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

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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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8

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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10

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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11

Han, Yu, and Véronique Lefebvre. "L-Sox5 and Sox6 Drive Expression of the Aggrecan Gene in Cartilage by Securing Binding of Sox9 to a Far-Upstream Enhancer." Molecular and Cellular Biology 28, no. 16 (June 16, 2008): 4999–5013. http://dx.doi.org/10.1128/mcb.00695-08.

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ABSTRACT The Sry-related high-mobility-group box transcription factor Sox9 recruits the redundant L-Sox5 and Sox6 proteins to effect chondrogenesis, but the mode of action of the trio remains unclear. We identify here a highly conserved 359-bp sequence 10 kb upstream of the Agc1 gene for aggrecan, a most essential cartilage proteoglycan and key marker of chondrocyte differentiation. This sequence directs expression of a minimal promoter in both embryonic and adult cartilage in transgenic mice, in a manner that matches Agc1 expression. The chondrogenic trio is required and sufficient to mediate the activity of this enhancer. It acts directly, Sox9 binding to a critical cis-acting element and L-Sox5/Sox6 binding to three additional elements, which are cooperatively needed. Upon binding to their specific sites, L-Sox5/Sox6 increases the efficiency of Sox9 binding to its own recognition site and thereby robustly potentiates the ability of Sox9 to activate the enhancer. L-Sox5/Sox6 similarly secures Sox9 binding to Col2a1 (encoding collagen-2) and other cartilage-specific enhancers. This study thus uncovers critical cis-acting elements and transcription factors driving Agc1 expression in cartilage and increases understanding of the mode of action of the chondrogenic Sox trio.
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12

Ma, Fang, Yali Zou, Ruilin Ma, Xin Chen, and Lanfang Ma. "Evolution, characterization and expression analysis of Sox gene family in rainbow trout (Oncorhynchus mykiss)." Czech Journal of Animal Science 67, No. 4 (April 30, 2022): 157–66. http://dx.doi.org/10.17221/4/2022-cjas.

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The Sox transcription factor family plays an important role in various biological processes such as animal sex determination and multiple organ development. We used online databases to analyze the gene structure, chemical characteristics, and evolutionary relationship of Sox family genes through bioinformatics, and we studied the expression profiles and regulatory mechanisms of Sox family genes. A total of 29 rainbow trout Sox genes were identified. The phylogenetic analysis found that Sox genes of rainbow trout were clustered in seven subfamilies (B1, B2, C, D, E, F and H), and the gene structure of each subfamily was relatively conserved. Furthermore, Sox1, Sox4, Sox6, Sox8, Sox9, Sox11, Sox17, Sox18, and Sox19 developed into two copies, which might be the result of teleost fish-specific genome replication. Multiple HMG box domain alignments indicated that the motifs for all Sox sequences are conserved. Gene expression studies reveal that Sox expression is tissue-specific and that multiple Sox genes are involved in rainbow trout gonad and central nervous system development. Our study provides valuable information on the evolution of teleosts, and will also help to further research the functional characteristics of Sox genes.
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13

Zhang, Zhilong, Min Chu, Qi Bao, Pengjia Bao, Xian Guo, Chunnian Liang, and Ping Yan. "Two Different Copy Number Variations of the SOX5 and SOX8 Genes in Yak and Their Association with Growth Traits." Animals 12, no. 12 (June 20, 2022): 1587. http://dx.doi.org/10.3390/ani12121587.

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Copy number variation (CNV) is a structural variant with significant impact on genetic diversity. CNV has been widely used in breeding for growth traits, meat production or quality, and coat color. SRY-like box genes (SOXs) are a class of transcription factors that play a regulatory role in cell fate specification and differentiation. SOX5 and SOX8 belong to subgroups D and E of the SOXs, respectively. Previous studies have shown that SOX5 and SOX8 are essential in the development of bones. In this study, we explored the association between the growth traits and CNVs of SOX5 and SOX8 in 326 Ashidan yaks and detected mRNA expression levels in different tissues. Our results illustrated that CNVs of SOX5 and SOX8 were significantly associated with withers height at 18 months of age and chest girth at 30 months of age (p < 0.05). The CNV combination of SOX5 and SOX8 was significantly associated with withers height at 18 months of age (p < 0.01). SOX5 expression in the lung was significantly higher than in the heart, spleen, kidney, and muscle (p < 0.05). SOX8 expression in the lung was significantly higher than in the liver and muscle (p < 0.05). Our results provide evidence that the CNVs of SOX5 and SOX8 genes could be used as new markers for the selection of yak growth traits.
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14

Li, Cui, Rong Chen, Hui Liu, Yao Huang, Jintao Yu, Weiwei Ouyang, and Chen Xue. "Response of chlorinated hydrocarbon transformation and microbial community structure in an aquifer to joint H2 and O2." RSC Advances 12, no. 36 (2022): 23252–62. http://dx.doi.org/10.1039/d2ra04185e.

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The joint H2/O2 can promote the transformation of TCE, tDCE and CF. A specific microbial community with higher diversity forms in the H2/O2 microcosm, and synchronously increases the anaerobic tceA and aerobic phe and soxB genes.
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15

Kamachi, Y., M. Uchikawa, J. Collignon, R. Lovell-Badge, and H. Kondoh. "Involvement of Sox1, 2 and 3 in the early and subsequent molecular events of lens induction." Development 125, no. 13 (July 1, 1998): 2521–32. http://dx.doi.org/10.1242/dev.125.13.2521.

