Relevant bibliographies by topics / Sox2 transcription factor

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'Sox2 transcription factor'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Sox2 transcription factor"

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Li, Pu-Yu, Ping Wang, She-Gan Gao, and Dao-Yin Dong. "Long Noncoding RNA SOX2-OT: Regulations, Functions, and Roles on Mental Illnesses, Cancers, and Diabetic Complications." BioMed Research International 2020 (November 26, 2020): 1–12. http://dx.doi.org/10.1155/2020/2901589.

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SRY-box transcription factor 2 (SOX2) overlapping transcript (SOX2-OT) is an evolutionarily conserved long noncoding RNA. Its intronic region contains the SOX2 gene, the major regulator of the pluripotency of embryonic stem cells. The human SOX2-OT gene comprises multiple exons and has multiple transcription start sites and generates hundreds of transcripts. Transcription factors (IRF4, AR, and SOX3), transcriptional inhibitors (NSPc1, MTA3, and YY1), and miRNAs (miR-211 and miR-375) have been demonstrated to control certain SOX2-OT transcript level at the transcriptional or posttranscriptional levels. Accumulated evidence indicates its crucial roles in the regulation of the SOX2 gene, miRNAs, and transcriptional process. Restricted expression of SOX2-OT transcripts in the brain results in the association between SOX2-OT single nucleotide polymorphisms and mental illnesses such as schizophrenia and anorexia nervosa. SOX2-OT is notably elevated in tumor tissues, and a high level of SOX2-OT is well correlated with poor clinical outcomes in cancer patients, leading to the establishment of its role as an oncogene and a prognostic or diagnostic biomarker for cancers. The emerging evidence supports that SOX2-OT mediates diabetic complications. In summary, SOX2-OT has diversified functions and could be a therapeutic target for various diseases.
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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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Tan, Cheng, and Shoji Takada. "Nucleosome allostery in pioneer transcription factor binding." Proceedings of the National Academy of Sciences 117, no. 34 (August 10, 2020): 20586–96. http://dx.doi.org/10.1073/pnas.2005500117.

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While recent experiments revealed that some pioneer transcription factors (TFs) can bind to their target DNA sequences inside a nucleosome, the binding dynamics of their target recognitions are poorly understood. Here we used the latest coarse-grained models and molecular dynamics simulations to study the nucleosome-binding procedure of the two pioneer TFs, Sox2 and Oct4. In the simulations for a strongly positioning nucleosome, Sox2 selected its target DNA sequence only when the target was exposed. Otherwise, Sox2 entropically bound to the dyad region nonspecifically. In contrast, Oct4 plastically bound on the nucleosome mainly in two ways. First, the two POU domains of Oct4 separately bound to the two parallel gyres of the nucleosomal DNA, supporting the previous experimental results of the partial motif recognition. Second, the POUSdomain of Oct4 favored binding on the acidic patch of histones. Then, simulating the TFs binding to a genomic nucleosome, theLIN28Bnucleosome, we found that the recognition of a pseudo motif by Sox2 induced the local DNA bending and shifted the population of the rotational position of the nucleosomal DNA. The redistributed DNA phase, in turn, changed the accessibility of a distant TF binding site, which consequently affected the binding probability of a second Sox2 or Oct4. These results revealed a nucleosomal DNA-mediated allosteric mechanism, through which one TF binding event can change the global conformation, and effectively regulate the binding of another TF at distant sites. Our simulations provide insights into the binding mechanism of single and multiple TFs on the nucleosome.
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Moosa, Mahdi, Phoebe Tsoi, Kyoung-Jae Choi, Allan Ferreon, and Josephine Ferreon. "Direct Single-Molecule Observation of Sequential DNA Bending Transitions by the Sox2 HMG Box." International Journal of Molecular Sciences 19, no. 12 (December 4, 2018): 3865. http://dx.doi.org/10.3390/ijms19123865.

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Sox2 is a pioneer transcription factor that initiates cell fate reprogramming through locus-specific differential regulation. Mechanistically, it was assumed that Sox2 achieves its regulatory diversity via heterodimerization with partner transcription factors. Here, utilizing single-molecule fluorescence spectroscopy, we show that Sox2 alone can modulate DNA structural landscape in a dosage-dependent manner. We propose that such stoichiometric tuning of regulatory DNAs is crucial to the diverse biological functions of Sox2, and represents a generic mechanism of conferring functional plasticity and multiplicity to transcription factors.
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Gandhi, Neha S., Edina Wang, Anabel Sorolla, Yu Jie Kan, Adil Malik, Jyotsna Batra, Kimberly A. Young, Wan Jun Tie, Pilar Blancafort, and Ricardo L. Mancera. "Design and Characterization of a Cell-Penetrating Peptide Derived from the SOX2 Transcription Factor." International Journal of Molecular Sciences 22, no. 17 (August 28, 2021): 9354. http://dx.doi.org/10.3390/ijms22179354.

