes transicions necessiten una repressió de l'E-Cadherina i es pot reproduir en cèl·lules en cultiu amb l'expressió ectòpica de Snail1, un repressor de l'E-Cadherina. Durant la transició produïda per Snail es produeix la ràpida activació de gens mesenquimals com Fibronectina i LEF1. L'expressió forçada d'E-Cadherina fa disminuir els nivells de RNA de Fibronectina i LEF1, indicant que en l'activació d'aquests dos gens està implicat un cofactor sensible a l'E-Cadherina. En concordança, la transcripció de Fibronectina i LEF1 és depenent de -Catenina i NFB. La sobreexpressió d'E-Cadherina inhibeix l'activitat transcripcional d'aquests dos factors i disminueix la seva interacció amb el promotor de Fibronectina. De manera similar a la -Catenina, NFB es detecta associat a l'E-Cadherina i altres components dels contactes intercel·lulars. Quan es trenquen les unions adherents, com quan es sobreexpressa Snail, la interacció E-Cadherina-NFB disminueix i augmenta l'activitat transcripcional de NFB i-Catenina.
Epithelial to mesenchymal transitions takes place during embryo development and in the late stages of tumorigenesis allowing metastasis formation. These transitions require E-Cadherin downregulation and can be reproduced in cell culture by ectopic expression of Snail1, an E-Cadherin gene repressor. During Snail-induced transition a rapid upregulation of mesenchymal genes such as Fibronectin and LEF1 has been characterized. Forced expression of E-Cadherin strongly down-regulates Fibronectin and LEF1 RNA levels, indicating that an E-Cadherin sensitive cofactor is involved in the activation of these genes. Accordingly, transcription of Fibronectin and LEF1 was dependent on -Catenin and NFB. E-Cadherin over-expression downregulated the transcriptional activity of both factors and decreased their interaction to Fibronectin promoter. Similarly to -Catenin, NFB was detected associated to E-Cadherin and other cell adhesion components. Association of NFB to E-Cadherin required the integrity of this complex; conditions that disrupts adherens junctions, such as Snail over-expression, decreased E-Cadherin-NFB interaction and up-regulates NFB and -Catenin transcriptional activity. Therefore, -Catenin and NFB transcriptional activities are required for expression of the studied mesenchymal genes and these activities are inactivated by immobilizing -Catenin and NFB to functional E-Cadherin structures.
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6

Boopathi, Ramachandran. "Structure de haute résolution du complexe nucleosome-H1 et son interaction avec le facteur de transcription Sox6." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV020/document.