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Activation of the first lens-specific gene of the chicken, delta 1-crystallin, is dependent on a group of lens nuclear factors, deltaEF2, interacting with the delta1-crystallin minimal enhancer, DC5. One of the deltaEF2 factors was previously identified as SOX2. We show that two related SOX proteins, SOX1 and SOX3, account for the remaining members of deltaEF2. Activation of the DC5 enhancer is dependent on their C-terminal domains. Expression of Sox1-3 in the eye region during lens induction was studied in comparison with Pax6 and delta1-crystallin. Pax6, known to be required for the inductive response of the ectoderm, is broadly expressed in the lateral head ectoderm from before lens induction. After tight association of the optic vesicle (around stage 10–11, 40 hours after egg incubation), expression of Sox2 and Sox3 is activated in the vesicle-facing ectoderm at stage 12 (44 hours). These cells, expressing together Pax6 and Sox2/3, subsequently give rise to the lens, beginning with formation of the lens placode and expression of delta-crystallin at stage 13 (48 hours). Sox1 then starts to be expessed in the lens-forming cells at stage 14. When the prospective retina area of the neural plate was unilaterally ablated at stage 7, expression of Sox2/3 was lost in the side of lateral head ectoderm lacking the optic cup, implying that an inductive signal from the optic cup activates Sox2/3 expression. In the mouse embryonic lens, this subfamily of Sox genes is expressed in an analogous fashion, although Sox3 transcripts have not been detected and Sox2 expression is down-regulated when Sox1 is activated. In ectodermal tissues of the chicken embryo, delta -crystallin expression occurs in a few ectopic sites. These are always characterized by overlapping expression of Sox2/3 and Pax6. Thus, an essential molecular event in lens induction is the ‘turning on’ of the transcriptional regulators SOX2/3 in the Pax6-expressing ectoderm and these SOX proteins activate crystallin gene expression. Continued activity, especially of SOX1, is then essential for further development of the lens.
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16

Zhang, Yuli, and Linlin Hou. "Alternate Roles of Sox Transcription Factors beyond Transcription Initiation." International Journal of Molecular Sciences 22, no. 11 (May 31, 2021): 5949. http://dx.doi.org/10.3390/ijms22115949.

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Sox proteins are known as crucial transcription factors for many developmental processes and for a wide range of common diseases. They were believed to specifically bind and bend DNA with other transcription factors and elicit transcriptional activation or repression activities in the early stage of transcription. However, their functions are not limited to transcription initiation. It has been showed that Sox proteins are involved in the regulation of alternative splicing regulatory networks and translational control. In this review, we discuss the current knowledge on how Sox transcription factors such as Sox2, Sry, Sox6, and Sox9 allow the coordination of co-transcriptional splicing and also the mechanism of SOX4-mediated translational control in the context of RNA polymerase III.
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17

Kamachi, Yusuke, Kathryn S. E. Cheah, and Hisato Kondoh. "Mechanism of Regulatory Target Selection by the SOX High-Mobility-Group Domain Proteins as Revealed by Comparison of SOX1/2/3 and SOX9." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 107–20. http://dx.doi.org/10.1128/mcb.19.1.107.

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ABSTRACT SOX proteins bind similar DNA motifs through their high-mobility-group (HMG) domains, but their action is highly specific with respect to target genes and cell type. We investigated the mechanism of target selection by comparing SOX1/2/3, which activate δ-crystallin minimal enhancer DC5, with SOX9, which activates Col2a1 minimal enhancer COL2C2. These enhancers depend on both the SOX binding site and the binding site of a putative partner factor. The DC5 site was equally bound and bent by the HMG domains of SOX1/2 and SOX9. The activation domains of these SOX proteins mapped at the distal portions of the C-terminal domains were not cell specific and were independent of the partner factor. Chimeric proteins produced between SOX1 and SOX9 showed that to activate the DC5 enhancer, the C-terminal domain must be that of SOX1, although the HMG domains were replaceable. The SOX2-VP16 fusion protein, in which the activation domain of SOX2 was replaced by that of VP16, activated the DC5 enhancer still in a partner factor-dependent manner. The results argue that the proximal portion of the C-terminal domain of SOX1/2 specifically interacts with the partner factor, and this interaction determines the specificity of the SOX1/2 action. Essentially the same results were obtained in the converse experiments in which COL2C2 activation by SOX9 was analyzed, except that specificity of SOX9-partner factor interaction also involved the SOX9 HMG domain. The highly selective SOX-partner factor interactions presumably stabilize the DNA binding of the SOX proteins and provide the mechanism for regulatory target selection.
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18

Ishikawa, Ryuichi, Maiko Kawasaki, Katsushige Kawasaki, Akane Yamada, Supaluk Trakanant, Fumiya Meguro, Atsushi Kitamura, Takehisa Kudo, Takeyasu Maeda, and Atsushi Ohazama. "Sox Genes Show Spatiotemporal Expression during Murine Tongue and Eyelid Development." International Journal of Dentistry 2018 (October 9, 2018): 1–13. http://dx.doi.org/10.1155/2018/1601363.

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The tongue is a critical organ, involved in functions such as speaking, swallowing, mastication, and degustation. Although Sox genes are known to play critical roles in many biological processes, including organogenesis, the expression of the Sox family members during tongue development remains unclear. We therefore performed a comparative in situ hybridization analysis of 17 Sox genes (Sox1–14, 17, 18, and 21) during murine tongue development. Sox2, 4, 6, 8, 9, 10, 11, 12, and 21 were found to be expressed in the tongue epithelium, whereas Sox2, 4–6, 8–11, 13, and 21 showed expression in the mesenchyme of the developing tongue. Expression of Sox1, 4, 6, 8–12, and 21 were observed in the developing tongue muscle. Sox5 and 13 showed expression only at E12, while Sox1 expression was observed only on E18. Sox6, 8, 9, and 12 showed expression at several stages. Although the expression of Sox2, 4, 10, 11, and 21 was detected during all the four stages of tongue development, their expression patterns differed among the stages. We thus identified a dynamic spatiotemporal expression pattern of the Sox genes during murine tongue development. To understand whether Sox genes are involved in the development of other craniofacial organs through similar roles to those in tongue development, we also examined the expression of Sox genes in eyelid primordia, which also contain epithelium, mesenchyme, and muscle. However, expression patterns and timing of Sox genes differed between tongue and eyelid development. Sox genes are thus related to organogenesis through different functions in each craniofacial organ.
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Underwood, Adam, Daniel T. Rasicci, David Hinds, Jackson T. Mitchell, Jacob K. Zieba, Joshua Mills, Nicholas E. Arnold, et al. "Evolutionary Landscape of SOX Genes to Inform Genotype-to-Phenotype Relationships." Genes 14, no. 1 (January 14, 2023): 222. http://dx.doi.org/10.3390/genes14010222.

