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Relevant bibliographies by topics / Retinoid pathway gene expression

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Academic literature on the topic 'Retinoid pathway gene expression'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "Retinoid pathway gene expression"

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Lefebvre, Bruno, Céline Brand, Sébastien Flajollet, and Philippe Lefebvre. "Down-Regulation of the Tumor Suppressor Gene Retinoic Acid Receptor β2 through the Phosphoinositide 3-Kinase/Akt Signaling Pathway." Molecular Endocrinology 20, no. 9 (September 1, 2006): 2109–21. http://dx.doi.org/10.1210/me.2005-0321.

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Abstract The retinoic acid receptor β2 (RARβ2) is a potent, retinoid-inducible tumor suppressor gene, which is a critical molecular relay for retinoid actions in cells. Its down-regulation, or loss of expression, leads to resistance of cancer cells to retinoid treatment. Up to now, no primary mechanism underlying the repression of the RARβ2 gene expression, hence affecting cellular retinoid sensitivity, has been identified. Here, we demonstrate that the phosphoinositide 3-kinase/Akt signaling pathway affects cellular retinoid sensitivity, by regulating corepressor recruitment to the RARβ2 promoter. Through direct phosphorylation of the corepressor silencing mediator for retinoic and thyroid hormone receptors (SMRT), Akt stabilized RAR/SMRT interaction, leading to an increased tethering of SMRT to the RARβ2 promoter, decreased histone acetylation, down-regulation of the RARβ2 expression, and impaired cellular differentiation in response to retinoid. The phosphoinositide 3-kinase/Akt signaling pathway, an important modulator of cellular survival, has thus a direct impact on cellular retinoid sensitivity, and its deregulation may be the triggering event in retinoid resistance of cancer cells.

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Mehta, Kapil, Teresa McQueen, Taghi Manshouri, Michael Andreeff, Steven Collins, and Maher Albitar. "Involvement of Retinoic Acid Receptor-α–Mediated Signaling Pathway in Induction of CD38 Cell-Surface Antigen." Blood 89, no. 10 (May 15, 1997): 3607–14. http://dx.doi.org/10.1182/blood.v89.10.3607.

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Abstract Human leukocyte antigen CD38, a 45-kD single-chain, transmembrane glycoprotein, is a bifunctional ectoenzyme that participates in signal transduction pathways involved in the regulation of cell growth and differentiation. In this study, we demonstrate the nature of retinoid receptors involved in retinoic acid–induced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60. We used a variant HL-60 cell line, HL-60R, in which retinoid receptor function has been abrogated by a trans-dominant negative mutation. We introduced the normal retinoic acid receptors (RAR)-α, -β, and -γ or retinoid X receptor (RXR)-α into HL-60R cells by retroviral vector-mediated gene transfer. Based on experiments using these cell lines and receptor-specific synthetic retinoids that preferentially bind to one of the RARs or RXRs, we conclude that RAR-α is involved in retinoid-induced CD38 expression in HL-60 cells. Further evidence included our demonstration that blocking of RAR-α with the antagonist Ro 41-5253 completely suppressed the retinoid-induced expression of CD38 mRNA transcript and the production of CD38 protein in HL-60 cells. Various tissues from transgenic mice that expressed an antisense construct of RAR-α lacked or produced very low levels of CD38. As expected, the tissues from transgenic mice contained 50% to 80% reduced levels of RAR-α. These results suggest that regulation of CD38 expression, both in vitro and in vivo, is under the direct control of RAR-α retinoid receptors.

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Mehta, Kapil, Teresa McQueen, Taghi Manshouri, Michael Andreeff, Steven Collins, and Maher Albitar. "Involvement of Retinoic Acid Receptor-α–Mediated Signaling Pathway in Induction of CD38 Cell-Surface Antigen." Blood 89, no. 10 (May 15, 1997): 3607–14. http://dx.doi.org/10.1182/blood.v89.10.3607.3607_3607_3614.

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Human leukocyte antigen CD38, a 45-kD single-chain, transmembrane glycoprotein, is a bifunctional ectoenzyme that participates in signal transduction pathways involved in the regulation of cell growth and differentiation. In this study, we demonstrate the nature of retinoid receptors involved in retinoic acid–induced expression of CD38 protein in the human myeloblastic leukemia cell line HL-60. We used a variant HL-60 cell line, HL-60R, in which retinoid receptor function has been abrogated by a trans-dominant negative mutation. We introduced the normal retinoic acid receptors (RAR)-α, -β, and -γ or retinoid X receptor (RXR)-α into HL-60R cells by retroviral vector-mediated gene transfer. Based on experiments using these cell lines and receptor-specific synthetic retinoids that preferentially bind to one of the RARs or RXRs, we conclude that RAR-α is involved in retinoid-induced CD38 expression in HL-60 cells. Further evidence included our demonstration that blocking of RAR-α with the antagonist Ro 41-5253 completely suppressed the retinoid-induced expression of CD38 mRNA transcript and the production of CD38 protein in HL-60 cells. Various tissues from transgenic mice that expressed an antisense construct of RAR-α lacked or produced very low levels of CD38. As expected, the tissues from transgenic mice contained 50% to 80% reduced levels of RAR-α. These results suggest that regulation of CD38 expression, both in vitro and in vivo, is under the direct control of RAR-α retinoid receptors.