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Comprendre la structure et l’organisation de la chromatine est une question fondamentale dans le domaine de la régulation de l’expression des gènes. La cristallographie par rayons-X et d’autres techniques biophysiques on permit de comprendre la structure du nucléosome avec une précision quasi atomique. Malgré de nombreuses études, les données structurelles au delà de la particule de cœur nucléosomale (NCP) demeurent imprécises. Au cours des dernières décennies plusieurs tentatives ont été faites pour montrer comment l’histone de liaison H1 interagit avec les particules nucléosomales pour les condenser en fibre de chromatine. Ces études ont mené à différents modèle décrivant la position de l’histone de liaison H1 sur la chromatine. De récentes avancées sur l’histone de liaison H1 suggèrent que le domaine globulaire de H1 (GH1) et la partie C-terminale interagit avec la dyade du nucléosome et les 2 bouts d’ADN de liaison (modèle à 3 contacts) qui sont contraintes de former une structure en tige. Cependant, la conformation et la position précise de l’histone de liaison H1 reste inconnues et la controverse à ce sujet persiste.Dans cette étude, nous avons déterminé la structure tridimensionnelle de nucléosomes contenant H1 par des techniques de cryo-microscopie électronique (cryo-EM) et de diffraction aux rayons-X dans des cristaux. Nous avons utilisé le chaperons d’histone, NAP1, pour déposer l’histone de liaison H1 sur les nucléosomes reconstitué à partir des histones de cœur recombinant et la séquence d’ADN positionnante 601 de 197 paires de bases (dite de Widom). Nos résultats de cryo-EM montrent que l’association de H1 compacte le nucléosome en réduisant la mobilité des ADNs et stabilisant ainsi les contacts entre les nucléotides précédant la sortie NCP et l’octamer d’histones. Nos résultats par diffusion de rayon-x dans des cristaux à une résolution de 7Ä montrent que la partie globulaire de H1 (GH1) est située sur la dyade et interagie simultanément avec les petits sillons de l’ADN à la dyade et les ADN de liaison à l’entrée et à la sortie du nucléosome. Les parties N- et C-terminales de H1 sont orientées vers l’extérieur du cœur du nucléosome à travers les différents ADN de liaison. Nous avons validé l’orientation de GH1 par des expériences de pontages ADN-proteine, après substitutions de cystéine par mutagénèse dirigée, empreinte par radicaux hydroxyles et « amarrage moléculaire ». Nos résultats révèlent l’effet de H1 sur la dynamique du nucléosome et apporte une vision détaillé de la conformation du « stem du nucléosome » lors de l’incorporation de H1.Nous avons également étudié l’association spécifique du facteur de transcription Sox6 à ces de reconnaissance consensus présent à l’intérieur du nucléosome, associé ou non avec l’histone de liaison H1 par une empreinte biphotonique avec laser UV. Nos résultats montrent que le domaine HMG de Sox6 se fixe spécifiquement sur son motif consensus situé profondément à l’intérieur du nucléosome à l’exception sur la dyade. Cette association n’est pas influencée par la « fermeture » des ADN de liaison avec l’histone H1 démontrant l’existence d’un autre façon de reconnaissance que le modèle de Widom basés sur fluctuations thermodynamiques des ADN de liaison. Le résultat que Sox6 est capable de surmonter la barrière nucléosomale (avec ou sans H1) suggère fortement que les facteurs de transcription de la famille Sox, de domaine de liaison de type HMG, jouent le rôle de facteurs « pionnier » dans la régulation de la transcription et en particulier dans l’initiation de la différentiation
Understanding the structural organization of chromatin is a fundamental issue in the field of gene regulation. X-ray crystallography and other biophysical techniques have enabled understanding of the nucleosome structure nearly at atomic precision. Despite numerous studies, the structural information beyond the nucleosome core particle (NCP) remains elusive. Over the last few decades several attempts have been made to reveal how the linker histone H1 interacts with the nucleosome particles and condenses them into a chromatin fiber. These studies have led to different models describing the position of linker histone H1 on chromatin. Recent advancements in linker histone H1 studies suggest that globular domain of histone H1 (GH1) interacts with the nucleosomal dyad and its C-terminal domain interacts with the linker DNA forming a stem like structure. However, the precise conformation of linker histone H1 and position of other domains still remains unknown.In this study, we resolved the three-dimensional structure of H1-containing nucleosomes by using cryo-electron microscopy (cryo-EM) and X-ray crystallography. We have used the chaperone NAP-1 to deposit linker histone H1 onto nucleosomes reconstituted from recombinant core histones and 197 base-pair of 601 strong nucleosome positioning DNA sequence. Our cryo-EM results showed that association of H1 gives a more compact appearance of the nucleosome as it restricts the mobility of the two linker DNAs keeping them in close proximity and thereby stabilizing contacts between the histone core and nucleotides preceding NCP exit. Our X-ray crystallography results at 7 Ä resolution reveal that the globular domain of histone H1 (GH1) is positioned onto the nucleosome pseudodyad and recognizes the nucleosome core and both linker arms by contacting the DNA backbone in the minor groove. The N- and C-terminal domains of H1 are oriented away from the nucleosome core towards different DNA linkers. We further validated the orientation of GH1 by cross-linking experiments followed after cysteine substitutions mutagenesis, hydroxyl radical footprinting and by molecular docking. Our results reveal the effect of H1 on nucleosome dynamics and also provide a detailed view of the nucleosome stem conformation upon H1 incorporation.We also studyed the nucleosome accessibility of transcription factor Sox6 and the impact of linker histone H1 incorporation to Sox6 binding on nucleosome by using UV laser biphotonic footprinting. Our results reveal that Sox6 HMG domain binds specifically to its consensus binding located deep inside of the nucleosomal DNA, but not at the nucleosomal dyad. Our in vitro footprinting results reveal that the “locking” of DNA linkers by incorporation of histone H1 on nucleosome does not show any impact on Sox6 HMG domain binding, evidencing an alternative to the Widom model based on thermal fluctuation “opening” of the nucleosome at the linkers.. The finding that Sox6 is able to overcome nucleosome (chromatosome) barrier in presence or absence of H1, strongly suggest that the HMG domain - based Sox family proteins it can act as a pioneer factor in transcription regulation, in particular in initiation of cell differentiation
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Dupasquier, Sébastien. "SOX9, un lien moléculaire entre voie Wnt/APC et PKCalpha dans l'épithélium intestinal sain et tumoral." Montpellier 1, 2008. http://www.theses.fr/2008MON1T041.