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The SOX transcription factor family is pivotal in controlling aspects of development. To identify genotype–phenotype relationships of SOX proteins, we performed a non-biased study of SOX using 1890 open-reading frame and 6667 amino acid sequences in combination with structural dynamics to interpret 3999 gnomAD, 485 ClinVar, 1174 Geno2MP, and 4313 COSMIC human variants. We identified, within the HMG (High Mobility Group)- box, twenty-seven amino acids with changes in multiple SOX proteins annotated to clinical pathologies. These sites were screened through Geno2MP medical phenotypes, revealing novel SOX15 R104G associated with musculature abnormality and SOX8 R159G with intellectual disability. Within gnomAD, SOX18 E137K (rs201931544), found within the HMG box of ~0.8% of Latinx individuals, is associated with seizures and neurological complications, potentially through blood–brain barrier alterations. A total of 56 highly conserved variants were found at sites outside the HMG-box, including several within the SOX2 HMG-box-flanking region with neurological associations, several in the SOX9 dimerization region associated with Campomelic Dysplasia, SOX14 K88R (rs199932938) flanking the HMG box associated with cardiovascular complications within European populations, and SOX7 A379V (rs143587868) within an SOXF conserved far C-terminal domain heterozygous in 0.716% of African individuals with associated eye phenotypes. This SOX data compilation builds a robust genotype-to-phenotype association for a gene family through more robust ortholog data integration.
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Hett, Anne Kathrin, and Arne Ludwig. "SRY-related (Sox) genes in the genome of European Atlantic sturgeon (Acipenser sturio)." Genome 48, no. 2 (April 1, 2005): 181–86. http://dx.doi.org/10.1139/g04-112.

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The Sox-gene family represents an ancient group of transcription factors involved in numerous developmental processes and sex determination in vertebrates. SOX proteins are characterized by a conserved high mobility group (HMG)-box domain, which is responsible for DNA binding and bending. We studied Sox genes in sturgeon, one of the most primitive groups of fishes characterized by a high chromosome number. Male and female genomes were screened for Sox genes using highly degenerate primers that amplified a broad range of HMG boxes. A total of 102 clones, representing 22 different sequences coding for 8 Sox genes, was detected and classified according to their orthologues. Sox2, Sox3, Sox4, Sox9, Sox11, Sox17, Sox19, and Sox21 were found in sturgeon; these genes represent Sox groups B, C, E, and F. In a phylogenetic analysis (neighbor-joining, maximum likelihood, maximum parsimony), these genes clustered with their mouse orthologues. In the case of Sox4, Sox17, and Sox21, we found evidence of gene duplication.Key words: Acipenseridae, gene evolution, sex determination, Sox genes.
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Amano, Katsuhiko, Kenji Hata, Atsushi Sugita, Yoko Takigawa, Koichiro Ono, Makoto Wakabayashi, Mikihiko Kogo, Riko Nishimura, and Toshiyuki Yoneda. "Sox9 Family Members Negatively Regulate Maturation and Calcification of Chondrocytes through Up-Regulation of Parathyroid Hormone–related Protein." Molecular Biology of the Cell 20, no. 21 (November 2009): 4541–51. http://dx.doi.org/10.1091/mbc.e09-03-0227.

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Sox9 is a transcription factor that plays an essential role in chondrogenesis and has been proposed to inhibit the late stages of endochondral ossification. However, the molecular mechanisms underlying the regulation of chondrocyte maturation and calcification by Sox9 remain unknown. In this study, we attempted to clarify roles of Sox9 in the late stages of chondrocyte differentiation. We found that overexpression of Sox9 alone or Sox9 together with Sox5 and Sox6 (Sox5/6/9) inhibited the maturation and calcification of murine primary chondrocytes and up-regulated parathyroid hormone–related protein (PTHrP) expression in primary chondrocytes and the mesenchymal cell line C3H10T1/2. Sox5/6/9 stimulated the early stages of chondrocyte proliferation and development. In contrast, Sox5/6/9 inhibited maturation and calcification of chondrocytes in organ culture. The inhibitory effects of Sox5/6/9 were rescued by treating with anti-PTHrP antibody. Moreover, Sox5/6/9 bound to the promoter region of the PTHrP gene and up-regulated PTHrP gene promoter activity. Interestingly, we also found that the Sox9 family members functionally collaborated with Ihh/Gli2 signaling to regulate PTHrP expression and chondrocyte differentiation. Our results provide novel evidence that Sox9 family members mediate endochondral ossification by up-regulating PTHrP expression in association with Ihh/Gli2 signaling.
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Lee, Wenqing Jean, Sumantra Chatterjee, Sook Peng Yap, Siew Lan Lim, Xing Xing, Petra Kraus, Wenjie Sun, et al. "An Integrative Developmental Genomics and Systems Biology Approach to Identify an In Vivo Sox Trio-Mediated Gene Regulatory Network in Murine Embryos." BioMed Research International 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/8932583.

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Embryogenesis is an intricate process involving multiple genes and pathways. Some of the key transcription factors controlling specific cell types are the Sox trio, namely, Sox5, Sox6, and Sox9, which play crucial roles in organogenesis working in a concerted manner. Much however still needs to be learned about their combinatorial roles during this process. A developmental genomics and systems biology approach offers to complement the reductionist methodology of current developmental biology and provide a more comprehensive and integrated view of the interrelationships of complex regulatory networks that occur during organogenesis. By combining cell type-specific transcriptome analysis and in vivo ChIP-Seq of the Sox trio using mouse embryos, we provide evidence for the direct control of Sox5 and Sox6 by the transcriptional trio in the murine model and by Morpholino knockdown in zebrafish and demonstrate the novel role of Tgfb2, Fbxl18, and Tle3 in formation of Sox5, Sox6, and Sox9 dependent tissues. Concurrently, a complete embryonic gene regulatory network has been generated, identifying a wide repertoire of genes involved and controlled by the Sox trio in the intricate process of normal embryogenesis.
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Bagchi, Angshuman, and Tapash Chandra Ghosh. "A structural study towards the understanding of the interactions of SoxY, SoxZ, and SoxB, leading to the oxidation of sulfur anions via the novel global sulfur oxidizing (sox) operon." Biochemical and Biophysical Research Communications 335, no. 2 (September 2005): 609–15. http://dx.doi.org/10.1016/j.bbrc.2005.07.115.