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Murphy, Philip T., Gary Lynch, Stephen Bergin, John Quinn, Siobhan Glavey, Philip W. Murphy, and Paul Kennedy. "Strong Correlation Between CTLA-4 and LEF1 Gene Expression Levels in CLL: Targeting of the Wnt/β-Catenin Pathway May Adversely Affect CTLA-4 Expression and Function." Blood 128, no. 22 (December 2, 2016): 5571. http://dx.doi.org/10.1182/blood.v128.22.5571.5571.

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Abstract Recently published clinical trials have confirmed the effectiveness of anti-CD38 monoclonal antibody therapy in myeloma. Furthermore, in vitro studies of chronic lymphocytic leukaemia (CLL) cells suggest that CD38 expression can be enhanced by treatment with retinoid derivatives and thus may enhance the cytotoxic effects of anti-CD38 therapy. However, retinoids have been shown to have diverse effects on cellular function and we have previously shown that the retinoid drug acitretin upregulates CD38 expression while also reducing cell homing to the chemokine CXCL12 in primary CLL cells. To investigate possible key mechanisms for these effects, we purified CD20+ B cells from the peripheral blood of 20 CLL patients (9 previously treated, 11 untreated) and, using flow cytometry, measured percentage cell surface expression of CD38 and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4, CD152). We also measured gene expression levels of the key retinoid receptor, stimulated by retinoic acid 6 (STRA6) and it's agonist, retinol-binding protein 4 (RBP4), as well as CTLA-4, cyclin D1 (CCND1) and the transcription factors, lymphoid enhancer factor 1 (LEF1) and signal transducer and activator of transcription 3 (STAT3) using RT-PCR. GAPDH was used as a reference gene. Mean percentage surface expression of CD38 and CTLA-4 was 21.96% and 45.25% respectively. Mean ∆CT gene expression levels of CCND1, CTLA-4, LEF1 and STAT3 were 12.03, 5.57 , 5.99 and 8.98 respectively. RBP4 and STRA6 gene expression levels were undetectable in all 20 patients. Gene expression of LEF1 showed significant correlations with CTLA-4 (rs=0.572, p=0.008), CCND1 (rs=0.61, p=0.004) and STAT3 (rs=0.587, p=0.006). There was also a significant correlation between gene expression of CCND1 and of STAT3 (r =0.499, p=0.025). No significant correlations were found between percentage surface expression of CTLA-4 and gene expression levels of either CTLA-4 or of LEF1. A weak negative correlation between percentage surface expression of CTLA-4 and of CD38 was not statistically significant. Comparing untreated and previously treated patients, there was no significant difference in gene expression levels of CTLA-4 and of LEF1 or in surface expression of CTLA-4. The failure to detect RBP4 and STRA6 gene expression in unstimulated peripheral blood CLL cells is evidence against an autocrine retinoid effect in CLL, although upregulation of STRA6 gene expression following stimulation by retinoids might be anticipated. The Wnt signalling pathway has been shown to be active in CLL, including aggressive disease subtypes, highlighting the potential benefits in targeting this pathway. Intriguingly, CTLA-4 expression, although found to be the most highly induced gene following treatment with recombinant Wnt-3a in melanoma cell lines, is associated with a favourable outcome in CLL, possibly by inhibiting cell proliferation and survival. In contrast, expression of LEF1, which is a direct target of the Wnt signalling pathway, is associated with disease progression in CLL. Our finding that CTLA-4 and LEF1 gene expression levels are strongly correlated suggests that further investigation of the relationship between CTLA-4 and the Wnt/β-Catenin pathway in CLL is required and that targeting of the Wnt/β-catenin pathway may have unwanted consequences on CTLA-4 expression and function. Disclosures Quinn: Celgene: Honoraria; Janssen Cilag: Honoraria.

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Aydemir, Gamze, Marta Domínguez, Angel R. de Lera, Johanna Mihaly, Dániel Törőcsik, and Ralph Rühl. "Apo-14´-Carotenoic Acid Is a Novel Endogenous and Bioactive Apo-Carotenoid." Nutrients 11, no. 9 (September 4, 2019): 2084. http://dx.doi.org/10.3390/nu11092084.