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Les cellules tumorales présentent des variations parfois importantes du taux de certaines protéines qui leur procurent un avantage sélectif de croissance par rapport aux cellules normales dont elles dérivent. Ces variations peuvent résulter d'altérations de l'ADN, premier support de l'information génétique, la transcription, la maturation et/ou la stabilité de l'ARN messager, ou encore la traduction et/ou la dégradation de la protéine. Les protéines kinases C (PKC) sont impliquées dans de nombreux processus cellulaires associés à la tumorigenèse, notamment le contrôle de la prolifération, de la différenciation et de l'apoptose. Or, d'importantes variations de leurs niveaux d'accumulation sont observées dans de nombreuses tumeurs humaines. Néanmoins, le lien causal entre les mécanismes régulant la transcription, la traduction ou encore la stabilité et la dégradation des PKC et ces variations est rarement établi. Nous avons pour notre part démontré que l'expression de PKCα est réprimée aussi bien in vitro qu'in vivo par le facteur de transcription SOX9 dans les cellules épithéliales intestinales. Cette répression ne nécessite pas l'interaction de SOX9 avec l'ADN via son domaine HMG mais est médiée par un nouveau mécanisme impliquant la région centrale de SOX9, très conservée entre les membres du groupe des SOXE (SOX8, 9, 10). Puisque SOX9 est une cible de la voie Wnt/APC dans les cellules épithéliales intestinales, nos résultats établissent un lien moléculaire entre voie Wnt/APC et PKCα et permettent d'expliquer pourquoi PKCα est diminuée dans les cancers colorectaux qui présentent pour 80% d'entre eux une activation constitutive de la voie Wnt/APC.
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Neirijnck, Yasmine. "Contrôle transcriptionnel du développement rénal par la famille de gènes Sox." Thesis, Nice, 2013. http://www.theses.fr/2013NICE4109.