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SOX2 is an oncogenic transcription factor overexpressed in nearly half of the basal-like triple-negative breast cancers associated with very poor outcomes. Targeting and inhibiting SOX2 is clinically relevant as high SOX2 mRNA levels are positively correlated with decreased overall survival and progression-free survival in patients affected with breast cancer. Given its key role as a master regulator of cell proliferation, SOX2 represents an important scaffold for the engineering of dominant-negative synthetic DNA-binding domains (DBDs) that act by blocking or interfering with the oncogenic activity of the endogenous transcription factor in cancer cells. We have synthesized an interference peptide (iPep) encompassing a truncated 24 amino acid long C-terminus of SOX2 containing a potential SOX-specific nuclear localization sequence, and the determinants of the binding of SOX2 to the DNA and to its transcription factor binding partners. We found that the resulting peptide (SOX2-iPep) possessed intrinsic cell penetration and promising nuclear localization into breast cancer cells, and decreased cellular proliferation of SOX2 overexpressing cell lines. The novel SOX2-iPep was found to exhibit a random coil conformation predominantly in solution. Molecular dynamics simulations were used to characterize the interactions of both the SOX2 transcription factor and the SOX2-iPep with FGF4-enhancer DNA in the presence of the POU domain of the partner transcription factor OCT4. Predictions of the free energy of binding revealed that the iPep largely retained the binding affinity for DNA of parental SOX2. This work will enable the future engineering of novel dominant interference peptides to transport different therapeutic cargo molecules such as anti-cancer drugs into cells.
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Dash, Soma, Lindy K. Brastrom, Shaili D. Patel, C. Anthony Scott, Diane C. Slusarski, and Salil A. Lachke. "The master transcription factor SOX2, mutated in anophthalmia/microphthalmia, is post-transcriptionally regulated by the conserved RNA-binding protein RBM24 in vertebrate eye development." Human Molecular Genetics 29, no. 4 (December 9, 2019): 591–604. http://dx.doi.org/10.1093/hmg/ddz278.

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Abstract Mutations in the key transcription factor, SOX2, alone account for 20% of anophthalmia (no eye) and microphthalmia (small eye) birth defects in humans—yet its regulation is not well understood, especially on the post-transcription level. We report the unprecedented finding that the conserved RNA-binding motif protein, RBM24, positively controls Sox2 mRNA stability and is necessary for optimal SOX2 mRNA and protein levels in development, perturbation of which causes ocular defects, including microphthalmia and anophthalmia. RNA immunoprecipitation assay indicates that RBM24 protein interacts with Sox2 mRNA in mouse embryonic eye tissue. and electrophoretic mobility shift assay shows that RBM24 directly binds to the Sox2 mRNA 3’UTR, which is dependent on AU-rich elements (ARE) present in the Sox2 mRNA 3’UTR. Further, we demonstrate that Sox2 3’UTR AREs are necessary for RBM24-based elevation of Sox2 mRNA half-life. We find that this novel RBM24–Sox2 regulatory module is essential for early eye development in vertebrates. We show that Rbm24-targeted deletion using a constitutive CMV-driven Cre in mouse, and rbm24a-CRISPR/Cas9-targeted mutation or morpholino knockdown in zebrafish, results in Sox2 downregulation and causes the developmental defects anophthalmia or microphthalmia, similar to human SOX2-deficiency defects. We further show that Rbm24 deficiency leads to apoptotic defects in mouse ocular tissue and downregulation of eye development markers Lhx2, Pax6, Jag1, E-cadherin and gamma-crystallins. These data highlight the exquisite specificity that conserved RNA-binding proteins like RBM24 mediate in the post-transcriptional control of key transcription factors, namely, SOX2, associated with organogenesis and human developmental defects.
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Yamatsuji, Tomoki, Etsuko Yokota, Takashi Sera, Noriaki Manabe, Takuya Fukazawa, and Yoshio Naomoto. "PS02.047: TARGETED SILENCING OF SOX2 BY AN ARTIFICIAL TRANSCRIPTION FACTOR SUPPRESSED THE GROWTH OF ESOPHAGEAL CANCER CELLS." Diseases of the Esophagus 31, Supplement_1 (September 1, 2018): 133–34. http://dx.doi.org/10.1093/dote/doy089.ps02.047.

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Abstract Background SOX2 is a transcription factor that is fundamental for early development and for the maintenance of stem cells in multiple adult tissues and also plays an important role in squamous cell differentiation. Amplification of chromosome 3q26 is the most common of the genetic alterations found in squamous cell carcinoma (SCC). SOX2 is a candidate oncogene present in this locus and amplification of SOX2 has been reported in lung and esophageal squamous cell SCC. In this study, we have developed a zinc finger-based artificial transcription factor (ATF) to selectively suppress SOX2 expression in cancer cells and termed the system ATF/SOX2. Methods We engineered the ATF using six zinc finger arrays designed to target a 19 bp site in the SOX2 distal promoter and a KOX transcriptional repressor domain. A recombinant adenoviral vector Ad-ATF/SOX2 that expresses ATF/SOX2 suppressed SOX2 at the mRNA and protein levels in esophageal SCC cells(TE1 and TE4) expressing SOX2. Results Ad-ATF/SOX2 decreased esophageal SCC cells proliferation and colony formation more effectively than the recombinant adenoviral vector Ad-shSOX2, which expresses SOX2 short hairpin RNA (shSOX2). Ad-ATF/SOX2 induced the cell cycle inhibitor CDKN1A more strongly than Ad-shSOX2. Moreover, Ad-ATF/SOX2 effectively inhibited tumor growth in a SCC xenograft mouse model. Conclusion In this study, we have shown that the targeted down-regulation of SOX2 using ATF based technologies can be used as an effective tool for the treatment of SCC in esophageal cancers that express SOX2. Our results indicate that ATF/SOX2 would lead to the development of an effective molecular-targeted therapy for esophageal SCC. Disclosure All authors have declared no conflicts of interest.
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Aguilar-Medina, Maribel, Mariana Avendaño-Félix, Erik Lizárraga-Verdugo, Mercedes Bermúdez, José Geovanni Romero-Quintana, Rosalío Ramos-Payan, Erika Ruíz-García, and César López-Camarillo. "SOX9 Stem-Cell Factor: Clinical and Functional Relevance in Cancer." Journal of Oncology 2019 (April 1, 2019): 1–16. http://dx.doi.org/10.1155/2019/6754040.

