Relevant bibliographies by topics / Suppressor cells Identification

Academic literature on the topic 'Suppressor cells Identification'

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Published: 4 June 2021
Last updated: 19 February 2022

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

Journal articles on the topic "Suppressor cells Identification":

1

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 deletion in a hepta-thymidine sequence centered 54 nucleotides upstream of the orfA transcription start site. This mutation increased the level of orfA-pit transcription. These data, together with previous biochemical evidence, show that theorfA-pit genes encode a Pi transport system that is expressed in wild-type cells grown with excess Pibut repressed in cells under conditions of Pi limitation. In phoCDET mutant cells, orfA-pitexpression is repressed, but this repression is alleviated by the second-site suppressor mutations. Suppression increasesorfA-pit expression compensating for the deficiencies in phosphate assimilation and symbiosis of the phoCDETmutants.
2

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 movement complementation ability of TCV CP. Other known suppressors of RNA silencing from a wide spectrum of viruses also complemented the movement of TCV-sGFP when delivered in trans by Agrobacterium tumefaciens. These include suppressors from nonplant viruses with no known plant movement function, demonstrating that this assay is based solely on RNA silencing suppression. While the TCV-sGFP construct is primarily used as an infectious RNA transcript, it was also subcloned for direct expression from Agrobacterium tumefaciens for simple quantification of suppressor activity based on fluorescence levels in whole leaves. Thus, this system provides the flexibility to assay for suppressor activity in either the cytoplasm or nucleus, depending on the construct employed.
3

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. In order to develop new therapeutical strategies for the treatment of aspergillosis this project aims to understand the influence of regulatory T cells on A. fumigatus infection in humans. Material/Methods: A. fumigatus-specific CD4+ T cell clones were established from PBMC of healthy donors. Based on this clone pool Treg clones were identified due to their inability to proliferate in the absence of costimulation assessed by 3[H]-TdR incorporation as well as their Ag-specific cytokine production and phenotype determined by flow cytometry. Treg function was analyzed by their ability to suppress proliferation of autologous CD4+ T cells using CFSE dilution. Results: We identified A. fumigatus-specific T cell clones that exhibited marginal detectable proliferation after restimulation with immobilized anti-CD3 mAb in the absence of costimulation. However, these T cell clones vigorously proliferated in response to restimulation with their cognate antigen. A more detailed characterization showed that these suppressor T cell clones produced high amounts of IL-10 and moderate levels of IFN-gamma upon Ag-specific restimulation and expressed low amounts of Foxp3 but not Helios, a transcription factor that had recently been linked to natural occurring Treg. Most importantly, these T cell clones suppressed Ag-specific expansion of CD4+ Teff. This effect was contact-independent since suppression of Ag-specific CD4+ T cell expansion detected in transwell experiments was comparable to cocultures that enabled cellular-contact. Furthermore, anti-CD3/CD28-induced proliferation of naïve CD4+ T cells was not reduced in the presence of culture supernatants obtained from suppressor T cell clones after their antigen-specific restimulation in the absence of DCs. Conclusions: We identified for the first time A. fumigatus-specific CD4+ T cell clones with a Tr1(-like) IL-10+IFN-gamma+Foxp3lowHelios− phenotype. These cells suppressed expansion of A. fumigatus-specific Teff in an Ag-specific manner mediated by soluble factors released from Tr1(-like) cell clones. Since these factors did not affect CD4+ T cell proliferation in the absence of DCs our data suggest, that Tr1(-like) cell clones rather negatively regulate the stimulatory capacity of DCs leading to a reduced expansion of Ag-specific CD4+ T cells. Therefore these Tr1(-like) cells might play a protective role during A. fumigatus infection in humans. Thus, adoptive transfer of A. fumigatus-specific Treg could be useful to enhance protective immunity in patients with chronic A. fumigatus infection. Disclosures: Topp: Micromet: Consultancy, Honoraria.
4

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. mds3 pmd1 double mutants are better suppressors of mck1 than is either single mutant, indicating that Mds3p and Pmd1p function synergistically. Northern blot analysis revealed that suppression is due to increased IME1 transcript accumulation. The roles of Mds3p and Pmd1p are not restricted to the MCK1 pathway because mds3 pmd1 mutations also suppress IME1 expression defects associated with MCK1-independent sporulation mutants. Furthermore, mds3 pmdl mutants express significant levels of IME1 even in vegetative cells and this unscheduled expression results in premature sporulation. These phenotypes, and interactions with RAS2-Val19 suggest that unscheduled derepression of IME1 is probably due to a defect in recognition of nutritional status.
5