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24

Milivojevic, Milena, Gordana Nikcevic, Natasa Kovacevic-Grujicic, A. Krstic, Marija Mojsin, Danijela Drakulic, and Milena Stevanovic. "Involvement of ubiquitous and tale transcription factors, as well as liganded RXRα, in the regulation of human SOX2 gene expression in the NT2/D1 embryonal carcinoma cell line." Archives of Biological Sciences 62, no. 2 (2010): 199–210. http://dx.doi.org/10.2298/abs1002199m.

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SOX2 is a key transcription factor in embryonic development representing a universal marker of pluripotent stem cells. Based on the functional redundancy and overlapping expression patterns of SOXB1 subgroup members during development, the goal of this study has been to analyze if some aspects of regulation of expression are preserved between human SOX2 and SOX3 genes. Thus, we have tested several transcription factors previously demonstrated to play roles in controlling SOX3 gene activity for potential participation in the regulation of SOX2 gene expression in NT2/D1 cells. Here we report on the activation of SOX2 expression by ubiquitous transcription factors (NF-Y, Sp1 and MAZ), TALE family members (Pbx1 and Meis1), as well as liganded RXR?. Elucidating components involved in the regulation of SOX gene expression represent a valuable contribution in unraveling the regulatory networks operating in pluripotent embryonic cells.
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Bhattaram, Pallavi, Alfredo Penzo-Méndez, Kenji Kato, Kaustav Bandyopadhyay, Abhilash Gadi, Makoto M. Taketo, and Véronique Lefebvre. "SOXC proteins amplify canonical WNT signaling to secure nonchondrocytic fates in skeletogenesis." Journal of Cell Biology 207, no. 5 (December 1, 2014): 657–71. http://dx.doi.org/10.1083/jcb.201405098.

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Canonical WNT signaling stabilizes β-catenin to determine cell fate in many processes from development onwards. One of its main roles in skeletogenesis is to antagonize the chondrogenic transcription factor SOX9. We here identify the SOXC proteins as potent amplifiers of this pathway. The SOXC genes, i.e., Sox4, Sox11, and Sox12, are coexpressed in skeletogenic mesenchyme, including presumptive joints and perichondrium, but not in cartilage. Their inactivation in mouse embryo limb bud caused massive cartilage fusions, as joint and perichondrium cells underwent chondrogenesis. SOXC proteins govern these cells cell autonomously. They replace SOX9 in the adenomatous polyposis coli–Axin destruction complex and therein inhibit phosphorylation of β-catenin by GSK3. This inhibition, a crucial, limiting step in canonical WNT signaling, thus becomes a constitutive event. The resulting SOXC/canonical WNT-mediated synergistic stabilization of β-catenin contributes to efficient repression of Sox9 in presumptive joint and perichondrium cells and thereby ensures proper delineation and articulation of skeletal primordia. This synergy may determine cell fate in many processes besides skeletogenesis.
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26

Grabarczyk, Daniel B., Paul E. Chappell, Steven Johnson, Lukas S. Stelzl, Susan M. Lea, and Ben C. Berks. "Structural basis for specificity and promiscuity in a carrier protein/enzyme system from the sulfur cycle." Proceedings of the National Academy of Sciences 112, no. 52 (December 11, 2015): E7166—E7175. http://dx.doi.org/10.1073/pnas.1506386112.

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The bacterial Sox (sulfur oxidation) pathway is an important route for the oxidation of inorganic sulfur compounds. Intermediates in the Sox pathway are covalently attached to the heterodimeric carrier protein SoxYZ through conjugation to a cysteine on a protein swinging arm. We have investigated how the carrier protein shuttles intermediates between the enzymes of the Sox pathway using the interaction between SoxYZ and the enzyme SoxB as our model. The carrier protein and enzyme interact only weakly, but we have trapped their complex by using a “suicide enzyme” strategy in which an engineered cysteine in the SoxB active site forms a disulfide bond with the incoming carrier arm cysteine. The structure of this trapped complex, together with calorimetric data, identifies sites of protein–protein interaction both at the entrance to the enzyme active site tunnel and at a second, distal, site. We find that the enzyme distinguishes between the substrate and product forms of the carrier protein through differences in their interaction kinetics and deduce that this behavior arises from substrate-specific stabilization of a conformational change in the enzyme active site. Our analysis also suggests how the carrier arm-bound substrate group is able to outcompete the adjacent C-terminal carboxylate of the carrier arm for binding to the active site metal ions. We infer that similar principles underlie carrier protein interactions with other enzymes of the Sox pathway.
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27

Ahmad, Azaz, Stephanie Strohbuecker, Claudia Scotti, Cristina Tufarelli, and Virginie Sottile. "In Silico Identification of SOX1 Post-Translational Modifications Highlights a Shared Protein Motif." Cells 9, no. 11 (November 13, 2020): 2471. http://dx.doi.org/10.3390/cells9112471.