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Transcriptional and epigenetic embryonic programs can be reactivated in cancer cells. As result, a specific subset of undifferentiated cells with stem-cells properties emerges and drives tumorigenesis. Recent findings have shown that ectoderm- and endoderm-derived tissues continue expressing stem-cells related transcription factors of the SOX-family of proteins such as SOX2 and SOX9 which have been implicated in the presence of cancer stem-like cells (CSCs) in tumors. Currently, there is enough evidence suggesting an oncogenic role for SOX9 in different types of human cancers. This review provides a summary of the current knowledge about the involvement of SOX9 in development and progression of cancer. Understanding the functional roles of SOX9 and clinical relevance is crucial for developing novel treatments targeting CSCs in cancer.
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POLAKOVA, INGRID, MARTINA DUSKOVA, and MICHAL SMAHEL. "Antitumor DNA vaccination against the Sox2 transcription factor." International Journal of Oncology 45, no. 1 (April 28, 2014): 139–46. http://dx.doi.org/10.3892/ijo.2014.2402.

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Lu, Yurong, Yiwen Zhu, Shihan Deng, Yuhuang Chen, Wei Li, Jing Sun, and Xiulong Xu. "Targeting the Sonic Hedgehog Pathway to Suppress the Expression of the Cancer Stem Cell (CSC)—Related Transcription Factors and CSC-Driven Thyroid Tumor Growth." Cancers 13, no. 3 (January 22, 2021): 418. http://dx.doi.org/10.3390/cancers13030418.

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The sonic hedgehog (Shh) pathway plays important roles in tumorigenesis, tumor growth, drug resistance, and metastasis. We and others have reported earlier that this pathway is highly activated in thyroid cancer. However, its role in thyroid cancer stem cell (CSC) self-renewal and tumor development remains incompletely understood. B lymphoma Mo-MLV insertion region 1 homolog (BMI1) and SRY-Box Transcription Factor 2 (SOX2) are two CSC-related transcription factors that have been implicated in promoting CSC self-renewal. The objective of our current investigation was to determine the role of the Shh pathway in regulating BMI1 and SOX2 expression in thyroid cancer and promoting thyroid tumor growth and development. Here we report that inhibition of the Shh pathway by Gli1 siRNA or by cyclopamine and GANT61 reduced BMI1 and SOX2 expression in SW1736 and KAT-18 cells, two anaplastic thyroid cancer cell lines. The opposite results were obtained in cells overexpressing Gli1 or its downstream transcription factor Snail. The Shh pathway regulated SOX2 and BMI1 expression at a transcriptional and post-transcriptional level, respectively. GANT61 treatment suppressed the growth of SW1736 CSC-derived tumor xenografts but did not significantly inhibit the growth of tumors grown from bulk tumor cells. Clinicopathological analyses of thyroid tumor specimens by immunohistochemical (IHC) staining revealed that BMI1 and SOX2 were highly expressed in thyroid cancer and correlated with Gli1 expression. Our study provides evidence that activation of the Shh pathway leads to increased BMI1 and SOX2 expression in thyroid cancer and promotes thyroid CSC-driven tumor initiation. Targeting the Shh pathway may have therapeutic value for treating thyroid cancer and preventing recurrence.
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Dissertations / Theses on the topic "Sox2 transcription factor"

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Lins, Katharina. "Regulation of POU transcription factor activity by OBF1 and Sox2." Thesis, Open University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402625.

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For a cell to exert a specialized function certain genes have to be expressed, others repressed. Transcription factors, regulating this expression, do not function alone, but are often part of multi-protein complexes. Regulating a single gene with more than one transcription factor is an efficient way to integrate responses to a variety of signals using a limited number of proteins. DNA binding proteins often interact with each other and with non-DNA binding proteins in a specific arrangement. The assembly of these complexes is often highly cooperative and promotes high levels of transcriptional synergy. The center of my thesis is the family of POU transcription factors. Specifically, I elaborate the interaction within the POU protein family, with members of other transcription factor families and with cofactors. In all cases, the assembly of the correct array of polypeptides on the DNA requires specific protein-protein and protein-DNA interactions. As an example of POU factors interacting with each other and with a cofactor I investigated the properties of a protein-DNA complex with the B-cell-specific cofactor OBF! and the Octl dimer. Depending on the DNA sequence they bind to, Octl dimers are arranged in configurations that are either accessible (PORE sequence) or inaccessible (MORE sequence) to OBF!. In Chapter 3 I show that the expression of Osteopontin, which contains a PORE sequence in its enhancer region, depends on the presence of OBFI in B-cells. OBFI alleviates DNA sequence requirements of the Octl dimer on PORE-related sequences in vitro. Furthermore, OBFI enhances POU dimer-DNA interactions and overrides Oct! interface mutations, which abolish PORE-mediated dimerization without OBFl. Based on the biochemical data, I propose a novel Oct! dimer arrangement when OBF 1 is bound. As an example of Oct factors interacting with members of another transcription factor family I studied the interactions of Sox2 with Octl and Oct4, respectively. POU and Sox transcription factors exemplify partnerships established between various transcriptional regulators during early embryonic development. The combination of Oct4 and Sox2 on DNA is considered to direct the establishment of the first three lineages in the mammalian embryo. Although functional cooperativity between key regulator proteins is pivotal for milestone decisions in mammalian development, little is known about the underlying molecular mechanisms. The data in Chapter 4 validate experimental highresolution structure determination, followed by model building. The study shows that Oct4 and Sox2 are able to dimerize on DNA in distinct conformational arrangements. The binding site characteristics of their target genes are responsible for the correct spatial alignment of the Velcro-like interaction domains on their surface. Interestingly, these surfaces frequently have redundant functions and are instrumental in recruiting various interacting protein partners. In Chapter 5 I investigated how Sox2 and Oct4 regulate transcription of a target gene. The first intron of Osteopontin contains a Sox-binding site and a unique PORE to which Oct4 can either bind as a monomer or a dimer. The study reveals that Sox2-specific repression depends on an upstream Sox site and an intact PORE, although neither the Sox nor the PORE sites are negative elements on their own. A mechanism is being proposed how Sox2 represses Oct4-mediated activation of Osteopontin.
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Rosso, Michele <1984&gt. "Role of the Transcription Factor Sox2 in the Osteogenic Lineage." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6489/4/rosso_michele_tesi.pdf.