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Carotenoids can be metabolized to various apo-carotenoids and retinoids. Apo-15´-carotenoic acid (retinoic acid, RA) is a potent activator of the retinoic acid receptor (RAR) in its all-trans- (ATRA) and 9-cis- (9CRA) forms. In this study we show firstly, that apo-14´-carotenoic acid (A14CA), besides retinoic acids, is present endogenously and with increased levels in the human organism after carrot juice supplementation rich in β-carotene. All-trans-A14C (ATA14CA) is just a moderate activator of RAR-transactivation in reporter cell lines but can potently activate retinoic acid response element (RARE)-mediated signalling in DR5/RARE-reporter mice and potently increase retinoid-reporter target gene expression in ATA14CA-supplemented mice and treated MM6 cells. Further metabolism to all-trans-13,14-dihydroretinoic acid (ATDHRA) may be the key for its potent effects on retinoid target gene activation in ATA14CA-treated MM6 cells and in liver of supplemented mice. We conclude that besides RAs, there are alternative ways to activate RAR-response pathways in the mammalian organism. ATA14CA alone and in combination with its metabolite ATDHRA may be an alternative pathway for potent RAR-mediated signalling.

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van der Wees, J., J. G. Schilthuis, C. H. Koster, H. Diesveld-Schipper, G. E. Folkers, P. T. van der Saag, M. I. Dawson, K. Shudo, B. van der Burg, and A. J. Durston. "Inhibition of retinoic acid receptor-mediated signalling alters positional identity in the developing hindbrain." Development 125, no. 3 (February 1, 1998): 545–56. http://dx.doi.org/10.1242/dev.125.3.545.

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Retinoids regulate gene expression via nuclear retinoic acid receptors, the RARs and RXRs. To investigate the functions of retinoid receptors during early neural development, we expressed a dominant negative RARbeta in early Xenopus embryos. We obtained evidence that dominant negative RARbeta specifically inhibits RAR/RXR heterodimer-mediated, but not RXR homodimer-mediated, transactivation. Both all-trans- and 9-cis-RA-induced teratogenesis were, however, efficiently opposed by ectopic expression of dominant negative RARbeta, indicating that only RAR/RXR transactivation is required for retinoid teratogenesis by each of these ligands. Experiments with two RXR-selective ligands confirmed that activation of RXR homodimers does not cause retinoid teratogenesis. Dominant negative RARbeta thus specifically interferes with the retinoid signalling pathway that is responsible for retinoid teratogenesis. Dominant negative RARbeta-expressing embryos had a specific developmental phenotype leading to disorganization of the hindbrain. Mauthner cell multiplications in the posterior hindbrain, and (both anteriorly and posteriorly) expanded Krox-20 expression domains indicated (partial) transformation of a large part of the hindbrain into (at least partial) rhombomere 3, 4 and/or 5 identity. In contrast, the fore- and midbrain and spinal cord appeared to be less affected. These data indicate that RARs play a role in patterning the hindbrain.

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Park, Dorothy J., Peter T. Vuong, Sven de Vos, Dan Douer, and H. Phillip Koeffler. "Comparative analysis of genes regulated by PML/RARα and PLZF/RARα in response to retinoic acid using oligonucleotide arrays." Blood 102, no. 10 (November 15, 2003): 3727–36. http://dx.doi.org/10.1182/blood-2003-02-0412.

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Abstract Acute promyelocytic leukemia (APL) is associated with chromosomal translocations involving retinoic acid receptor α (RARα) and its fusion partners including promyelocytic leukemia (PML) and promyelocytic leukemia zinc finger (PLZF). Using oligonucleotide arrays, we examined changes in global gene expression mediated by the ectopic expression of either PML/RARα (retinoid-sensitive) or PLZF/RARα (retinoid-resistant) in U937 cells. Of more than 5000 genes analyzed, 16 genes were commonly up-regulated, and 57 genes were down-regulated by both fusion proteins suggesting their role in the APL phenotype. In our APL model, for example, TNFAIP2, TNFR2, ELF4, RARγ, and HoxA1 were down-regulated by both fusion proteins in the absence of retinoic acid (RA). RA strongly up-regulated these genes in PML/RARα, but not in PLZF/RARα expressing U937 cells. Expression studies in NB4, retinoid-resistant NB4-R2, normal human CD34+ cells, and APL patient samples strongly suggest their role in the regulation of granulocytic differentiation. Furthermore, combined treatment with tumor necrosis factor α (TNFα) and RA synergistically enhanced granulocytic differentiation in NB4 cells but not in NB4-R2 cells. Our data indicate that APL pathogenesis and retinoid-induced granulocytic differentiation of APL cells involve genes in the cell death pathway, and that cooperation between the RA and TNFα signaling pathways exists. Targeting both the retinoid-dependent differentiation and the cell death pathways may improve leukemic therapy, especially in retinoid-resistant acute myeloid leukemia. (Blood. 2003;102:3727-3736)

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Quere, Ronan, Aurelie Baudet, Bruno Cassinat, Gerald Bertrand, Jacques Marti, Laurent Manchon, David Piquemal, Christine Chomienne, and Therese Commes. "Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity." Blood 109, no. 10 (January 11, 2007): 4450–60. http://dx.doi.org/10.1182/blood-2006-10-051086.