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The transcription factor SOX1 is a key regulator of neural stem cell development, acting to keep neural stem cells (NSCs) in an undifferentiated state. Postnatal expression of Sox1 is typically confined to the central nervous system (CNS), however, its expression in non-neural tissues has recently been implicated in tumorigenesis. The mechanism through which SOX1 may exert its function is not fully understood, and studies have mainly focused on changes in SOX1 expression at a transcriptional level, while its post-translational regulation remains undetermined. To investigate this, data were extracted from different publicly available databases and analysed to search for putative SOX1 post-translational modifications (PTMs). Results were compared to PTMs associated with SOX2 in order to identify potentially key PTM motifs common to these SOXB1 proteins, and mapped on SOX1 domain structural models. This approach identified several putative acetylation, phosphorylation, glycosylation and sumoylation sites within known functional domains of SOX1. In particular, a novel SOXB1 motif (xKSExSxxP) was identified within the SOX1 protein, which was also found in other unrelated proteins, most of which were transcription factors. These results also highlighted potential phospho-sumoyl switches within this SOXB1 motif identified in SOX1, which could regulate its transcriptional activity. This analysis indicates different types of PTMs within SOX1, which may influence its regulatory role as a transcription factor, by bringing changes to its DNA binding capacities and its interactions with partner proteins. These results provide new research avenues for future investigations on the mechanisms regulating SOX1 activity, which could inform its roles in the contexts of neural stem cell development and cancer.
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Zhao, Suling, Jennifer Nichols, Austin G. Smith, and Meng Li. "SoxB transcription factors specify neuroectodermal lineage choice in ES cells." Molecular and Cellular Neuroscience 27, no. 3 (November 2004): 332–42. http://dx.doi.org/10.1016/j.mcn.2004.08.002.

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29

Neriec, Nathalie, and Claude Desplan. "Different ways to make neurons: parallel evolution in the SoxB family." Genome Biology 15, no. 5 (2014): 116. http://dx.doi.org/10.1186/gb4177.

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30

Richards, Gemma Sian, and Fabian Rentzsch. "Regulation of Nematostella neural progenitors by SoxB, Notch and bHLH genes." Development 142, no. 19 (October 1, 2015): 3332–42. http://dx.doi.org/10.1242/dev.123745.

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31

Flici, Hakima, Christine E. Schnitzler, R. Cathriona Millane, Graham Govinden, Amy Houlihan, Stephanie D. Boomkamp, Sanbing Shen, Andreas D. Baxevanis, and Uri Frank. "An Evolutionarily Conserved SoxB-Hdac2 Crosstalk Regulates Neurogenesis in a Cnidarian." Cell Reports 18, no. 6 (February 2017): 1395–409. http://dx.doi.org/10.1016/j.celrep.2017.01.019.

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32

Qin, Sha, Gaoming Liu, Haoer Jin, Xue Chen, Jiang He, Juxiong Xiao, Yan Qin, Yitao Mao, and Luqing Zhao. "The Dysregulation of SOX Family Correlates with DNA Methylation and Immune Microenvironment Characteristics to Predict Prognosis in Hepatocellular Carcinoma." Disease Markers 2022 (April 13, 2022): 1–21. http://dx.doi.org/10.1155/2022/2676114.

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Background. Due to the molecular heterogeneity of hepatocellular carcinoma (HCC), majority of patients respond poorly among various of therapy. This study is aimed at conducting a comprehensive analysis about roles of SOX family in HCC for obtaining more therapeutic targets and biomarkers which may bring new ideas for the treatment of HCC. Methods. UALCAN, Kaplan Meier plotter, cBioPortal, STRING, WebGestalt, Metascape, TIMER 2.0, DiseaseMeth, MethSurv, HPA, CCLE database, and Cytoscape software were used to comprehensively analyze the bioinformatic data. Results. SOX2, SOX4, SOX8, SOX10, SOX11, SOX12, SOX17, and SOX18 were significantly differentially expressed in HCC and normal tissues and were valuable for the grade and survival of HCC patients. In addition, the gene alterations of SOX family happened frequently, and SOX4 and SOX17 had the highest mutation rate. The function of SOX family on HCC may be closely correlated with the regulation of angiogenesis-related signaling pathways. Moreover, SOX4, SOX8, SOX11, SOX12, SOX17, and SOX18 were correlation with 8 types of immune cells (including CD8+ T cell, CD4+ T cell, B cell, Tregs, neutrophil, macrophage, myeloid DC, and NK cell), and we found that most types of immune cells had a positive correlation with SOX family. Notably, CD4+ T cell and macrophage were positively related with all these SOX family. NK cells were negatively related with most SOX family genes. DNA methylation levels in promoter area of SOX2, SOX4, and SOX10 were lower in HCC than normal tissues, while SOX8, SOX11, SOX17, and SOX18 had higher DNA methylation levels than normal tissues. Moreover, higher DNA methylation level of SOX12 and SOX18 demonstrated worse survival rates in patients with HCC. Conclusion. SOX family genes could predict the prognosis of HCC. In addition, the regulation of angiogenesis-related signaling pathways may participate in the development of HCC. DNA methylation level and immune microenvironment characteristics (especially CD4+ T cell and macrophage immune cell infiltration) could be a novel insight for predicting prognosis in HCC.
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33

Kishi, M., K. Mizuseki, N. Sasai, H. Yamazaki, K. Shiota, S. Nakanishi, and Y. Sasai. "Requirement of Sox2-mediated signaling for differentiation of early Xenopus neuroectoderm." Development 127, no. 4 (February 15, 2000): 791–800. http://dx.doi.org/10.1242/dev.127.4.791.

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From early stages of development, Sox2-class transcription factors (Sox1, Sox2 and Sox3) are expressed in neural tissues and sensory epithelia. In this report, we show that Sox2 function is required for neural differentiation of early Xenopus ectoderm. Microinjection of dominant-negative forms of Sox2 (dnSox2) mRNA inhibits neural differentiation of animal caps caused by attenuation of BMP signals. Expression of dnSox2 in developing embryos suppresses expression of N-CAM and regional neural markers. We have analyzed temporal requirement of Sox2-mediated signaling by using an inducible dnSox2 construct fused to the ligand-binding domain of the glucocorticoid receptor. Attenuation of Sox2 function both from the late blastula stage and from the late gastrula stage onwards causes an inhibition of neural differentiation in animal caps and in whole embryos. Additionally, dnSox2-injected cells that fail to differentiate into neural tissues are not able to adopt epidermal cell fate. These data suggest that Sox2-class genes are essential for early neuroectoderm cells to consolidate their neural identity during secondary steps of neural differentiation.
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Uchida, Takeshi, Motonari Tsubaki, Tatsuki Kurokawa, Hiroshi Hori, Junshi Sakamoto, Teizo Kitagawa, and Nobuhito Sone. "Active site structure of SoxB-type cytochrome bo3 oxidase from thermophilic Bacillus." Journal of Inorganic Biochemistry 82, no. 1-4 (November 2000): 65–72. http://dx.doi.org/10.1016/s0162-0134(00)00145-8.