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The Sox2 transcription factor is modified by sumoylation at the K247 position although the addition of SUMO1 and Pias1 promotes the sumoylation of Sox2 at the additional K123 site. The role of sumoylation on Sox2 biological functions was analyzed by comparing the activity of WT and sumoylation mutants on the transcription of the FGF4 gene in HeLa cells and on the downregulation of the Wnt pathwayvin 293T cells. When SUMO1 and PIAS1 promote the sumoylation of WT Sox2, the transcriptional activity of the FGF4 promoter is inhibited showing that Sox2 sumoylation is necessary for the repression function. However, there is no effect of Sox2 sumoylation on β-Catenin activity. Since we were interested in osteoblast differentiation we set up an inducible system for Sox2 in primary osteoblasts. Following Sox2 doxycycline induction, 158 genes were differentially expressed: 120 up-regulated and 38 down-regulated. We annotated as direct Sox2 targets a number of genes involved in osteoblast biology and we further analyzed 3 of them involved in the BMP pathway. The results show that Sox2 regulates the BMP pathway without affecting SMAD phosphorylation, and that Sox2 sumoylation is not necessary for this function. We also found that genes involved in the Hippo pathway were direct Sox2 targets. As the Hippo pathway is activated by Sox2 and Sox2 interacts with the NF2 promoter, we checked the effect of Sox2 on the expression of NF2. We showed that Sox2 down-regulates the transcriptional activity of the NF2 promoter, allowing the transcription of the YAP/TEAD genes in osteoblasts, thus acting as an upstream regulator of the Hippo pathway. We conclude that Sox2 induction in osteoblasts triggers FGF dependent inhibition of the BMP, Wnt and Hippo pathways.
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Rosso, Michele <1984&gt. "Role of the Transcription Factor Sox2 in the Osteogenic Lineage." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6489/.

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The Sox2 transcription factor is modified by sumoylation at the K247 position although the addition of SUMO1 and Pias1 promotes the sumoylation of Sox2 at the additional K123 site. The role of sumoylation on Sox2 biological functions was analyzed by comparing the activity of WT and sumoylation mutants on the transcription of the FGF4 gene in HeLa cells and on the downregulation of the Wnt pathwayvin 293T cells. When SUMO1 and PIAS1 promote the sumoylation of WT Sox2, the transcriptional activity of the FGF4 promoter is inhibited showing that Sox2 sumoylation is necessary for the repression function. However, there is no effect of Sox2 sumoylation on β-Catenin activity. Since we were interested in osteoblast differentiation we set up an inducible system for Sox2 in primary osteoblasts. Following Sox2 doxycycline induction, 158 genes were differentially expressed: 120 up-regulated and 38 down-regulated. We annotated as direct Sox2 targets a number of genes involved in osteoblast biology and we further analyzed 3 of them involved in the BMP pathway. The results show that Sox2 regulates the BMP pathway without affecting SMAD phosphorylation, and that Sox2 sumoylation is not necessary for this function. We also found that genes involved in the Hippo pathway were direct Sox2 targets. As the Hippo pathway is activated by Sox2 and Sox2 interacts with the NF2 promoter, we checked the effect of Sox2 on the expression of NF2. We showed that Sox2 down-regulates the transcriptional activity of the NF2 promoter, allowing the transcription of the YAP/TEAD genes in osteoblasts, thus acting as an upstream regulator of the Hippo pathway. We conclude that Sox2 induction in osteoblasts triggers FGF dependent inhibition of the BMP, Wnt and Hippo pathways.
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MARIANI, JESSICA. "Transcriptional regulation, target genes and functional roles of the SOX2 transcription factor in mouse neural stem cells maintenance and neuronal differentiation." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/8321.

