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Littérature scientifique sur le sujet « Suppressor cells Identification »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 19 février 2022

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Articles de revues sur le sujet "Suppressor cells Identification"

Bardin, Sylvie D., Ralf T. Voegele, and Turlough M. Finan. "Phosphate Assimilation in Rhizobium(Sinorhizobium) meliloti: Identification of apit-Like Gene." Journal of Bacteriology 180, no. 16 (August 15, 1998): 4219–26. http://dx.doi.org/10.1128/jb.180.16.4219-4226.1998.

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ABSTRACT Rhizobium meliloti mutants defective in thephoCDET-encoded phosphate transport system form root nodules on alfalfa plants that fail to fix nitrogen (Fix−). We have previously reported that two classes of second-site mutations can suppress the Fix− phenotype ofphoCDET mutants to Fix+. Here we show that one of these suppressor loci (sfx1) contains two genes, orfA and pit, which appear to form an operon transcribed in the order orfA-pit. The Pit protein is homologous to various phosphate transporters, and we present evidence that three suppressor mutations arose from a single thymidine d

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Powers, Jason G., Tim L. Sit, Feng Qu, T. Jack Morris, Kook-Hyung Kim, and Steven A. Lommel. "A Versatile Assay for the Identification of RNA Silencing Suppressors Based on Complementation of Viral Movement." Molecular Plant-Microbe Interactions® 21, no. 7 (July 2008): 879–90. http://dx.doi.org/10.1094/mpmi-21-7-0879.

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The cell-to-cell movement of Turnip crinkle virus (TCV) in Nicotiana benthamiana requires the presence of its coat protein (CP), a known suppressor of RNA silencing. RNA transcripts of a TCV construct containing a reporter gene (green fluorescent protein) (TCV-sGFP) in place of the CP open reading frame generated foci of three to five cells. TCV CP delivered in trans by Agrobacterium tumefaciens infiltration potentiated movement of TCV-sGFP and increased foci diameter, on average, by a factor of four. Deletion of the TCV movement proteins in TCV-sGFP (construct TCVΔ92-sGFP) abolished the movem

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Bedke, Tanja, Sarah Lurati, Claudia Stuehler, Nina Khanna, Hermann Einsele, and Max S. Topp. "Identification and Characterization of Human Aspergillus Fumigatus-Specific Tr1-(Like) Cells." Blood 118, no. 21 (November 18, 2011): 181. http://dx.doi.org/10.1182/blood.v118.21.181.181.

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Abstract Abstract 181 Introduction: The ubiquitous mold Aspergillus fumigatus (A. fumigatus) induces two forms of pathogenesis: invasive aspergillosis in neutropenic patients and allergic aspergillosis in patients with chronic obstructive lung disease as well as in immunosuppressed patients. Mouse models of aspergillosis suggest that not only effector T cells (Teff) but also regulatory T cells (Treg) play a crucial role for the regulation of a protective T cell-mediated immunity to A. fumigatus. However, it is little-known about the involvement of Treg during A. fumigatus infection in humans.

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Benni, Mei Li, and Lenore Neigeborn. "Identification of a New Class of Negartive Regulators Affecting Sporulation-Specific Gene Expression in Yeast." Genetics 147, no. 3 (November 1, 1997): 1351–66. http://dx.doi.org/10.1093/genetics/147.3.1351.

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We characterized two yeast loci, MDS3 and PMD1, that negatively regulate sporulation. Initiation of sporulation is mediated by the meiotic activator IME1, which relies on MCK1 for maximal expression. We isolated the MDS3-1 allele (encoding a truncated form of Mds3p) as a suppressor that restores IME1 expression in mck1 mutants. mds3 null mutations confer similar suppression phenotypes as MDS3-1, indicating that Mds3p is a negative regulator of sporulation and the MDS3-1 allele confers a dominant-negative phenotype. PMD1 is predicted to encode a protein sharing significant similarity with Mds3p

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He, B., Y. Chiba, H. Li, S. de Vega, K. Tanaka, K. Yoshizaki, M. Ishijima, et al. "Identification of the Novel Tooth-Specific Transcription Factor AmeloD." Journal of Dental Research 98, no. 2 (November 14, 2018): 234–41. http://dx.doi.org/10.1177/0022034518808254.