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AbstractDisease relapse sometimes occurs after acute promyelocytic leukemia (APL) therapy with all-trans retinoic acid (ATRA). Among the diagnostic parameters predicting relapse, heterogeneity in the in vitro differentiation rate of blasts is an independent factor. To identify biologic networks involved in resistance, we conducted pharmacogenomic studies in APL blasts displaying distinct ATRA sensitivities. Although the expression profiles of genes invested in differentiation were similarly modulated in low- and high-sensitive blasts, low-sensitive cells showed higher levels of transcription of ATRA-target genes, transcriptional regulators, chromatin remodelers, and transcription factors. In opposition, only high-sensitive blasts expressed the CYP26A1 gene, encoding the p450 cytochrome which is known to be involved in retinoic acid catabolism. In NB4 cells, ATRA treatment activates a novel signaling pathway, whereby interleukin-8 stimulates the expression of the homeobox transcription factor HOXA10v2, an effective enhancer of CYP26A1 transcription. These data were corroborated in primary APL cells, as maturation levels correlated with CYP26A1 expression. Treatment with a retinoic acid metabolism blocking agent (RAMBA) results in high-nucleoplasmic concentrations of retinoid and growth of NB4-resistant subclones. Hence, for APL blasts associated with poor prognosis, the low CYP26A1 expression may explain high risk of resistance installation, by increased retinoid pressure. Pharmacogenomic profiles of genes involved in retinoid acid metabolism may help to optimize anticancer therapies, including retinoids.

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Lehrke, Ingo, Matthias Schaier, Kerstin Schade, Christian Morath, Ruediger Waldherr, Eberhard Ritz, and Juergen Wagner. "Retinoid receptor-specific agonists alleviate experimental glomerulonephritis." American Journal of Physiology-Renal Physiology 282, no. 4 (April 1, 2002): F741—F751. http://dx.doi.org/10.1152/ajprenal.00026.2001.

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Retinoids are potent antiproliferative and anti-inflammatory compounds. We previously demonstrated that the natural pan-agonists all- trans retinoic acid (RA) and 13- cis RA efficiently preserve renal structure and function in rat mesangioproliferative glomerulonephritis. We examine effects of synthetic retinoid receptor-specific agonists 1) to identify common and receptor subtype-specific pathways in this model and 2) to characterize effects of retinoids on the renal endothelin (ET) system. Vehicle-injected control rats were compared with rats treated with daily subcutaneous injections of agonists specific for retinoid A (Ro-137410) and retinoid X (Ro-257386) receptors and the complex anti-activator protein-1 active retinoid BMS-453 7 days after induction of anti-Thy1.1 nephritis ( n = 7–9/group). The different retinoids lowered glomerular ET-1 and ET type A and B receptor gene expression in control and nephritic rats with comparable efficacy. Reduction of glomerular c-Fos and GATA-2 mRNA expression levels suggests downregulation of transcription factors required for ET expression. The different retinoids were similar in their action on the glomerular capillary occlusion score, number of total glomerular cells, and glomerular infiltrating macrophage count. They differed in their ability to normalize blood pressure (Ro-257386 > BMS-453 > arotinoid), albuminuria (BMS-453 > Ro-257386 > arotinoid), and creatinine clearance (arotinoid > BMS-453 > Ro-257386). No signs of toxicity were observed. We conclude that all retinoid agonists with different subtype specificity are highly efficient in reducing renal damage and proliferation of mesangial cells. Retinoid X and A receptor-specific pathways are apparently involved in the antiproliferative, anti-inflammatory, and anti-ET action. Further studies are indicated to define the potential use of retinoid agonists in inflammatory renal disease.

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Hoffman, Lisa M., Kamal Garcha, Konstantina Karamboulas, Matthew F. Cowan, Linsay M. Drysdale, William A. Horton, and T. Michael Underhill. "BMP action in skeletogenesis involves attenuation of retinoid signaling." Journal of Cell Biology 174, no. 1 (July 3, 2006): 101–13. http://dx.doi.org/10.1083/jcb.200604150.

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The bone morphogenetic protein (BMP) and growth and differentiation factor (GDF) signaling pathways have well-established and essential roles within the developing skeleton in coordinating the formation of cartilaginous anlagen. However, the identification of bona fide targets that underlie the action of these signaling molecules in chondrogenesis has remained elusive. We have identified the gene for the retinoic acid (RA) synthesis enzyme Aldh1a2 as a principal target of BMP signaling; prochondrogenic BMPs or GDFs lead to attenuation of Aldh1a2 expression and, consequently, to reduced activation of the retinoid signaling pathway. Consistent with this, antagonism of retinoid signaling phenocopies BMP4 action, whereas RA inhibits the chondrogenic stimulatory activity of BMP4. BMP4 also down-regulates Aldh1a2 expression in organ culture and, consistent with this, Aldh1a2 is actively excluded from the developing cartilage anlagens. Collectively, these findings provide novel insights into BMP action and demonstrate that BMP signaling governs the fate of prechondrogenic mesenchyme, at least in part, through regulation of retinoid signaling.