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Les anomalies congénitales du rein et du tractus urinaire (CAKUT) sont l’une des malformations les plus fréquentes chez l’homme, et résultent d’un défaut du programme de dévelopement des organes. La famille de gènes Sox code pour 20 facteurs de transcription qui assurent des fonctions multiples et essentielles pendant l’organogenèse chez l’homme et la souris. Nous avons précedemment montré que Sox8 et Sox9 sont nécessaires au branchement de l’uretère, et la perte de ces gènes résulte en une agénésie rénale. L’objectif de ce projet de thèse était de caractériser le role des gènes Sox-C (Sox4/11/12) in vivo chez la souris. L’analyse des patrons d’expression a révélé que Sox4 , Sox11 et Sox12 sont co-exprimés dans les cellules progénitirices des néphrons, destinées à subir une transition mésenchyme epithelium (MET) pour former des vésicules qui s'allongent pour aboutir au néphron fonctionnel. L’analyse phénotypique a révélé une redondance fonctionnelle entre Sox4 et Sox11 pendant les processus de MET et de maturation des néphrons: les double mutants développent une hypodysplasie rénale dûe à une réduction dramatique du nombre et de la taille des néphrons. Le pool de progéniteurs de néphrons est intact chez ces mutants mais incapable de s’engager dans la nephrogenèse, probablement dû à un changement d’identité cellulaire. Par ailleurs, en l’absence de Sox11, des bourgeons uretéraux ectopiques se forment, conduisant à des reins duplex, phénotype présent dans une proportion de patients CAKUT. De manière importante, nous avons identifié une série de variants SOX11 dans une cohorte de patients CAKUT, suggérant l'implication de mutations SOX11 dans cette maladie chez l'homme
Congenital abnormalities of the kidney and the urinary tract (CAKUT) belong to the mostcommon birth defects in human and are caused by defects in the program governing organ development. The Sox gene family encodes 20 transcription factors that ensure multiple and essential functions during mouse and human organogenesis. We have previously shown that the homologous genes Sox8 and Sox9 are required for the branching process of the ureter and their loss results in renal agenesis. In this thesis project, we aimed to identify and characterize the role of the Sox-C genes (Sox4/11/12), in vivo using mouse models. Expression analysis revealed that Sox4, Sox11 and Sox12 are coexpressed in the self-renewing nephron precursors cells that are destined to undergo mesenchyme-to-eptihelial transition (MET) to form vesicles that elongate to give rise to the functional nephrons. Phenotypical analysis revealed a functional redundancy between Sox4 and Sox11 in MET and nephron maturation processes: double mutants display renal hypodysplasia, due to a dramatic reduction in the number and size of nephrons. The nephron precursor pool is intact in these mutants but unable to commit to nephrogenesis, probably because of a cell identity change. In addition, in the absence of Sox11, ectopic ureteric buds form, leading to duplex kidneys, a phenotype found in a proportion of CAKUT patients. Importantly, mutation analysis of a cohort suffering from CAKUT syndrome identified a series of SOX11 variants, thus suggesting an involvement of SOX11 mutations in this human disease
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Hess, Samuel Joseph. "Sox2 target network in regulating adult Schwann cell plasticity : new insights into peripheral nerve regeneration and pathology." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25778.

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Terminally differentiated Schwann cells (SCs), the glial cells in the adult peripheral nerves, display a remarkable plasticity by adopting a de-differentiated phenotype following injury and becoming specialised to repair-type cells for promoting nerve regeneration. Adult SC plasticity is also hijacked by leprosy-causing Mycobacterium leprae during peripheral nerve infection, which make SCs susceptible to reprogramming and generation of progenitor/stem-like cells for bacterial advantage. Interestingly, de-differentiated SCs generated during nerve injury and infection reactivated stem cell transcription factor Sox2, which is essential for maintaining pluripotency in embryonic stem cells (ESCs). In this study we address what role Sox2 plays and how it is involved in adult SC plasticity. We identified that Sox2 binds to a network of gene targets in de-differentiated adult SCs across the mouse genome. This Sox2 target network is distinct from Sox2 target genes in core ESC pluripotency, and appears to be modulated by SC microenvironmental changes and pathological conditions, as nerve crush injury and infection-induced reprogramming expanded Sox2 binding to target genes. In vivo knockdown by shRNA of Sox2 in wild type adult nerves demonstrated reduction in SC de-differentiation. Mutant mice defective in natural nerve degeneration, de-differentiation and regeneration (Wallerian degeneration slow mice; Wlds) not only show impaired Sox2 binding to its target genes but also a delay in Sox2 and target gene expression after nerve crush injury. Together, these in vivo data reveal an impact of Sox2 and its target network on SC plasticity. Furthermore, altered expression of many of these target genes after Sox2 knockdown in wild type adult Schwann cells in vitro and in vivo as well as in injured Wlds nerves suggests a functional role of a Sox2 target network in nerve injury-repair processes. This includes Sox2 target genes such as Megf10, Btc, Atf3 and Nestin. By acting on these genes Sox2 may coordinate relevant gene functions ranging from phagocytosis/clearance, proliferation, transcription and cytoskeletal dynamics. Thus, this study proposes a novel concept of how reactivation of an embryonic stem cell regulator like Sox2 in adult tissues coordinates a gene network regulating Schwann cell plasticity and multiple biological functions facilitating the nerve injury-repair process. These findings may aid in developing strategies towards promoting nerve regeneration, or designing treatments for neuropathies in which deregulation of Schwann cell de-differentiation contributes to pathogenesis.
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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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Books on the topic "SoxB"

1

SOB. Alexander, AR: Sibling Rivalry Press, 2011.