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Basic-helix-loop-helix (bHLH) transcription factors play an important role in various organs’ development; however, a tooth-specific bHLH factor has not been reported. In this study, we identified a novel tooth-specific bHLH transcription factor, which we named AmeloD, by screening a tooth germ complementary DNA (cDNA) library using a yeast 2-hybrid system. AmeloD was mapped onto the mouse chromosome 1q32. Phylogenetic analysis showed that AmeloD belongs to the achaete-scute complex-like ( ASCL) gene family and is a homologue of ASCL5. AmeloD was uniquely expressed in the inner enamel epitheli

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Movahedi, Kiavash, Martin Guilliams, Jan Van den Bossche, Rafael Van den Bergh, Conny Gysemans, Alain Beschin, Patrick De Baetselier, and Jo A. Van Ginderachter. "Identification of discrete tumor-induced myeloid-derived suppressor cell subpopulations with distinct T cell–suppressive activity." Blood 111, no. 8 (April 15, 2008): 4233–44. http://dx.doi.org/10.1182/blood-2007-07-099226.

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Abstract The induction of CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) is an important immune-evading mechanism used by tumors. However, the exact nature and function of MDSCs remain elusive, especially because they constitute a heterogeneous population that has not yet been clearly defined. Here, we identified 2 distinct MDSC subfractions with clear morphologic, molecular, and functional differences. These fractions consisted of either mononuclear cells (MO-MDSCs), resembling inflammatory monocytes, or low-density polymorphonuclear cells (PMN-MDSCs), akin to immature neutrophils. Inte

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Anger, Natalia, and Joanna Rossowska. "Myeloid-derived suppressor cells as a target for anticancer therapy." Postępy Higieny i Medycyny Doświadczalnej 72 (December 31, 2018): 1179–98. http://dx.doi.org/10.5604/01.3001.0012.8267.

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Myeloid-derived suppressor cells are heterogenic immature myeloid cells, which possess suppressor activity and play an important role in both, tumor progression and metastasis. The accumulation of MDSCs is induced primarily by factors that are secreted by the tumor microenvironment, which disturb myelopoiesis that occurs in the bone marrow and enables the migration of immature myeloid cells into the tumor. MDSCs promote tumor growth by inhibiting the activity of immunocompetent cells, as well as by activating non-immunological processes, such as tumor angiogenesis, the degradation of extracell

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Kansa, Geoffrey S., and Edgar G. Engleman. "Phenotypic identification of suppressor-effector, suppressor-amplifier and suppressor-inducer T cells of B cell differentiation in man." European Journal of Immunology 17, no. 4 (1987): 453–57. http://dx.doi.org/10.1002/eji.1830170403.

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Zimring, James C., and Judith A. Kapp. "Identification and Characterization of CD8⁺ Suppressor T Cells." Immunologic Research 29, no. 1-3 (2004): 303–12. http://dx.doi.org/10.1385/ir:29:1-3:303.

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Blanchard, Thomas G., Steven J. Czinn, Vivekjyoti Banerjee, Neha Sharda, Andrea C. Bafford, Fahad Mubariz, Dennis Morozov, Antonino Passaniti, Hafiz Ahmed, and Aditi Banerjee. "Identification of Cross Talk between FoxM1 and RASSF1A as a Therapeutic Target of Colon Cancer." Cancers 11, no. 2 (February 8, 2019): 199. http://dx.doi.org/10.3390/cancers11020199.

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Metastatic colorectal cancer (mCRC) is characterized by the expression of cellular oncogenes, the loss of tumor suppressor gene function. Therefore, identifying integrated signaling between onco-suppressor genes may facilitate the development of effective therapy for mCRC. To investigate these pathways we utilized cell lines and patient derived organoid models for analysis of gene/protein expression, gene silencing, overexpression, and immunohistochemical analyses. An inverse relationship in expression of oncogenic FoxM1 and tumor suppressor RASSF1A was observed in various stages of CRC. This

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Thèses sur le sujet "Suppressor cells Identification"

Francis, Christopher Ryan. "Identification and analysis of prohibitin in B16 Mouse Melanoma Cells." [Huntington, WV : Marshall University Libraries], 2008. http://www.marshall.edu/etd/descript.asp?ref=868.

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Thesis (M.S.)--Marshall University, 2008.<br>Title from document title page. Includes abstract. Document formatted into pages: contains vi, 69 p. : ill. Includes bibliographical references (p. 59-65).

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Sherger, Matthew George. "Identification of Myeloid Derived Suppressor Cells in Tumor Bearing Dogs." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1337617975.

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Zhang, Liyi, and 張麗儀. "Identification and characterization of tumor suppressor gene and cancer stemness gene in esophageal squamous cell carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/208563.