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Dissertations / Theses on the topic "Retinoid pathway gene expression"

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Sokolova, Natalia Valerievna. "The role of vitamin A in embryonic lung development in mice." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320687.

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Hörnberg, Maria. "Effects of retinoic acid in the mouse olfactory sensory systems /." Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1371.

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Wang, Xiao Elston Timothy C. "Mathematical modeling of signaling pathway dynamics and stochastic gene expression." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2006. http://dc.lib.unc.edu/u?/etd,367.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2006.
Title from electronic title page (viewed Oct. 10, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Statistics and Operations Research." Discipline: Statistics and Operations Research; Department/School: Statistics and Operations Research.

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Wright, Alan. "Bayesian pathway analysis in epigenetics." Thesis, University of Plymouth, 2013. http://hdl.handle.net/10026.1/1286.

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A typical gene expression data set consists of measurements of a large number of gene expressions, on a relatively small number of subjects, classified according to two or more outcomes, for example cancer or non-cancer. The identification of associations between gene expressions and outcome is a huge multiple testing problem. Early approaches to this problem involved the application of thousands of univariate tests with corrections for multiplicity. Over the past decade, numerous studies have demonstrated that analyzing gene expression data structured into predefined gene sets can produce benefits in terms of statistical power and robustness when compared to alternative approaches. This thesis presents the results of research on gene set analysis. In particular, it examines the properties of some existing methods for the analysis of gene sets. It introduces novel Bayesian methods for gene set analysis. A distinguishing feature of these methods is that the model is specified conditionally on the expression data, whereas other methods of gene set analysis and IGA generally make inferences conditionally on the outcome. Computer simulation is used to compare three common established methods for gene set analysis. In this simulation study a new procedure for the simulation of gene expression data is introduced. The simulation studies are used to identify situations in which the established methods perform poorly. The Bayesian approaches developed in this thesis apply reversible jump Markov chain Monte Carlo (RJMCMC) techniques to model gene expression effects on phenotype. The reversible jump step in the modelling procedure allows for posterior probabilities for activeness of gene set to be produced. These mixture models reverse the generally accepted conditionality and model outcome given gene expression, which is a more intuitive assumption when modelling the pathway to phenotype. It is demonstrated that the two models proposed may be superior to the established methods studied. There is considerable scope for further development of this line of research, which is appealing in terms of the use of mixture model priors that reflect the belief that a relatively small number of genes, restricted to a small number of gene sets, are associated with the outcome.

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Georgiades, Pantelis. "Studies of the expression and function of the retinoid-X-receptor y gene in rodent embryonic development." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244677.

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Livingstone, Julie. "Gene expression and bioinformatics analysis of the isoflavonoid pathway in soybean." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66992.

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The phenylpropanoid pathway is highly researched due to t he putative nutraceutical benefits of its secondary metabolites. The enzymes of this pathway are member of gene families, but the exact number of gene homologues has to date been unknown. In this study, expressed sequence tags (ESTs) were used to identify all homologues in the isoflavonoid pathway of soybean (Glycine max L. Merr.). Gene expression of all homologues in whole tissues, and at a cellular level in the pod was also investigated using laser capture microdissection (LCM) and real time reverse-transcription polymerase chain reaction (qRT-PCR). Computational promoter analysis was undertaken to identify common regulatory motifs among the gene homologues. We have identified novel 2-hydroxyisoflavanone dehydratase and isoflavone-7-O-glucosyltransferase homologues. Differential expression of multiple gene homologues was discovered in numerous tissues. Our promoter analysis discovered five motifs which were previously identified within the promoter regions of the phenylpropanoid pathway in other plant species.
La plupart des gènes de la voie métabolique des phenylpropanoïdes chez le soya incluent plusieurs homologues, mais leur nombre exact pour chacun des gènes demeure inconnu. L'expression de tous les homologues fut observée dans plusieurs tissus et au niveau cellulaire dans la cosse utilisant les méthodes de « laser capture microdissection » et de « real-time reverse-transcription polymerase chain reaction ». Une analyse de promoteurs in silico a été réalisée afin d'identifier des motifs régulateur commun chez les homologues. Cette étude a identifié un gène 2-hydroxyisoflavanone dehydratase nouveau en plus de cinq gènes isoflavone-7-O-glucosyltransferase. En outre, l'expression différentielle de plusieurs des homologues fut observée surtout dans les racines, les cotylédons et dans la couche exocarpe de la cosse. L'analyse de promoteur a découvert cinq motifs, qui ont auparavant été identifiés aussi dans des promoteurs de la voie métabolique des phenylpropanoid de d'autres espèces de plantes.

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Stenico, Verena <1983&gt. "Genus Bifidobacterium: taxonomy studies and gene expression analysis on folate pathway." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6604/.