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 epithelium (IEE), but its expression was suppressed after IEE cell differentiation into ameloblasts. Furthermore, AmeloD expression showed an inverse expression pattern with the epithelial cell-specific cell–cell adhesion molecule E-cadherin in the dental epithelium. Overexpression of AmeloD in dental epithelial cell line CLDE cells resulted in E-cadherin suppression. We found that AmeloD bound to E-box cis-regulatory elements in the proximal promoter region of the E-cadherin gene. These results reveal that AmeloD functions as a suppressor of E-cadherin transcription in IEE cells. Our study demonstrated that AmeloD is a novel tooth-specific bHLH transcription factor that may regulate tooth development through the suppression of E-cadherin in IEE cells.
6

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. Interestingly, both MO-MDSCs and PMN-MDSCs suppressed antigen-specific T-cell responses, albeit using distinct effector molecules and signaling pathways. Blocking IFN-γ or disrupting STAT1 partially impaired suppression by MO-MDSCs, for which nitric oxide (NO) was one of the mediators. In contrast, while IFN-γ was strictly required for the suppressor function of PMN-MDSCs, this did not rely on STAT1 signaling or NO production. Finally, MO-MDSCs were shown to be potential precursors of highly antiproliferative NO-producing mature macrophages. However, distinct tumors differentially regulated this inherent MO-MDSC differentiation program, indicating that this phenomenon was tumor driven. Overall, our data refine tumor-induced MDSC functions by uncovering mechanistically distinct MDSC subpopulations, potentially relevant for MDSC-targeted therapies.
7

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 extracellular matrix and the formation of premetastatic niche. Due to their significant impact on the development of cancer, MDSCs became clinically relevant in tumor diagnostics. In recent years, various therapeutic strategies were developed in order to inhibit the proliferation, accumulation or suppressor activity of MDSCs, as well as to render the differentiation or total depletion of these cells. The proposed therapies often combine factors that reduce MDSCs suppression with conventional chemotherapy or with immune checkpoints inhibitors. In this review, we describe the current state of knowledge about factors that enable the accumulation of MDSCs, methods of phenotypic identification of these cells, as well as the mechanisms of suppression used by them. Moreover, we provide insight into the therapeutic approaches, which aim to restore the reactivity of the immune system by reducing the suppressor effects of MDSCs.
8

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 inverse correlation was also observed in mCRC cells lines (T84, Colo 205) treated with Akt inhibitor. Inhibition of FoxM1 expression in mCRC cells as well as in our ex vivo model resulted in increased RASSF1A expression. Reduced levels of RASSF1A expression were found in normal cells (RWPE-1, HBEpc, MCF10A, EC) stimulated with exogenous VEGF165. Downregulation of FoxM1 also coincided with increased YAP phosphorylation, indicative of tumor suppression. Conversely, downregulation of RASSF1A coincided with FoxM1 overexpression. These studies have identified for the first time an integrated signaling pathway between FoxM1 and RASSF1A in mCRC progression, which may facilitate the development of novel therapeutic options for advanced colon cancer therapy.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Suppressor cells Identification":

1

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.
Title from document title page. Includes abstract. Document formatted into pages: contains vi, 69 p. : ill. Includes bibliographical references (p. 59-65).
2

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 and cancer stemness genes which help us to develop new targeted agents to achieving objective, long-lasting therapeutic responses in ESCC. To obtain an accurate overview of genetic changes occurring in ESCC patients, our group performed microarray-based mRNA expression profiling and high-throughout transcriptome sequencing (RNA-Seq) to compare differentially expressed genes between ESCC tumors and their corresponding non-tumorous tissues. Prostate stem cell antigen (PSCA) was considered to be a candidate of primary interest due to significantly reduced expression in both microarray and RNA-Seq data. In this study, we examined the role of PSCA on the pathogenesis of esophageal cancer. Our results showed that PSCA was frequently down-regulated in ESCC. Its expression was negatively regulated by transcription factor SOX5. Also, we provided evidence that down-regulation of PSCA was associated with poor clinical outcomes of patients with ESCC. Both in vitro and in vivo assays revealed that PSCA could arrest cell cycle progression and promote differentiation. To further elucidate the mechanism involved in biological function of PSCA, we performed co-immunoprecipitation and mass spectroscopy to identify proteins that associate with PSCA. This study found that RB1CC1, a key signaling node to regulate cellular proliferation and differentiation, interacted specifically with PSCA both in vitro and in vivo. Binding of PSCA and RB1CC1 in cytoplasm resulted in stabilization and translocation of RB1CC1 into nucleus and then further regulates the crucial cell cycle and differentiation genes. Furthermore, in order to identify the cancer stemness genes specifically expressed in CSCs of ESCC, we utilized gene expression analysis to profile 34 stemness-associated genes in ESCC specimens. Developmental pluripotency associated 4 (DPPA4), a well known pluripotent marker of stem cell, was considered as the best candidate. Our following histopathological study demonstrated that DPPA4 rigorously marked the rare CSCs, in contrast to core stemness factors (OCT4 and SOX2) and previous reported CSC markers (CD90 and CD44), which expressed in a large population of cancer cells. Moreover, the expression of DPPA4 was also found to have prognostic value in ESCC, as the appearance of DPPA4+ cells was significantly associated with poor differentiation, advanced stage and higher incidences of lymph node metastasis. Finally, our functional studies showed that ESCC cells expressing exogenous DPPA4 conferred an enhanced ability to initiate tumor, self-renew, resist chemotherapy and metastasize through lymphatic system. In summary, this study provide evidence indicating that novel tumor suppressor gene PSCA and cancer stemness gene DPPA4 may contribute to the development and progression of ESCC. Additionally, they may serve as potential targets for development of effective therapeutic strategies.
published_or_final_version
Clinical Oncology
Doctoral
Doctor of Philosophy
4