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35

Krishnani, Kishore K., Gopalapillay Gopikrishna, Subramanian M. Pillai, and Baijnath P. Gupta. "Abundance of sulphur-oxidizing bacteria in coastal aquaculture using soxB gene analyses." Aquaculture Research 41, no. 9 (August 2010): 1290–301. http://dx.doi.org/10.1111/j.1365-2109.2009.02415.x.

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36

Guimont, Philippe, Francine Grondin, and Claire M. Dubois. "Sox9-dependent transcriptional regulation of the proprotein convertase furin." American Journal of Physiology-Cell Physiology 293, no. 1 (July 2007): C172—C183. http://dx.doi.org/10.1152/ajpcell.00349.2006.

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The proprotein convertase furin participates in the maturation/bioactivation of a variety of proproteins involved in chondrogenesis events. These include parathyroid hormone-related peptide (PTHrP), an autocrine/paracrine factor that is crucial to both normal cartilage development and cartilage-related pathological processes. Despite the known importance of furin activity in the bioactivation of the polypeptides, the mechanisms that control furin regulation in chondrogenesis remain unknown. To gain insight into the molecular regulation of furin, we used the mouse prechondrogenic ATDC5 cell line, an established in vitro model of cartilage differentiation. Peak expression of both furin mRNA and furin PTHrP maturation was observed during chondrocyte nodule formation stage, an event that correlated with increased mRNA levels of Sox9, a potent high-mobility-group (HMG) box-containing transcription factor required for cartilage formation. Inhibition of furin activity led to a diminution in maturation of PTHrP, suggesting a relationship between Sox9-induced regulation of furin and chondrogenesis events. Transient transfection of Sox9 in nonchondrogenic cells resulted in a marked increase in furin mRNA and in the transactivation of the furin P1A promoter. Direct Sox9 action on the P1A promoter was narrowed down to a critical paired site with Sox9 binding capability in vitro and in vivo. Sox9 transactivation effect was inhibited by L-Sox5 and Sox-6, two Sox9 homologs also expressed in ATDC5 cells. Sox6 inhibitory effect was reduced when using Sox6-HMG-box mutants, indicating a repressive effect through direct HMG-box/DNA binding. Our work suggests a mechanism by which furin is regulated during chondrogenesis. It also adds to the complexity of Sox molecule interaction during gene regulation.
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Arefin, Badrul, Farjana Parvin, Shahrzad Bahrampour, Caroline Bivik Stadler, and Stefan Thor. "Drosophila Neuroblast Selection Is Gated by Notch, Snail, SoxB, and EMT Gene Interplay." Cell Reports 29, no. 11 (December 2019): 3636–51. http://dx.doi.org/10.1016/j.celrep.2019.11.038.

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38

Das, Debanu, Fumiaki Yumoto, Kristopher Kuchenbecker, Ashley Deacon, Robert Fletterick, and Ian Wilson. "Understanding disease mutations from the crystal structure of SOX9 with DNA." Acta Crystallographica Section A Foundations and Advances 70, a1 (August 5, 2014): C1398. http://dx.doi.org/10.1107/s205327331408601x.

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SRY(Sex determining Region Y)-box or SOX transcription factors are important in early development and maintenance of different cell pools after birth. Of the ~20 SOX proteins (SRY, SOX1-SOX15, SOX17, SOX18, SOX21 and SOX30), SOX2, SOX9 and SOX10 mutations are primarily disease-associated: SOX2 with Combined Pituitary Hormone Deficiency, Microphthalmia, Septo-optic dysplasia and anophthalmic syndrome; SOX9 with Campomelic Dysplasia (affects development of the reproductive and skeletal system); and SOX10 (~94% sequence identity to SOX9) with Waardenburg Syndrome (affects audition and pigmentation in hair, eyes and skin; and specifically with WS types 2 and 4). As part of our Protein Structure Initiative (PSI)-Biology partnership, we performed structural and mutational analyses including x-ray crystallography and surface plasmon resonance assays, on the DNA-binding HMG domain of SOX9 with duplex DNA. Crystals were obtained in C222 space group and the structure was determined by molecular replacement to 2.77 Å resolution with final Rcryst/Rfree of 24.8/27.8%. The overall structure of the SOX9-DNA complex is similar to other SOX/SRY protein complexes. The SOX9-DNA protein-DNA interactions suggested a panel of mutations to assay for biochemical activity, which allowed us to understand the molecular basis of five mutations identified in Campomelic Dysplasia. These mutated residues have direct contact with DNA as well as indirect contacts, i.e., these mutations lead to allosteric secondary structure changes in the protein, which affect residues in direct contact with DNA. Due to the very high sequence identity between SOX9 and SOX10, our crystal structure also helps to rationalize the effect of SOX10 mutations in Waardenburg Syndrome. This work is supported by NIH grants U54 GM094586 and U01 GM094614. SSRL operations are funded by DOE BES, and the SSRL SMB program by DOE BER, NIH NCRR BTP and NIH NIGMS.
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39

Stancheva, G., T. Goranova, M. Laleva, M. Kamenova, A. Mitkova, N. Velinov, G. Poptodorov, R. Kaneva, V. Mitev, and N. Gabrovsky. "698: Gene expression of SOX2, SOX6, SOX8 and SOX9 and their prognostic role in patients with gliomas." European Journal of Cancer 50 (July 2014): S168. http://dx.doi.org/10.1016/s0959-8049(14)50616-8.

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40

Mandal, Subhrangshu, Moidu Jameela Rameez, Sumit Chatterjee, Jagannath Sarkar, Prosenjit Pyne, Sabyasachi Bhattacharya, Rahul Shaw, and Wriddhiman Ghosh. "Molecular mechanism of sulfur chemolithotrophy in the betaproteobacterium Pusillimonas ginsengisoli SBSA." Microbiology 166, no. 4 (April 1, 2020): 386–97. http://dx.doi.org/10.1099/mic.0.000890.