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Folates (vitamin B9) are essential water soluble vitamins, whose deficiency in humans may contribute to the onset of several diseases, such as anaemia, cancer, cardiovascular diseases, neurological problems as well as defects in embryonic development. Human and other mammals are unable to synthesize ex novo folate obtaining it from exogenous sources, via intestinal absorption. Recently the gut microbiota has been identified as an important source of folates and the selection and use of folate producing microorganisms represents an innovative strategy to increase human folate levels. The aim of this thesis was to gain a fundamental understanding of folate metabolism in Bifidobacterium adolescentis. The work was subdivided in three main phases, also aimed to solve different problems encountered working with Bifidobacterium strains. First, a new identification method (based on PCR-RFLP of hsp60 gene) was specifically developed to identify Bifidobacterium strains. Secondly, Bifidobacterium adolescentis biodiversity was explored in order to recognize representing strains of this species to be screened for their folate production ability. Results showed that this species is characterized by a wide variability and support the idea that a possible new taxonomic re-organization would be required. Finally B. adolescentis folate metabolism was studied using a double approach. A quantitative analysis of folate content was complemented by the examination of expression levels of genes involved in folate related pathways. For the normalization process, required to increase the robustness of the qRT-PCR analysis, an appropriate set of reference genes was tested using two different algorithms. Results demonstrate that B.adolescentis strains may represent an endogenous source of natural folate and they could be used to fortify fermented dairy products. This bio-fortification strategy presents many advantages for the consumer, providing native folate forms more bio-available, and not implicated in the discussed controversy concerning the safety of high intake of synthetic folic acid.

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Stelios, Pavlidis. "Pathway based microarray analysis based on multi-membership gene regulation." Thesis, Brunel University, 2012. http://bura.brunel.ac.uk/handle/2438/6968.

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Recent developments in automation and novel experimental techniques have led to the accumulation of vast amounts of biological data and the emergence of numerous databases to store the wealth of information. Consequentially, bioinformatics have drawn considerable attention, accompanied by the development of a plethora of tools for the analysis of biological data. DNA microarrays constitute a prominent example of a high-throughput experimental technique that has required substantial contribution of bioinformatics tools. Following its popularity there is an on-going effort to integrate gene expression with other types of data in a common analytical approach. Pathway based microarray analysis seeks to facilitate microarray data in conjunction with biochemical pathway data and look for a coordinated change in the expression of genes constituting a pathway. However, it has been observed that genes in a pathway may show variable expression, with some appearing activated while others repressed. This thesis aims to add some contribution to pathway based microarray analysis and assist the interpretation of such observations, based on the fact that in all organisms a substantial number of genes take part in more than one biochemical pathway. It explores the hypothesis that the expression of such genes represents a net effect of their contribution to all their constituent pathways, applying statistical and data mining approaches. A heuristic search methodology is proposed to manipulate the pathway contribution of genes to follow underlying trends and interpret microarray results centred on pathway behaviour. The methodology is further refined to account for distinct genes encoding enzymes that catalyse the same reaction, and applied to modules, shorter chains of reactions forming sub-networks within pathways. Results based on various datasets are discussed, showing that the methodology is promising and may assist a biologist to decipher the biochemical state of an organism, in experiments where pathways exhibit variable expression.

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Newton, Sherylanne. "Noise-induced hearing loss : changes in gene expression in the auditory pathway." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40895.

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Noise induced hearing loss is classically divided into permanent or temporary forms. Individuals with permanent threshold shifts (PTS) will permanently lose auditory sensitivity, whereas individuals with temporary threshold shifts (TTS) will experience elevated hearing thresholds immediately following noise exposure, which resolves over several weeks. TTS causes little lasting damage to the hair cell, stereocilia or supporting structures which form the organ of Corti within the inner ear, and was therefore considered “no harm, no foul”. However, recent evidence suggests that TTS and PTS also leads to, what has been termed, “silent damage”; neuropathic damage which causes the loss of synaptic innervation at the inner hair cell and a slowly developing neuronal death. This study investigates the gene expression changes which accompany this type of noise-induced damage in the spiral ganglion neuron (SGN). Previous studies of gene expression changes following noise insult have used whole cochlea preparations which do not differentiate between changes in different cochlear structures. Here we have used micro-dissection of the modiolus to focus on the SGNs and to minimise contribution from other cochlea structures. In order to maximise the amount of data collected from each experimental animal, cochlear nucleus (CN) samples were taken in parallel to look at noise-induced changes at this first region of the central auditory system. A 1.5hr noise exposure of 105 dB SPL broadband noise elicited a moderate form of PTS, characterized by an immediate threshold shift of up to 44 dB SPL, which partially recovers over 28 days. Tissue was collected at 1day, 7days and 28days following exposure and RNA-Sequencing was performed. Over the 28-day period 421 genes were significantly changed in the modiolus; these were suggestive of a chronic immune response and for the first time, fibrinogen and lipid dysregulation. In the cochlear nucleus, just 184 genes were altered over 28-days; changes to Trpv4, Trpm3 and TrkA may contribute to increases in cell excitability in the CN following noise exposure.