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Esophageal squamous cell carcinoma (ESCC), the major histological subtype of esophageal cancer, is one of the most common malignancies with poor prognosis in the world. Despite continued development of diagnosis and treatment, ESCC remains the sixth leading cause of cancer death worldwide. Current treatment regimens in ESCC are often characterized by ineffectiveness and poor selectivity. Therapeutic methods directed at cancer-associated genes or cancer stem cells (CSCs) may be effective approaches to cure this deadly cancer. Therefore, this study aims to identify specific ESCC-related genes an

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Ring, Giselle Natasha. "Identification and characterization of TMEM 85, a novel suppressor of bax-mediated cell death in yeast." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112352.

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The ability to evade apoptosis is an acquired characteristic associated with many normal and pathophysiological processes. TMEM 85 represents a novel transmembrane domain containing human protein isolated in our previous screen for Bax suppressors, but whose function is currently unknown. Using viability and growth assays, we confirmed that TMEM 85 is anti-apoptotic. Four unique human cDNA sequences containing regions distinct from and of perfect identity to our cDNA were present in the database. Analysis of TMEM 85 suggests that it consists of five exons, alternatively spliced to produce at l

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Guo, Tianhuan, and 郭天欢. "Identification of tumor suppressor genes in the commonly deleted region of chromosome 6q in NK-cell malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43785761.

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Guo, Tianhuan. "Identification of tumor suppressor genes in the commonly deleted region of chromosome 6q in NK-cell malignancies." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43785761.

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Dahmani, Rajae. "Identification d’une nouvelle isoforme du gène suppresseur de tumeur LKB1 ayant des propriétés oncogéniques." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T053/document.

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LKB1 est un gène suppresseur de tumeur qui code une kinase « maitre » dont l’activité contrôle la polarité et la prolifération cellulaire en les coordonnant avec l’état métabolique de la cellule. Ce travail a abouti à l’identification d’une nouvelle isoforme LKB1 appelée ∆N-LKB1 qui est générée par transcription alternative et initiation interne de la traduction de l'ARNm LKB1. La protéine ∆N-LKB1 est délétée de sa partie N-terminale incluant une partie de son domaine kinase. Bien que la protéine N-LKB1 soit catalytiquement inactive, elle potentialise l'effet activateur de la protéine LKB1 su

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Wong, Chun-lam, and 黃俊霖. "Identification and functional analysis of candidate tumor suppressor genes in chromosome 9 in esophageal squamous cell carcinoma (ESCC)." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45204214.

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Hamze, Zeinab. "Études fonctionnelles du gène suppresseur de tumeurs MEN1 : « Identification des bases moléculaires de la spécificité endocrine de sa fonction suppresseur de tumeurs »." Thesis, Lyon 1, 2011. http://www.theses.fr/2011LYO10094.

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La Néoplasie Endocrinienne Multiple de type1 (NEM1) est une maladie à transmission autosomique dominante liée à l'inactivation du gène MEN1 codant pour la protéine ménine. Bien que ménine soit exprimée dans tous les tissus testés de l'organisme, elle n'a un effet oncosuppresseur que dans les cellules endocrines. L'hypothèse de mon travail est que ménine interagit avec des fonctions endocrines spécifiques. J'ai ciblé mes études sur une lignée de cellules β pancréatiques INS-1 dans laquelle j'ai étudié la réponse cellulaire au glucose et la régulation du facteur de transcription MAFA en fonction

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Nothdurft, Silke [Verfasser], and Martin [Akademischer Betreuer] Schuler. "Identification and characterization of aryl hydrocarbon receptor (AHR) as a suppressor of non-small-cell lung cancer metastasis / Silke Nothdurft ; Betreuer: Martin Schuler." Duisburg, 2021. http://d-nb.info/1240145101/34.

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Chapitres de livres sur le sujet "Suppressor cells Identification"

Horwitz, Benjamin A., and Sophie Lev. "Identification of Differentially Expressed Fungal Genes In Planta by Suppression Subtraction Hybridization." In Molecular and Cell Biology Methods for Fungi, 115–23. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-611-5_8.

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van Cleef, Koen W. R., Joël T. van Mierlo, Marius van den Beek, and Ronald P. van Rij. "Identification of Viral Suppressors of RNAi by a Reporter Assay in Drosophila S2 Cell Culture." In Antiviral RNAi, 201–13. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-037-9_12.

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Mihailescu, Dan, Arthur B. Schneider, and Leon Fogelfeld. "Pathogenesis of thyroid cancer." In Oxford Textbook of Endocrinology and Diabetes, 600–609. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.3324.

