Littérature scientifique sur le sujet « Groucho/TLE »
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Articles de revues sur le sujet "Groucho/TLE"
Desjobert, Cecile, Peter Noy, Tracey Swingler, Hannah Williams, Kevin Gaston et Padma-Sheela Jayaraman. « The PRH/Hex repressor protein causes nuclear retention of Groucho/TLE co-repressors ». Biochemical Journal 417, no 1 (12 décembre 2008) : 121–32. http://dx.doi.org/10.1042/bj20080872.
Texte intégralChen, Guoqing, et Albert J. Courey. « Groucho/TLE family proteins and transcriptional repression ». Gene 249, no 1-2 (mai 2000) : 1–16. http://dx.doi.org/10.1016/s0378-1119(00)00161-x.
Texte intégralHUSAIN, Junaid, Rita LO, Diane GRBAVEC et Stefano STIFANI. « Affinity for the nuclear compartment and expression during cell differentiation implicate phosphorylated Groucho/TLE1 forms of higher molecular mass in nuclear functions ». Biochemical Journal 317, no 2 (15 juillet 1996) : 523–31. http://dx.doi.org/10.1042/bj3170523.
Texte intégralHeimbucher, Thomas, Christina Murko, Baubak Bajoghli, Narges Aghaallaei, Anja Huber, Ronald Stebegg, Dirk Eberhard, Maria Fink, Antonio Simeone et Thomas Czerny. « Gbx2 and Otx2 Interact with the WD40 Domain of Groucho/Tle Corepressors ». Molecular and Cellular Biology 27, no 1 (23 octobre 2006) : 340–51. http://dx.doi.org/10.1128/mcb.00811-06.
Texte intégralGRBAVEC, Diane, Rita LO, Yanling LIU, Andy GREENFIELD et Stefano STIFANI. « Groucho/transducin-like Enhancer of split (TLE) family members interact with the yeast transcriptional co-repressor SSN6 and mammalian SSN6-related proteins : implications for evolutionary conservation of transcription repression mechanisms ». Biochemical Journal 337, no 1 (17 décembre 1998) : 13–17. http://dx.doi.org/10.1042/bj3370013.
Texte intégralHoffman, Brad G., Bogard Zavaglia, Mike Beach et Cheryl D. Helgason. « Expression of Groucho/TLE proteins during pancreas development ». BMC Developmental Biology 8, no 1 (2008) : 81. http://dx.doi.org/10.1186/1471-213x-8-81.
Texte intégralCinnamon, Einat, et Ze’ev Paroush. « Context-dependent regulation of Groucho/TLE-mediated repression ». Current Opinion in Genetics & ; Development 18, no 5 (octobre 2008) : 435–40. http://dx.doi.org/10.1016/j.gde.2008.07.010.
Texte intégralFisher, A. L., S. Ohsako et M. Caudy. « The WRPW motif of the hairy-related basic helix-loop-helix repressor proteins acts as a 4-amino-acid transcription repression and protein-protein interaction domain. » Molecular and Cellular Biology 16, no 6 (juin 1996) : 2670–77. http://dx.doi.org/10.1128/mcb.16.6.2670.
Texte intégralJennings, Barbara H., et David Ish-Horowicz. « The Groucho/TLE/Grg family of transcriptional co-repressors ». Genome Biology 9, no 1 (2008) : 205. http://dx.doi.org/10.1186/gb-2008-9-1-205.
Texte intégralPatel, Sanjeevkumar R., Samina S. Bhumbra, Raghavendra S. Paknikar et Gregory R. Dressler. « Epigenetic Mechanisms of Groucho/Grg/TLE Mediated Transcriptional Repression ». Molecular Cell 45, no 2 (janvier 2012) : 185–95. http://dx.doi.org/10.1016/j.molcel.2011.11.007.
Texte intégralThèses sur le sujet "Groucho/TLE"
Grbavec, Diane C. « Characterization of molecular mechanisms involving the transcriptional repression functions of mammalian Groucho/TLE proteins ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0035/NQ64564.pdf.
Texte intégralAlmqvist, Jenny. « Epstein-Barr virus nuclear antigen 1, Oct & ; Groucho/TLE in control of promoter regulation / ». Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-523-2/.
Texte intégralPerin, Alessandro. « Controllo del self-renewal e della tumorigenicità delle glioblastoma “stem-like” cells ad opera di FOXG1 ». Doctoral thesis, Università degli studi di Trieste, 2012. http://hdl.handle.net/10077/7398.
Texte intégralGlioblastoma (GBM) is the most common and malignant primary brain tumour. GBM prognosis remains dismal despite available treatments, be- cause of tumour recurrence. According to the "Glioma Stem-like Cell" (GSC) hypothesis, GBM recurrence is sustained by a fraction of cells that share similarities with normal Neural Stem Cells / Neural Precursors (NSCs). In potential agreement with this possibility, primary cell cultures with characteristics of GSCs can be established from GBM. These cells display typical hallmarks of NSCs, namely unlimited self-renewal and ability to differentiate into different neural lineages in vitro. Most importantly, GSCs are highly tumorigenic when transplanted intracranially in vivo and their in vitro self-renewal potential correlates positively with tumorigenicity and negatively with prognosis in Glioma patients. We hypothesize that the tumour-forming potential of GSCs may result from the deregulation of molecular mechanisms normally involved in NSC self-renewal, proliferation and/or differentiation. In this regard, the fork-head transcription factor, FOXG1, promotes the self-renewal of both embryonic and adult NSCs. Here we show that FOXG1 mRNA and protein are up-regulated in human Gliomas and that elevated FOXG1 expression is a bad prognostic factor in GBM patients. We show further that FOXG1 is expressed in a sub-population of GBM cells with NSC-like characteristics, as well as in cultured GSCs. More importantly, knockdown of FOXG1 significantly decreases GSC self-renewal, with a concomitant increase of the cell-cycle inhibitor, p21Cip1. We also show that FOXG1 is co-expressed in GBM and GSCs with the transcriptional co-repressor TLE, a protein known to work together with FOXG1 during forebrain development. The effect of FOXG1 knockdown on GSC self-renewal is phenocopied by TLE knockdown, as well as by the forced over-expression of the previously characterized TLE:FOXG1 antagonist, GRG6, a protein with little or no expression in GBM. More importantly, mouse orthotopic implantations of human GSCs, which were either silenced for FOXG1 or over-expressing GRG6, gave rise to smaller tumours when compared to control condition; this tumor size reduction resulted in prolonged mice survival. Together, these results suggest that FOXG1 and TLE are important regulators of GBM tumorigenesis.
XXIV Ciclo
1977