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The aims of this PhD research were: to examine molecular mechanisms underlying the transcriptional regulation of the Sox2 gene during forebrain development; to examine the role of Sox2 for the proper neuronal differentiation of neural stem cells; and to examine the role of Sox2 in controlling the maintenance of neural stem cells (in vivo and in vitro). The aim of the first work (Chapter 1) was to investigate the transcription factors and the regulatory sequences that control transcription of the Sox2 gene in the developing brain and neural stem cells. Our laboratory previously identified Sox2 regulatory sequences able to drive expression of a reporter β-geo transgene to neural stem cells of the brain in transgenic mice. I focused on two mouse forebrain-specific enhancers able to recapitulate Sox2 telencephalic expression throughout forebrain development, also active in neural stem cells of the adult and embryonic brain (Sox2 5’ and 3’ enhancers). This work showed that Emx2 acts as a direct transcriptional repressor of both Sox2 telencephalic enhancers, acting in two different ways to repress their transcriptional activity: by directly binding to a specific site within these regulatory elements, thus preventing the binding of activators, or possibly by protein to protein interaction sequestring the activators, thus antagonizing their activity. By the study of double mutant mice (expressing reduced levels of Sox2 and Emx2) we further found that Emx2 deficiency counteracts (at least in part) the deleterious effects of Sox2 deficiency on neural stem cell proliferation ability in the postnatal hippocampus, and also rescued other brain morphological abnormalities of Sox2-deficient mutants. It is likely possible that a simultaneous decrease of Emx2 levels (a Sox2 repressor) may antagonize these defects, by restoring Sox2 levels. In the second line of my research (Chapter 2) we performed in vitro differentiation studies on neural stem cells cultured from embryonic and adult brains of Sox2 “knockdown” mutants (expressing reduced levels of Sox2) where Sox2 deficiency impairs neuronal differentiation. In particular, my contribution to this work was to evaluate the in vitro differentiation defects of Sox2 mutant neurospheres by immunofluorescence staining for different glial and neuronal markers. Strikingly, I observed that mutant cells produce reduced numbers of mature neurons (in particular GABAergic neurons), but generate normal glia. Most of the cells belonging to the neuronal lineage failed to progress to mature neurons showing morphological abnormalities. To evaluate if restoration of Sox2 levels is able to rescue the differentiation defects of mutant cells, I engineered Sox2-expressing lentiviral vector, which I used to infect neural cells at early or late differentiation stages. I found that, Sox2 overexpression is able to rescue the neuronal maturation defects of mutant cells only if administered at early stages of differentiation. Further, I observed that Sox2 suppresses the endogenous GFAP gene, a marker of glial differentiation. These results suggests that Sox2 is required in early in vitro differentiating neuronal cells, for maturation and for suppression of alternative lineage markers. The third research (Chapter 3) investigated neurogenesis and neural stem cells properties in mice carrying a conditional mutation in the Sox2 gene (Sox2flox). Here, Sox2 was deleted via a nestin-Cre transgene that leads to complete Sox2 loss in the central nervous system by 12.5 dpc. These studies showed that embryonic neurogenesis was not importantly defective, however shortly after birth, NSC and neurogenesis are completely lost in the hippocampus. The expression of cytokine-encoding genes, essential for stem cell niche, is also strongly perturbed and leads to impaired stem cell maintenance (in vivo and in vitro). In vitro, NSC cultures derived from Sox2-deleted forebrain become rapidly exhausted, losing their proliferation and self-renewal properties. In Sox2-deleted neurospheres, Shh is extremely downregulated. However, the conditioned medium from wild type NSC cultures or the administration of a Shh agonist efficiently rescue the proliferation defects. These results suggest that the effect of Sox2 on neural stem cells growth and maintenance is partially mediated by Shh secretion, and that the Shh gene must be a direct target of Sox2. To confirm this hypothesis, I infected Sox2-deleted NSC with a Sox2-IRES-GFP expressing lentivirus just prior to the beginning of the growh decline, and I observed that the re-expression of Sox2 induces the ability to re-express Shh and rescues the formation of neurosphere. These findings indicate that NSC control their status, at least in part, through non cell-autonomous mechanisms (such as activation of important cytochine-encoding genes) which depend on Sox2.
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Hütz, Katharina Antonia. "The role of the transcription factor SOX2 in tumorigenesis and development of the stomach." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-175561.

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BADIOLA, SANGA ALEXANDRA. "Study of the role of the SOX2 transcription factor in neural and mammary cancer stem cells using SOX2 conditional knock-out in mouse." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/52431.

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The stem cell-determining transcription factor Sox2 is required for the maintenance of normal stem cells. In this study, we investigated the requirement for Sox2 in neural and breast cancer stem-like cells. In the first case, using a conditional genetic deletion mutant in a mouse model of platelet-derived growth factor-induced malignant oligodendroglioma. Taken together, our results showed that Sox2 is essential for tumor initiation by mouse pHGG cells, and we illustrated a Sox2-directed strategy of immunotherapy to eradicate tumor-initiating cells. In the second case, we used a Sox2 conditional deletion by an MMTV-Cre transgene (active in mammary tissue) to address Sox2 requirement within a widely studied mouse model of mammary tumor, produced by expression of a transgene encoding a mutated ErbB2/Neu oncogene, driven to mammary tissue by the MMTV promoter. Our results point to a heterogeneity within mammary tumors regarding Sox2 expression and function, in particular within ErbB2/Neu-positive tumors, that it will be important to consider when hypothesizing therapy approaches.
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CACCIA, ROBERTA. "Defects in neuronal differentiation and axonal connectivity in mice mutant in the Sox2 transcription factor gene: in vitro and in vivo studies." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2010. http://hdl.handle.net/10281/10334.

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Sox2 is an important transcription factor expressed in the central nervous system from the beginning of its development. We generated Sox2 mutant mice carrying a “knockdown” mutation together with a null mutation, which express 20-30% of the normal amount of Sox2. These mice show brain abnormalities including decreased cortical size, defects in neurogenesis and cell death in thalamus (Ferri et al., 2004). We also generated Sox2 conditional mutant mice, in wich the Sox2 locus is flanked by loxP sites, and it can be ablated by driven expression of a Cre recombianse. These mice show brain abnormalities including e decreased size of posterior cortex. (Favaro et al.). Around the time of neurogenesis, neocortex and dorsal thalamus start to become connected through reciprocal axonal projections. The complete process in mice occurs between E13 and E18. I hypothesize that in Sox2 mutants the thalamocortical and corticothalamic connections may be affected. I studied if the cortical neurons are able to grow and form correct connections in Sox2 hypomorphic mice and in conditional Sox2 mutant mice, in which Sox2 in completely ablated in the central nervous system from E12,5 via a Nestin Cre transgene, or is deleted from specific regions of the brain via Cre driven by genes specifically expressed in cortex or thalamus
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BERTOLINI, JESSICA ARMIDA. "Functional characterization of regulatory sequences targeted by the transcription factor SOX2, identified by studies of long-range chromatin interactions in brain-derived neural stem/precursor cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/83922.