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Seixas, Noémia. Beethoven sob. Lisboa: Ulmeiro, 1989.

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Davis, Carol Anne. Sob story. London: Snowbooks, 2006.

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Silva, Alencar e. Sob vésper: Poesia. Manaus: Edições Puxirum, 1986.

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Chicago White Sox. Edina, Minn: ABDO Pub. Co., 2011.

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Kawai, Mitsuko. Sob dois horizontes. São Paulo: Editora do Escritor, 1988.

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Italia, Bob. Boston Red Sox. Edina, MN: Abdo & Daughters, 1997.

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Chicago White Sox. Minneapolis, Minnesota: Sportszone, an imprint of ABDO Publishing, 2015.

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Gilbert, Sara. Chicago White Sox. Mankato, MN: Creative Paperbacks, 2014.

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Abramson, Phyllis Leslie. Sob sister journalism. New York: Greenwood Press, 1990.

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Book chapters on the topic "SoxB"

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Lefebvre, Véronique, Benoit de Crombrugghe, and Richard R. Behringer. "The transcription factors L-Sox5 and Sox6 are essential for cartilage formation." In The Many Faces of Osteoarthritis, 91–100. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8133-3_10.

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Nongmeikapam, Kishorjit, Wahengbam Kanan Kumar, and Aheibam Dinamani Singh. "Prn-Sorb-Slam." In Autonomous Driving and Advanced Driver-Assistance Systems (ADAS), 167–92. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003048381-8.

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Chiang, Pen-Chi, and Xiang Gao. "SOx Control." In Air Pollution Control and Design, 7–47. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-13-7488-3_2.

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Hall, Beverley. "Sorb-German Bilingual Education." In Bilingual Education, 151–56. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-4531-2_15.

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Shimozaki, Koji. "Sox2 (SRY-Box 2)." In Encyclopedia of Signaling Molecules, 5093–100. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101970.

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Shimozaki, Koji. "Sox2 (SRY-Box 2)." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101970-1.

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Jozsa, Frank P. "Boston Red Sox." In SpringerBriefs in Economics, 9–15. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25996-3_2.

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Jozsa, Frank P. "Chicago White Sox." In SpringerBriefs in Economics, 41–48. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25996-3_6.

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Ray, Sujay, Arundhati Banerjee, and Angshuman Bagchi. "Molecular Level Insight into the Interactions of SoxC and SoxD from Epsilonproteobacteria Sulfurimonas denitrificans: A Biomolecular Computational Approach." In Advances in Intelligent Systems and Computing, 401–10. New Delhi: Springer India, 2015. http://dx.doi.org/10.1007/978-81-322-2517-1_39.

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Schrum, Kelly. "Introduction." In Some Wore Bobby Sox, 1–10. New York: Palgrave Macmillan US, 2004. http://dx.doi.org/10.1007/978-1-349-73134-3_1.

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Conference papers on the topic "SoxB"

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Jiang, Shih-Sheng, Wen-Tsen Fang, I.-Shou Chang, and Chih-Ting Huang. "Abstract 1292: Mutually exclusive expression of SOX2 and SOX9 in lung adenocarcinoma cells and its implications." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1292.

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Hanlin, Heath. "Sorb." In ACM SIGGRAPH 99 Electronic art and animation catalog. New York, New York, USA: ACM Press, 1999. http://dx.doi.org/10.1145/312379.313083.

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Capasso, Giulio, Jani Achrén, Mirko Colapietro, Sergio D'Orsi, Sergio Campana, Riccardo Claudi, Pietro Schipani, et al. "SOXS control electronics design." In Software and Cyberinfrastructure for Astronomy V, edited by Juan C. Guzman and Jorge Ibsen. SPIE, 2018. http://dx.doi.org/10.1117/12.2312780.