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Chemolithotrophic sulfur oxidation represents a significant part of the biogeochemical cycling of this element. Due to its long evolutionary history, this ancient metabolism is well known for its extensive mechanistic and phylogenetic diversification across a diverse taxonomic spectrum. Here we carried out whole-genome sequencing and analysis of a new betaproteobacterial isolate, Pusillimonas ginsengisoli SBSA, which is found to oxidize thiosulfate via the formation of tetrathionate as an intermediate. The 4.7 Mb SBSA genome was found to encompass a soxCDYZAXOB operon, plus single thiosulfate dehydrogenase (tsdA) and sulfite : acceptor oxidoreductase (sorAB) genes. Recombination-based knockout of tsdA revealed that the entire thiosulfate is first converted to tetrathionate by the activity of thiosulfate dehydrogenase (TsdA) and the Sox pathway is not functional in this bacterium despite the presence of all necessary sox genes. The ∆soxYZ and ∆soxXA knockout mutants exhibited a wild-type-like phenotype for thiosulfate/tetrathionate oxidation, whereas ∆soxB, ∆soxCD and soxO::KanR mutants only oxidized thiosulfate up to tetrathionate intermediate and had complete impairment in tetrathionate oxidation. The substrate-dependent O2 consumption rate of whole cells and the sulfur-oxidizing enzyme activities of cell-free extracts, measured in the presence/absence of thiol inhibitors/glutathione, indicated that glutathione plays a key role in SBSA tetrathionate oxidation. The present findings collectively indicate that the potential glutathione : tetrathionate coupling in P. ginsengisoli involves a novel enzymatic component, which is different from the dual-functional thiol dehydrotransferase (ThdT), while subsequent oxidation of the sulfur intermediates produced (e.g. glutathione : sulfodisulfane molecules) may proceed via the iterative action of soxBCD .
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41

Iwafuchi-Doi, Makiko, Yuzo Yoshida, Daria Onichtchouk, Manuel Leichsenring, Wolfgang Driever, Tatsuya Takemoto, Masanori Uchikawa, Yusuke Kamachi, and Hisato Kondoh. "The Pou5f1/Pou3f-dependent but SoxB-independent regulation of conserved enhancer N2 initiates Sox2 expression during epiblast to neural plate stages in vertebrates." Developmental Biology 352, no. 2 (April 2011): 354–66. http://dx.doi.org/10.1016/j.ydbio.2010.12.027.

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Smits, Patrick, Peter Dy, Srijeet Mitra, and Véronique Lefebvre. "Sox5 and Sox6 are needed to develop and maintain source, columnar, and hypertrophic chondrocytes in the cartilage growth plate." Journal of Cell Biology 164, no. 5 (March 1, 2004): 747–58. http://dx.doi.org/10.1083/jcb.200312045.

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Sox5 and Sox6 encode Sry-related transcription factors that redundantly promote early chondroblast differentiation. Using mouse embryos with three or four null alleles of Sox5 and Sox6, we show that they are also essential and redundant in major steps of growth plate chondrocyte differentiation. Sox5 and Sox6 promote the development of a highly proliferating pool of chondroblasts between the epiphyses and metaphyses of future long bones. This pool is the likely cellular source of growth plates. Sox5 and Sox6 permit formation of growth plate columnar zones by keeping chondroblasts proliferating and by delaying chondrocyte prehypertrophy. They allow induction of chondrocyte hypertrophy and permit formation of prehypertrophic and hypertrophic zones by delaying chondrocyte terminal differentiation induced by ossification fronts. They act, at least in part, by down-regulating Ihh signaling, Fgfr3, and Runx2 and by up-regulating Bmp6. In conclusion, Sox5 and Sox6 are needed for the establishment of multilayered growth plates, and thereby for proper and timely development of endochondral bones.
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43

Overton, Paul M., Lisa A. Meadows, Joachim Urban, and Steven Russell. "Evidence for differential and redundant function of the Sox genesDichaeteandSoxNduring CNS development inDrosophila." Development 129, no. 18 (September 15, 2002): 4219–28. http://dx.doi.org/10.1242/dev.129.18.4219.

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Group B Sox-domain proteins encompass a class of conserved DNA-binding proteins expressed from the earliest stages of metazoan CNS development. In all higher organisms studied to date, related Group B Sox proteins are co-expressed in the developing CNS; in vertebrates there are three (Sox1, Sox2 and Sox3) and in Drosophila there are two (SoxNeuro and Dichaete). It has been suggested there may be a degree of functional redundancy in Sox function during CNS development. We describe the CNS phenotype of a null mutation in the Drosophila SoxNeuro gene and provide the first direct evidence for both redundant and differential Sox function during CNS development in Drosophila. In the lateral neuroectoderm, where SoxNeuro is uniquely expressed, SoxNeuro mutants show a loss or reduction of achaete expression as well as a loss of many correctly specified lateral neuroblasts. By contrast, in the medial neuroectoderm, where the expression of SoxNeuro and Dichaete overlaps, the phenotypes of both single mutants are mild. In accordance with an at least partially redundant function in that region, SoxNeuro/Dichaete double mutant embryos show a severe neural hypoplasia throughout the central nervous system, as well as a dramatic loss of achaete expressing proneural clusters and medially derived neuroblasts. However, the finding that Dichaete and SoxN exhibit opposite effects on achaete expression within the intermediate neuroectoderm demonstrates that each protein also has region-specific unique functions during early CNS development in the Drosophila embryo.
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44

Danopoulos, Soula, Irving Alonso, Matthew E. Thornton, Brendan H. Grubbs, Saverio Bellusci, David Warburton, and Denise Al Alam. "Human lung branching morphogenesis is orchestrated by the spatiotemporal distribution of ACTA2, SOX2, and SOX9." American Journal of Physiology-Lung Cellular and Molecular Physiology 314, no. 1 (January 1, 2018): L144—L149. http://dx.doi.org/10.1152/ajplung.00379.2017.