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Sox2 codifica per un fattore trascrizionale necessario per la pluripotenza delle cellule staminali embrionali. Mutazioni eterozigoti in Sox2 nell’uomo causano difetti nello sviluppo dell’occhio (anoftalmia, microftalmia) e dell’ippocampo, con insorgenza di patologie come epilessia, problemi nel controllo motorio e difetti di apprendimento. Tramite “knock-out” condizionale di Sox2 in topo, abbiamo osservato l’importanza di Sox2 per lo sviluppo del cervello e per il “self-renewal” delle staminali neurali. Di recente è emerso che elementi regolatori possono trovarsi molto lontano dai geni che controllano lungo il cromosoma. Mutazioni in tali elementi talvolta causano patologie dovute a deregolazione del gene associato. In collaborazione con la Dr. C.-L. Wei (California), abbiamo comparato le interazioni “long-range” nella cromatina di cellule di precursori neurali (NPCs) di topi “wild-type” (wt) e Sox2-deleti, usando la tecnica ChIA-PET: su 7000 interazioni mappate in NPCs wt, 2700 erano perse in NPCs Sox2-delete. Tra queste 2700 interazioni, molte coinvolgevano geni legati allo sviluppo neurale e sequenze identificate come enhancer telencefalici per la presenza di siti di legame per p300. Abbiamo poi determinato la mappa genomica dei siti di legame per SOX2 nella cromatina di NPCs wt (in collaborazione con il Dr. F. Guillemot; Londra). Circa metà delle interazioni “long-range” SOX2-dipendenti presentava un picco di ChIP-seq per SOX2, suggerendo un ruolo diretto di SOX2 nel loro mantenimento. Il mio progetto di tesi intende definire se sequenze distali, associate in modo SOX2-dipendente a geni neurali (candidati “target” per SOX2), sono elementi di regolazione trascrizionale attivi durante lo sviluppo embrionale del cervello e se la loro attività è regolata da SOX2. Abbiamo selezionato 13 putativi elementi regolatori distali (DREs), tra le interazioni ChIA-PET perse nelle NPCs Sox2-delete, per caratterizzarli funzionalmente in esperimenti di transgenesi in zebrafish. Ho condotto questi esperimenti in vivo nel laboratorio della Dr. P. Bovolenta a Madrid, supportata da una “EMBO short-term fellowship”. Abbiamo clonato le 13 DREs in un plasmide (ZED), a monte di un promotore minimo e del gene GFP. Il plasmide è stato iniettato in embrioni allo stadio di 1 cellula e il DNA si è integrato nel genoma di pesce. Gli embrioni sono stati osservati durante lo sviluppo per analizzare se, e dove, la sequenza testata guidava l’espressione di GFP. La GFP era espressa riproducibilmente in 12 DREs su 13 nel cervello in via di sviluppo e/o in regioni neurali più posteriori, sovrapponendosi al pattern di espressione del gene associato. Ciò indica che i DREs da soli guidano l’espressione del gene reporter. Ho quindi selezionato embrioni GFP+ transienti (F0) di 8 DREs per ottenere linee transgeniche stabili F1. Per testare se l’attività enhancer dei DREs è regolata da SOX2, ho usato un approccio “perdita di funzione”. Ho iniettato un oligonucleotide antisenso (morfolino), specificamente diretto contro l’mRNA di Sox2, in embrioni F2 di zebrafish allo stadio di 1 cellula. In 2 linee stabili su 8, l’espressione telencefalo-specifica di GFP era ridotta a precoci stadi di sviluppo. Abbiamo anche clonato alcuni DREs in vettori luciferasi per esperimenti di transfezione in colture cellulari. Uno dei DREs mostrava un aumento di attività luciferasica in cotransfezione con vettori di espressione per Sox2 e Mash1, suggerendo un meccanismo di regolazione in cui SOX2 opera insieme al cofattore MASH1. Possiamo concludere che alcuni DREs testati, selezionati tra le interazioni “long-range” di ChIA-PET perse nelle NPCs Sox2-delete, agiscono come elementi regolatori in esperimenti in vivo e sono direttamente regolati da SOX2.
Sox2 encodes a transcription factor required for embryonic stem cell pluripotency. Heterozygous Sox2 mutations in humans cause defects in the development of eyes (anophthalmia, microphthalmia) and hippocampus, with neurological pathology including epilepsy, motor control problems and learning disabilities. Using a Sox2 conditional knock-out in mouse, we discovered that Sox2 is important for brain development and for neural stem cell maintenance. Recently, it was found that transcriptional regulatory elements are not always localized in proximity of the gene they control, but often they lie very far from it on the linear chromosome map. Mutations in these elements can cause pathology, due to the deregulation of the associated gene. In collaboration with Dr. C.-L. Wei’s lab (California), we compared long-range DNA interactions in chromatin of wild-type mouse neural stem/precursor cells (NPCs) and Sox2-deleted cells, using the ChIA-PET technique: out of a total of 7000 long-range interactions mapped in wild-type NPCs, 2700 were lost in Sox2-deleted cells. Many of the lost interactions involved genes important for neural development and sequences already identified as forebrain enhancers by p300 binding in mouse developing telencephalon. In parallel, we determined the genome-wide map of SOX2 binding sites in chromatin of wild-type NPCs, by ChIP-seq (in collaboration with Dr. F. Guillemot; London). At least half of the SOX2-dependent long-range interactions contain a SOX2 ChIP-seq peak, suggesting that SOX2 has a direct role in their maintenance. My project seeks to define if distal sequences, associated in a SOX2-dependent way to neural genes (candidates to be putative SOX2 targets), represent transcriptional regulatory elements active during embryonic brain development and if their activity is regulated by SOX2. We selected 13 putative distal regulatory elements (DREs), among the ChIA-PET interactions lost in Sox2-deleted cells, to functionally characterize them in transgenic experiments in zebrafish. I did the transgenesis experiments in Dr. P. Bovolenta’s lab in Madrid, supported by an EMBO short-term fellowship. We cloned the 13 DREs upstream of a minimal promoter and a GFP gene (in a “ZED” plasmid). The plasmid is injected in 1-cell stage embryos and the DNA is integrated into the fish genome. After injection, the embryos are observed during development to analyze if, and where, the tested sequences drive GFP expression. I found that 12 out of 13 DREs give rise to reproducible GFP expression in the developing forebrain and/or in more posterior neural regions, matching the expression pattern of the associated gene. This indicates that the selected DREs alone are able to guide reporter gene expression. I collected the transient GFP+ embryos (F0) of 8 DREs to obtain F1 stable transgenic lines. To test if the enhancer activity of DREs is regulated by SOX2, I used a loss of function experiment. I injected a morpholino antisense oligonucleotide, specifically directed against the Sox2 mRNA, in F2 zebrafish embryos at 1-cell stage. Two, out of 8, stable lines showed a reduced GFP expression specifically in forebrain in early developmental stages. We have also cloned some of the selected DREs in a luciferase vector to test them by transfection in cultured cells. One of the DREs showed a significant increase in luciferase activity if co-transfected with Sox2 and Mash1 expressing vectors, suggesting a regulatory mechanism operated by SOX2 on this element in presence of the cofactor MASH1. We can conclude that some of the tested DREs, involved in ChIA-PET interactions lost in Sox2-deleted cells, work as regulatory elements in in vivo experiments and are directly regulated by SOX2.
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Hütz, Katharina Antonia [Verfasser], and Thomas [Akademischer Betreuer] Cremer. "The role of the transcription factor SOX2 in tumorigenesis and development of the stomach / Katharina Antonia Hütz. Betreuer: Thomas Cremer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/106031858X/34.