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Shen, Ying. "Regulation of EphA4 expression through the APC-mediated ubiquitin-proteasome pathway /." View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?BICH%202007%20SHEN.

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Books on the topic "Retinoid pathway gene expression"

1

Valkonen, Mari. Functional studies of the secretory pathway of filamentous fungi: The effect of unfolded protein response on protein production. Espoo [Finland]: VTT Technical Research Centre of Finland, 2003.

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Alizadeh-Azami, Solmaz. Is there a common antipsychotic pathway for neuronal gene expression in vitro? 2006.

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Methylation pathway perturbations with folate deficiency: A role for epigenetics in endothelial gene expression. Ottawa: National Library of Canada, 2003.

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Lotfi, Shamim. Molecular mechanisms underlying the expression of proglucagon gene: Role of the Epac signaling pathway in the intestinal endocrine L cells. 2005.

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Merl, Dan, Joseph Lucas, Joseph Nevins, Haige Shen, and Mike West. Trans-study projection of genomic biomarkers in analysis of oncogene deregulation and breast cancer. Edited by Anthony O'Hagan and Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.6.

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This article focuses on the use of Bayesian concepts and methods in the trans-study projection of genomic biomarkers for the analysis of oncogene deregulation in breast cancer. The objective of the study is to determine the extent to which patterns of gene expression associated with experimentally induced oncogene pathway deregulation can be used to investigate oncogene pathway activity in real human cancers. This is often referred to as the in vitro to in vivo translation problem, which is addressed using Bayesian sparse factor regression analysis for model-based translation and refinement of in vitro generated signatures of oncogene pathway activity into the domain of human breast tumour tissue samples. The article first provides an overview of the role of oncogene pathway deregulation in human cancers before discussing the details of modelling and data analysis. It then considers the findings based on biological evaluation and Bayesian pathway annotation analysis.

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Menon, Deepa U. Autism and Intellectual Disabilities. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0053.

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PTEN (phosphatase and tensin homologue) on chromosome 10q23.3 is a tumor suppressor gene that encodes for a dual specificity phosphatase that regulates the phosphatidylinositol 3- kinase pathway and has an important role in brain development by affecting neuronal survival, neurite outgrowth, synaptic plasticity, and learning memory. Germline mutations of the PTEN gene have been implicated in a group of related tumor syndromes with autosomal dominant inheritance and variable expression and include the Cowden syndrome, Bannayan-Riley-Ruvalcaba syndrome, Proteus syndrome, and Juvenile Polyposis syndrome. These syndromes are collectively called the PTEN hamartoma tumor syndromes (PHTS) because they have a predisposition to tumors and hamartomas. PTEN germ line mutations have also been recently linked to autism and macrocephaly and the prevalence of PTEN mutation in children with autism spectrum disorder, and macrocephaly is reported to range from 1.1% to 16.7%.

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Kan, Carol, and Ma-Li Wong. Genetics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0004.

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An association between type 2 diabetes mellitus (T2DM) and depression has been reported in epidemiological studies. Finding a genetic overlap between T2DM and depression will provide evidence to support a common biological pathway to both disorders. Genetic correlations observed from twin studies indicate that a small magnitude of the variance in liability can be attributed to genetic factors. However, no genetic overlap has been observed between T2DM and depression in genome-wide association studies using both the polygenic score and the linkage disequilibrium score regression approaches. Clarifying the shared heritability between these two complex traits is an important next step towards better therapy and treatment. Another area that needs to be explored is gene–environment interaction, since genotypes can affect an individual’s responses to the environment and environment can differentially affect genotypes expression.

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Book chapters on the topic "Retinoid pathway gene expression"

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Nugent, Paul, and Robert M. Greene. "Use of Antisense Oligonucleotides to Study the Role of CRABPs in Retinoic Acid-Induced Gene Expression." In Retinoid Protocols, 191–202. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1385/0-89603-438-0:191.

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Brody, Edward, Joëlle Marie, Maria S. Goux-Pelletan, and Béatrice Clouet d’Orval. "Alternative Splicing to Tissue Specific Splicing - An Evolutionary Pathway?" In Evolutionary Tinkering in Gene Expression, 203–13. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5664-6_19.

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Tsybovsky, Yaroslav, and Krzysztof Palczewski. "Retinoid Pathway Gene Mutations and the Pathophysiology of Related Visual Diseases." In The Retinoids, 529–42. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118628003.ch24.

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Adametz, David, Mélanie Rey, and Volker Roth. "Information Bottleneck for Pathway-Centric Gene Expression Analysis." In Lecture Notes in Computer Science, 81–91. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-11752-2_7.

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AlAjlan, Amani, and Ghada Badr. "Data Mining in Pathway Analysis for Gene Expression." In Lecture Notes in Computer Science, 69–77. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20910-4_6.

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Yu, Xiang Sean, Raymond K. Blanchard, Yexun Wang, and Min You. "Gene Expression Arrays for Pathway Analysis in Cancer Research." In Principles of Molecular Oncology, 135–52. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-470-4_7.