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Both epidemiological and molecular biological studies have been used to understand the origins of thyroid cancer. Epidemiological studies have been used to identify factors that predispose to thyroid cancer. That is principally how we know that exposure to radiation leads to thyroid cancer (see Chapter 3.2.5). In fact, radiation is the only environmental factor for which the proof is incontrovertible. Molecular biological studies, reviewed in the second part of this chapter, have been used to investigate the events within thyroid cells that are initiated by predisposing factors, e.g. radiation, and lead, by one or multiple steps, to transformation and cancer. These studies have focused on cancer-related genes, particularly proto-oncogenes and tumour suppressor genes, and have led to the identification of potential therapeutic agents. They have also focused on the cellular pathways and processes, including epigenetic changes and microRNA expression, which accompany transformation of the thyroid cell. Epidemiology and molecular biology have interacted productively in the studies that have followed the Chernobyl accident. This interaction is described in the third part of this chapter in which the mutations found in radiation-related thyroid cancers are reviewed.

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Lok, Hong, Arthur Kwok Leung Cheung, Josephine Mun Yee Ko, Yue Cheng, and Maria Li. "Identification of Tumor Suppressor Genes via Cell Fusion and Chromosomal Transfer." In Tumor Suppressor Genes. InTech, 2012. http://dx.doi.org/10.5772/38925.

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Actes de conférences sur le sujet "Suppressor cells Identification"

BURRER, Renaud, Océane ARIBO, Assil BENCHAABEN, Maroua TLIBA, Domenico LAZZARO, and Jean-Philippe COTON. "Abstract LB-352: Identification of myeloid-derived suppressor cells in solid tumors by multiplex IHC." 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-lb-352.

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Gao, Boning, Chunxian Huang, Luc Girard, Adi F. Gazdar, Jerry W. Shay, and John D. Minna. "Abstract 2342: Identification of oncogenes and tumor suppressor genes using immortalized lung bronchial epithelial cells and small airway epithelial cells." 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.am2012-2342.

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Boutte, Angela, and Charles Lin. "Abstract 1459: Proteomic identification of a novel antitumor protein from myeloid-derived suppressor cells in breast cancer." 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.am10-1459.

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Li, Yongsheng, Guifang Yan, Huakan Zhao, and Qi Zhang. "Abstract 4732: Myeloid-derived suppressor cells potentiate colorectal carcinogenesis: Identification of a novel RIPK3-PGE2 circuit in tumor microenvironment." 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.am2018-4732.

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LaBagnara, Michael, Keith Lambert, Sudeepta Sridhara, Michael Tobias, Raj Murali, and Meena Jhanwar-Uniyal. "Abstract 1927: Tumor suppressor PTEN regulates cancer stem cells of glioblastoma multiforme: identification of signaling pathways as targets of therapy." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1927.

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Bellacosa, Alfonso. "Abstract PL04-04: Altered gene expression patterns in phenotypically normal cells from individuals heterozygous for mutations in tumor suppressor genes: Identification of candidate biomarkers of cancer risk." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Nov 7-10, 2010; Philadelphia, PA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-10-pl04-04.

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Rodenberg, J., I. Uray, R. Bissonnette, and P. Brown. "Identification of Critical Transducers of Rexiniod-Mediated Growth Suppression in Normal Breast Cells." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-3134.

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Rodenberg, Jennifer M., Ivan P. Uray, Reid P. Bissonnette, and Powel H. Brown. "Abstract A91: Identification of nuclear hormone receptors critical for rexiniod‐mediated growth suppression of normal human breast cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-a91.

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Chesnokov, Alexander, Oleg Ivanov, Vyacheslav Kolyadin, Alexey Lemus, Vitaly Pavlenko, Sergey Semenov, Vyacheslav Stepanov, et al. "HLRW Management During MR Reactor Decommissioning in NRC “Kurchatov Institute”." In ASME 2013 15th International Conference on Environmental Remediation and Radioactive Waste Management. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icem2013-96046.

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A program of decommissioning of MR research reactor in the Kurchatov institute started in 2008. The decommissioning work presumed a preliminary stage, which included: removal of spent fuel from near reactor storage; removal of spent fuel assemble of metal liquid loop channel from a core; identification, sorting and disposal of radioactive objects from gateway of the reactor; identification, sorting and disposal of radioactive objects from cells of HLRW storage of the Kurchatov institute for radwaste creating form the decommissioning of MR. All these works were performed by a remote controlled

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Rapports d'organisations sur le sujet "Suppressor cells Identification"

Liu, Xuedong. Identification of the Downstream Promoter Targets of Smad Tumor Suppressors in Human Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada433854.

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