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Zayed, Hebatalla [Verfasser], Iver [Gutachter] Petersen, Peter [Gutachter] Elsner, and Alexander [Gutachter] Marx. "Stem cell transcription factor SOX2 in synovial sarcoma and other soft tissue tumors / Hebatalla Zayed ; Gutachter: Iver Petersen, Peter Elsner, Alexander Marx." Jena : Friedrich-Schiller-Universität Jena, 2019. http://d-nb.info/120588419X/34.

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Book chapters on the topic "Sox2 transcription factor"

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Wegner, Michael, and C. Claus Stolt. "Sox Transcription Factors in Neural Development." In Transcription Factors in the Nervous System, 181–203. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2006. http://dx.doi.org/10.1002/3527608036.ch10.

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

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Lucchesi, John C. "Stem cells." In Epigenetics, Nuclear Organization & Gene Function, 191–204. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0017.

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The zygote and the very early cells are totipotent because they can produce a whole organism. Later, cells become pluripotent because they can differentiate into different subgroups of tissues. These cells can be extracted as embryonic stem cells (ESCs). Their pluripotent nature is due to the action of the pioneer transcription factors Oct4, Sox2 and Nanog. Multipotent or progenitor stem cells are present in adult organisms where they can differentiate into the various cells present in specific tissues. Differentiation depends on their microenvironment or niche. Differentiation of stem cells requires the silencing of the pluripotency genes and the activation of genes that are characteristic of different cell types. The genome of stem cells exhibits the same features of topological organization that are found in somatic cells. At the onset and throughout differentiation, the topological organization of the ESC genome changes, reflecting the changes in transcriptional activity that underlie the progression of pluripotent cells to multipotent progenitor cells and then to differentiated cells.
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Lefebvre, Véronique. "Roles and regulation of SOX transcription factors in skeletogenesis." In Vertebrate Skeletal Development, 171–93. Elsevier, 2019. http://dx.doi.org/10.1016/bs.ctdb.2019.01.007.

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Ferletta, Maria. "The Role of Sox Transcription Factors in Brain Tumourigenesis." In Molecular Targets of CNS Tumors. InTech, 2011. http://dx.doi.org/10.5772/23616.

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Lucchesi, John C. "Nuclear reprogramming and induced pluripotency." In Epigenetics, Nuclear Organization & Gene Function, 205–12. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0018.

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Four core transcription factors known to maintain the pluripotent state in embryonic stem cells (ESCs)—Oct4, Sox2, Klf4 and c-Myc—were used to induce pluripotent stem cells in adult-derived fibroblasts. Induced pluripotent stem cells (iPSCs), like ESCs, have less condensed and more transcriptionally active chromatin than differentiated cells. The number of genes with bivalent promoter marks increases during reprogramming, reflecting the switch of differentiation-specific active genes to an inactive, but poised, status. The levels of DNA methyl transferases and demethylases are increased, underlying the changes in the pattern of DNA methylation that occur late during reprogramming. The potential therapeutic applications of iPSCs include reprogramming a patient’s own cells to avoid the problem of rejection following injection to restore tissue or organ function. iPSCs derived from individuals at risk of developing late-onset neurological diseases could be differentiated in culture to predict the future occurrence of the disease. Caveats involve the fact that long-term culturing often results in genomic mutations that may, by chance, involve tumor suppressors or oncogenes.
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Oh, Chun-do, Frank C. Ko, and Di Chen. "Regulation of Cartilage Matrix Protein by Transcription Factors, SOX9 and β-Catenin." In Encyclopedia of Bone Biology, 609–20. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-801238-3.62215-8.

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Kobayashi, Hideyuki. "Pluripotent Stem Cells Induced from Testicular Tissue of a Man with Klinefelter Syndrome (47, XXY) by Four Transcription Factors (OCT4, SOX2, KLF4, and C-MYC)." In Methodological Advances in the Culture, Manipulation and Utilization of Embryonic Stem Cells for Basic and Practical Applications. InTech, 2011. http://dx.doi.org/10.5772/13851.

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Sybirna, Anastasiya, Frederick C. K. Wong, and M. Azim Surani. "Genetic basis for primordial germ cells specification in mouse and human: Conserved and divergent roles of PRDM and SOX transcription factors." In Current Topics in Developmental Biology, 35–89. Elsevier, 2019. http://dx.doi.org/10.1016/bs.ctdb.2019.04.004.

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Conference papers on the topic "Sox2 transcription factor"

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Calderon-Aparicio, Ali J., Hiroyuki Yamamoto, Humberto de vitto, Tianshun Zhang, Qiushi Wang, Ann M. Bode, and Zigang Dong. "Abstract 2469: RCC2 promotes esophageal cancer growth by regulating activity and expression of the Sox2 transcription factor." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2469.