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Young, David, Marco Landoni, Stephen Smartt, Sergio Campana, Riccardo U. Claudi, Pietro Schipani, Matteo Aliverti, et al. "The SOXS data-reduction pipeline." In Software and Cyberinfrastructure for Astronomy VI, edited by Juan C. Guzman and Jorge Ibsen. SPIE, 2020. http://dx.doi.org/10.1117/12.2561015.

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Cosentino, Rosario, Matteo Aliverti, Salvatore Scuderi, Sergio Campana, Riccardo U. Claudi, Pietro Schipani, Andrea Baruffolo, et al. "The VIS detector system of SOXS." In Ground-based and Airborne Instrumentation for Astronomy VII, edited by Hideki Takami, Christopher J. Evans, and Luc Simard. SPIE, 2018. http://dx.doi.org/10.1117/12.2312539.

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Claudi, Riccardo, Federico Biondi, Nancy Elias-Rosa, Matteo Genoni, Matteo Munari, Kalyan Radhakrishnan, Davide Ricci, et al. "Operational modes and efficiency of SOXS." In Ground-based and Airborne Instrumentation for Astronomy VIII, edited by Christopher J. Evans, Julia J. Bryant, and Kentaro Motohara. SPIE, 2020. http://dx.doi.org/10.1117/12.2562321.

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Cortes, Carlos, and Hideharu Amano. "Switching region analysis for SOTB technology." In 2017 International Caribbean Conference on Devices, Circuits and Systems (ICCDCS). IEEE, 2017. http://dx.doi.org/10.1109/iccdcs.2017.7959717.

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Gupta, Sumit. "SOX Compliant Agile Processes." In Agile 2008 Conference. IEEE, 2008. http://dx.doi.org/10.1109/agile.2008.48.

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Petersen, Rebecca. "Loss of Sox4 Impacts Early Ocular Development." In Virtual 12th Light Sheet Fluorescence Microscopy Conference 2020. Royal Microscopical Society, 2020. http://dx.doi.org/10.22443/rms.lsfm2020.18.

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Brucalassi, Anna, Oz Diner, Hanindyo Kuncarayakti, Adam Rubin, José Antonio Araiza-Durán, Andrea Bianco, Mirko Colapietro, et al. "Architecture of the SOXS instrument control software." In Software and Cyberinfrastructure for Astronomy V, edited by Juan C. Guzman and Jorge Ibsen. SPIE, 2018. http://dx.doi.org/10.1117/12.2310092.

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Reports on the topic "SoxB"

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Gupta, R. P., S. K. Gangwal, and G. P. Khare. Fluidized-bed testing of Z-SORB III sorbent. Office of Scientific and Technical Information (OSTI), August 1994. http://dx.doi.org/10.2172/78556.

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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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Prensner, John. The Role of Sox4 In Prostate Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada560517.

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Campbell, W. M., J. J. O`Donnell, S. Katta, T. Grindley, G. Delzer, and G. Khare. Desulfurization of hot fuel with Z-Sorb III sorbent. Office of Scientific and Technical Information (OSTI), December 1993. http://dx.doi.org/10.2172/10192619.

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Lee, G. K., and R. J. Philp. Low NOx/SOx burner trials: CFB Gagetown. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1988. http://dx.doi.org/10.4095/304408.

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Lee, G. K. The Rockwell low NOx /SOx burner development. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1986. http://dx.doi.org/10.4095/302630.

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Onaitis, Mark. The Role of Sox2 in Lung Cancer Initiation and Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada598798.

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Onaitis, Mark. The Role of Sox2 in Lung Cancer Initiation and Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada599530.

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Onaitis, Mark. The Role of Sox2 in Lung Cancer Initiation and Progression. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada603904.

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Lee, G. K., and R. J. Philp. Gagetown low NOx/SOx burner project test program. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1987. http://dx.doi.org/10.4095/304366.

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You might also be interested in the extended bibliographies on the topic 'SoxB' for particular source types:
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