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Žgombić, Mirna, and Gregg Duester. "DNA Elements Mediating Retinoid and Thyroid Hormone Regulation of Alcohol Dehydrogenase Gene Expression." In Advances in Experimental Medicine and Biology, 571–80. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2904-0_60.

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Zyla, Joanna, Kinga Leszczorz, and Joanna Polanska. "Robustness of Pathway Enrichment Analysis to Transcriptome-Wide Gene Expression Platform." In Advances in Intelligent Systems and Computing, 176–85. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-54568-0_18.

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Karagiannaki, Ioulia, Yannis Pantazis, Ekaterini Chatzaki, and Ioannis Tsamardinos. "Pathway Activity Score Learning for Dimensionality Reduction of Gene Expression Data." In Discovery Science, 246–61. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-61527-7_17.

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Abstract Molecular gene-expression datasets consist of samples with tens of thousands of measured quantities (e.g., high dimensional data). However, there exist lower-dimensional representations that retain the useful information. We present a novel algorithm for such dimensionality reduction called Pathway Activity Score Learning (PASL). The major novelty of PASL is that the constructed features directly correspond to known molecular pathways and can be interpreted as pathway activity scores. Hence, unlike PCA and similar methods, PASL’s latent space has a relatively straight-forward biological interpretation. As a use-case, PASL is applied on two collections of breast cancer and leukemia gene expression datasets. We show that PASL does retain the predictive information for disease classification on new, unseen datasets, as well as outperforming PLIER, a recently proposed competitive method. We also show that differential activation pathway analysis provides complementary information to standard gene set enrichment analysis. The code is available at https://github.com/mensxmachina/PASL.

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Wykoff, Charles C., Christopher W. Pugh, Adrian L. Harris, Patrick H. Maxwell, and Peter J. Ratcliffe. "The HIF Pathway: Implications for Patterns of Gene Expression in Cancer." In Novartis Foundation Symposia, 212–31. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868716.ch15.

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Conference papers on the topic "Retinoid pathway gene expression"

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Yu, Le, S. Marshall, T. Forster, and P. Ghazal. "Modelling of macrophage gene expression in the interferon pathway." In 2006 IEEE International Workshop on Genomic Signal Processing and Statistics. IEEE, 2006. http://dx.doi.org/10.1109/gensips.2006.353148.

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Yue Zhao, Tham H. Hoang, Pujan Joshi, Seung-Hyun Hong, and Dong-Guk Shin. "Deep pathway analysis incorporating mutation information and gene expression data." In 2016 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2016. http://dx.doi.org/10.1109/bibm.2016.7822528.

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KURHEKAR, M. P., S. ADAK, S. JHUNJHUNWALA, and K. RAGHUPATHY. "GENOME-WIDE PATHWAY ANALYSIS AND VISUALIZATION USING GENE EXPRESSION DATA." In Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2001. http://dx.doi.org/10.1142/9789812799623_0043.

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Kim, Hyunsoo, and Markus Bredel. "Predicting survial by cancer pathway gene expression profiles in the TCGA." In 2012 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2012. http://dx.doi.org/10.1109/bibmw.2012.6470256.

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Zhang, Mingrui, Beya Adamu, Chi-Cheng Lin, and Ping Yang. "Gene expression analysis with integrated fuzzy C-means and pathway analysis." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090211.

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Wu, Zhong, John DiCarlo, Yexun Wang, and Vikram Devgan. "Abstract A43: Gene expression signature for Wnt/β-catenin signaling pathway." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a43.

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Joshi, Pujan, Honglin Wang, Brent Basso, Seung-Hyun Hong, Charles Giardina, and Dong-Guk Shin. "A Framework for Route Based Pathway Analysis of Gene Expression Data." In ICCBB '20: 2020 4th International Conference on Computational Biology and Bioinformatics. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3449258.3449262.

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Baarsma, HA, H. Meurs, AJ Halayko, and R. Gosens. "Wnt Pathway Gene Expression in Airway Smooth Muscle and Bronchial Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3895.

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Roelofs, Pieter A., William L. Brown, Paul N. Span, John W. Martens, Chai Y. Goh, Boon H. Chua, Dennis Kappei, and Reuben S. Harris. "Abstract 286: Regulation of APOBEC3B gene expression through the Rb/E2F pathway." 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.am2020-286.

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Yang, Sihyung, April E. Cho, Eunhye Lee, Soojeong Lim, Raymond F. Novak, and So Hee Kim. "Abstract 3408: Gene expression profiling of MCF10A series of Ha-Ras transformed human breast epithelial cells: Gene expression involved in EMT pathway." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3408.

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Reports on the topic "Retinoid pathway gene expression"

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Dixon, Richard A. Systematic Modification of Monolignol Pathway Gene Expression for Improved Lignocellulose Utilization. Office of Scientific and Technical Information (OSTI), August 2010. http://dx.doi.org/10.2172/985404.

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