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Yokota, Etsuko, Tomoki Yamatsuji, Munenori Takaoka, Minoru Haisa, Nagio Takigawa, Noriko Miyake, Tomoko Ikeda, et al. "Abstract 1922: Targeted silencing of SOX2 by an artificial transcription factor showed antitumor effect in lung and esophageal squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1922.

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Pistilli, Barbara, Giovanni Benedetti, Mauro Finicelli, Tiziana Squillaro, Andrea Marcellusi, Tommasina Biscotti, Alfredo Santinelli, et al. "Abstract P2-06-05: Expression of the pluripotency transcription factor SOX2 in primary breast cancers (BCs): Correlation with clinicopathological features (CPfs) and recurrence." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p2-06-05.

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Ahmad, Salma, Hanan Nazar, Nouralhuda Alatieh, Maryam Al-Mansoob, Zainab Farooq, Muna Yusuf, and Allal Ouhtit. "Validation of Novel Transcriptional Targets that Underpin CD44-promoted breast cancer cell invasion." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0153.

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Introduction: Breast cancer (BC) is the most common cancer worldwide, and metastasis is its worst aspect and the first cause of death. Metastasis is a multistep process, where an invasion is a recurring event. The process of BC cell invasion involves three major factors, including cell adhesion molecules (CAM), proteinases and Growth factors.CD44, a family of CAM proteins and the hyaluronic acid (HA) cell surface receptor, acts as cell differentiation, cell migration/invasion and apoptosis regulator. Rationale: We have previously established a tetracycline (Tet)-OFF-regulated expression system, both in vitro and in vivo (Hill et al, 2006). As a complementary approach, the highly metastatic MDA-MB-231 BC cells expressing high levels of endogenous CD44s (the standard form of CD44), was cultured in the presence and absence of 50 µg/ml of HA. RNA samples were isolated from both cell experimental models, and microarray analysis (12K CHIP from Affymetrix) was applied. More than 200 CD44s transcriptional target genes were identified and were sub-divided into groups of genes based on their function: cell motility, cytoskeletal organization, ability to degrade ECM, and cell survival. Hypothesis: Among these 200 identified genes, we selected seven genes (ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1, and SOD2) and hypothesized that based on evidence from literature, these genes are potential novel targets of CD44-downstream signaling mediating BC cell invasion. Specific Aims: Pursuant to this goal, we proposed the following objectives: 1- Structural validation of ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1 and SOD2 as novel transcriptional targets of CD44/HA-downstream signaling at both RNA and Protein level using reverse transcription polymerase chain reaction (RT-PCR) and Western Blot respectively. 2-Functional validation of ICAP-1, KYNU, AHR, SIRT1, SRSF8, PRAD1and SOD2 as novel transcriptional targets that underpin CD44-promoted BC cell migration using wound healing assay after the transfection with siRNA. Innovation/Consclusion: This study validated seven transcriptional targets of CD44/HA-downstream signaling promoting BC cell invasion. Ongoing experiments aim to dissect the signaling pathways that link CD44 activation by HA to the transcription of these seven genes.
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Manzar, Nishat, Ritika Tiwari, Vipul Bhatia, Anjali Yadav, Shannon Carskadon, Nilesh Gupta, Amina Zoubeidi, et al. "Abstract C128: Reprogramming transcription factors SOX2 and REST modulates SPINK1 expression in governing cellular plasticity in prostate cancer." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-c128.

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Chetty, Chandramu, Praveen Bhoopathi, Meena Gujrati, Dzung H. Dinh, Jasti S. Rao, and Sajani S. Lakka. "Abstract 1313: SPARC enhances radiosensitivity by inhibiting radiation-induced SOX-4 transcription factor in medulloblastoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1313.

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Abdel-Sayed, Philippe, Arne Vogel, and Dominique P. Pioletti. "Dissipation Can Act as a Mechanobiological Signal in Cartilage Differentiation." In ASME 2013 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/imece2013-62268.

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Knee cartilage is a soft tissue having viscoelastic properties. Under cyclic loadings, viscoelastic materials dissipate mechanical loadings through heat generation. In knee cartilage, this heat might not be convected because of the tissue avascularity, resulting thus to a local temperature increase. As cells are sensitive to temperature, these thermo-mechanical phenomena of energy dissipation could influence their metabolism. The goal of this study is to evaluate the effect of thermogenesis on chondrogenic differentiation. First, we focused our work in quantifying the heat generated in cartilage as a result to deformation. On a cellular level, the effect of thermal alterations on cell metabolism was assessed looking at the gene expression of transcription factors involved in chondrogenesis. Hence, human chondro-progenitor cells were cultured at 33°C and 37°C for 48 h and 96 h. An up-regulation in mRNA expression levels of Sox9 and its co-activator PGC-1α has been observed. These results point to a thermal contribution to chondrogenic gene expression.
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Lara, Haydee, Tamara Matysiak-Budnik, and Scott T. Magness. "Abstract 5057: Single-cell RNA-seq analysis of heterogeneous populations within gastroenteropancreatic neuroendocrine tumors: the role of Sox transcription factors." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5057.

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Das, Koushik K., Steffen Heeg, Maximilian Reichert, Shigetsugu Takano, Basil S. Bakir, Gregory P. Botta, Christopher Hahn, Andrew D. Rhim, and Anil K. Rustgi. "Abstract A11: Ets transcription factor Etv5 regulates ductal morphogenesis and differentiation in association with Sox9 in vitro and increases susceptibility and delays recovery from pancreatitis in vivo." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a11.

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Reports on the topic "Sox2 transcription factor"

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Scharer, Christopher. Identification of the Transformational Properties and Transcriptional Targets of the Oncogenic SRY Transcription Factor SOX4. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada497252.

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Scharer, Christopher. Identification of the Transformational Properties and Transcriptional Targets of the Oncogenic SRY Transcription Factor SOX4. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada524928.

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

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