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Lung morphogenesis relies on a number of important processes, including proximal-distal patterning, cell proliferation, migration and differentiation, as well as epithelial-mesenchymal interactions. In mouse lung development, SOX2+ cells are localized in the proximal epithelium, whereas SOX9+ cells are present in the distal epithelium. We show that, in human lung, expression of these transcription factors differs, in that during the pseudoglandular stage distal epithelial progenitors at the tips coexpress SOX2 and SOX9. This double-positive population was no longer present by the canalicular stages of development. As in mouse, the human proximal epithelial progenitors express solely SOX2 and are surrounded by smooth muscle cells (SMCs) both in the proximal airways and at the epithelial clefts. Upon Ras-related C3 botulinum toxin substrate 1 inhibition, we noted decreased branching, as well as increased SMC differentiation, attenuated peristalsis, and a reduction in the distal double-positive SOX2/SOX9 progenitor cell population. Thus, the presence of SOX2/SOX9 double-positive progenitor cells in the distal epithelium during the pseudoglandular stage of human lung development appears to be critical to proximal-distal patterning and lung branching. Moreover, SMCs promote a SOX2 proximal phenotype and seem to suppress the SOX9+ population.
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45

Archer, Tenley C., Jing Jin, and Elena S. Casey. "Interaction of Sox1, Sox2, Sox3 and Oct4 during primary neurogenesis." Developmental Biology 350, no. 2 (February 2011): 429–40. http://dx.doi.org/10.1016/j.ydbio.2010.12.013.

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46

Ikeda, Toshiyuki, Satoru Kamekura, Akihiko Mabuchi, Ikuyo Kou, Shoji Seki, Tsuyoshi Takato, Kozo Nakamura, Hiroshi Kawaguchi, Shiro Ikegawa, and Ung-il Chung. "The combination of SOX5, SOX6, and SOX9 (the SOX trio) provides signals sufficient for induction of permanent cartilage." Arthritis & Rheumatism 50, no. 11 (November 2004): 3561–73. http://dx.doi.org/10.1002/art.20611.

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47

Richards, G. S., and F. Rentzsch. "Transgenic analysis of a SoxB gene reveals neural progenitor cells in the cnidarian Nematostella vectensis." Development 141, no. 24 (November 13, 2014): 4681–89. http://dx.doi.org/10.1242/dev.112029.

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48

Meyer, Birte, Johannes F. Imhoff, and Jan Kuever. "Molecular analysis of the distribution and phylogeny of the soxB gene among sulfur-oxidizing bacteria – evolution of the Sox sulfur oxidation enzyme system." Environmental Microbiology 9, no. 12 (December 2007): 2957–77. http://dx.doi.org/10.1111/j.1462-2920.2007.01407.x.

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49

Ducluzeau, Anne-Lise, Barbara Schoepp-Cothenet, Robert van Lis, Frauke Baymann, Michael J. Russell, and Wolfgang Nitschke. "The evolution of respiratory O 2 /NO reductases: an out-of-the-phylogenetic-box perspective." Journal of The Royal Society Interface 11, no. 98 (September 6, 2014): 20140196. http://dx.doi.org/10.1098/rsif.2014.0196.

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Complex life on our planet crucially depends on strong redox disequilibria afforded by the almost ubiquitous presence of highly oxidizing molecular oxygen. However, the history of O 2 -levels in the atmosphere is complex and prior to the Great Oxidation Event some 2.3 billion years ago, the amount of O 2 in the biosphere is considered to have been extremely low as compared with present-day values. Therefore the evolutionary histories of life and of O 2 -levels are likely intricately intertwined. The obvious biological proxy for inferring the impact of changing O 2 -levels on life is the evolutionary history of the enzyme allowing organisms to tap into the redox power of molecular oxygen, i.e. the bioenergetic O 2 reductases, alias the cytochrome and quinol oxidases. Consequently, molecular phylogenies reconstructed for this enzyme superfamily have been exploited over the last two decades in attempts to elucidate the interlocking between O 2 levels in the environment and the evolution of respiratory bioenergetic processes. Although based on strictly identical datasets, these phylogenetic approaches have led to diametrically opposite scenarios with respect to the history of both the enzyme superfamily and molecular oxygen on the Earth. In an effort to overcome the deadlock of molecular phylogeny, we here review presently available structural, functional, palaeogeochemical and thermodynamic information pertinent to the evolution of the superfamily (which notably also encompasses the subfamily of nitric oxide reductases). The scenario which, in our eyes, most closely fits the ensemble of these non-phylogenetic data, sees the low O 2 -affinity SoxM- (or A-) type enzymes as the most recent evolutionary innovation and the high-affinity O 2 reductases (SoxB or B and cbb 3 or C) as arising independently from NO-reducing precursor enzymes.
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50

Sock, Elisabeth, Katy Schmidt, Irm Hermanns-Borgmeyer, Michael R. Bösl, and Michael Wegner. "Idiopathic Weight Reduction in Mice Deficient in the High-Mobility-Group Transcription Factor Sox8." Molecular and Cellular Biology 21, no. 20 (October 15, 2001): 6951–59. http://dx.doi.org/10.1128/mcb.21.20.6951-6959.2001.

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ABSTRACT Sox8, Sox9, and Sox10 constitute subgroup E within the Sox family of transcription factors. Many Sox proteins are essential regulators of development. Sox9, for instance, is required for chondrogenesis and male sex determination; Sox10 plays key roles in neural crest development and peripheral gliogenesis. The function of Sox8 has not been studied so far. Here, we generated mice deficient in this third member of subgroup E. In analogy to the case for the related Sox9 and Sox10, we expected severe developmental defects in these mice. Despite strong expression of Sox8 in many tissues, including neural crest, nervous system, muscle, cartilage, adrenal gland, kidney, and testis, homozygous mice developed normally in utero, were born at Mendelian frequencies, and were viable. A substantial reduction in weight was observed in these mice; however, this reduction was not attributable to significant structural deficits in any of the Sox8-expressing tissues. Because of frequent coexpression with either Sox9 or Sox10, the mild phenotype of Sox8-deficient mice might at least in part be due to functional redundancy between group E Sox proteins.
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