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 least four different mRNA's and proteins (TMEM 85v1-v4). RT-PCR analysis using RNA isolated from mice and humane tissues show that all transcripts are expressed. Yeast contain an orthologue of the human TMEM 85v1 protein, YGL213C. Surprisingly, the viability assay indicated that mutants lacking YGL231c do not show a hyper-responsive apoptotic phenotype, however its overexpression shows that it is nevertheless anti-apoptotic. Using a yeast strain expressing chromosomally TAP-tagged YGL231c, we found no up-regulation of the endogenous gene due to stress. The deletion mutant is also known to expresses a synthetically lethal phenotype in the presence of alpha-synuclein. While expression of alpha-synuclein caused significant death in both the wild type and deletion mutants, TMEM 85v2 was unable to exhibit a protective role. These findings demonstrate the complexity of the TMEM 85 gene and its anti-apoptotic function in both yeast and human.
5

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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6

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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7

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 sur sa cible principale l’APMK, senseur énergétique de la cellule, via une interaction directe avec le domaine d'auto-inhibition de l’AMPK. En revanche, ∆N-LKB1 interfère négativement avec la capacité de LKB1 à induire la polarité cellulaire. Enfin, en utilisant des approches in vitro et in vivo, nous avons montré que N-LKB1 possède une propriété oncogénique intrinsèque. N-LKB1 est exprimée seule dans la lignée NCI-H460 issue du cancer du poumon. L’inhibition de l’expression de N-LKB1 dans les cellules NCI-H460 induit une diminution de la survie de ces cellules et inhibe leur pouvoir oncogénique quand elles sont greffées dans la souris nude. Nous avons donc identifié une nouvelle isoforme LKB1 qui stimule l’adaptation métabolique LKB1-dépendante, mais qui inhibe la polarité cellulaire contrôlée par LKB1. Le suppresseur de tumeur LKB1 ainsi que l’oncogène N-LKB1 sont codé par le même gène, ce qui peut expliquer certains des effets paradoxaux de LKB1 durant la tumorigenèse
The LKB1 tumor suppressor gene encodes a master kinase that coordinates the regulation of energetic metabolism, cell growth and cell polarity. We now report the identification of a novel isoform of LKB1 named N-LKB1 that is generated through alternative transcription and internal initiation of translation of the LKB1 mRNA. The N-LKB1 protein lacks the N-terminal region and a portion of the kinase domain. Although N-LKB1 is catalytically inactive, it potentiates the stimulating effect of LKB1 on the AMP-activated protein kinase (AMPK) metabolic sensor through a direct interaction with the regulatory auto-inhibitory domain of AMPK. Contrasting, N-LKB1 negatively interferes with the LKB1 polarizing activity. Finally, combining in vitro and in vivo approaches, we showedthat N-LKB1 has an intrinsic oncogenic property. N-LKB1 is expressed solely in the lung cancer cell line, NCI-H460. Silencing of N-LKB1 decreased survival of NCI-H460 cells and inhibited their tumorigenicity when engrafted in nude mice. In conclusion, we have identified a novel LKB1 isoform that enhances the LKB1-controlled AMPK metabolic activity but inhibits LKB1-induced polarizing activity. Both, the LKB1 tumor suppressor and the oncogene, N-LKB1, are expressed from the same locus and this may account for some of the paradoxical effects of LKB1 during tumorigenesis
8

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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9

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 de la variation de l'expression de ménine. Nos résultats ont démontré que l'inhibition de ménine augmente l'incorporation de BrdU en réponse au glucose dans les cellules INS-1, ainsi que l'expression de plusieurs gènes impliqués dans la prolifération de ces cellules. Cette inhibition de ménine est associée avec une réduction dramatique de l'expression de MafA, et celle de certains gènes cibles de MafA. Par ailleurs, la surexpression de la forme sauvage, et non pas des formes mutées de ménine, stimule l'expression de MafA. La variation de l'expression de MafA étant également associée à une variation du taux de prolifération cellulaire. D'autre part, les études in vivo ont montré une bonne corrélation entre le niveau d'expression de ménine et celui de MafA dans les insulinomes du rat et de l'homme. En conclusion, mon travail de thèse a permis de mieux clarifier la fonction biologique de ménine dans les cellules β, et de mettre en évidence l'implication potentielle du facteur MafA dans la tumorigénèse des insulinomes
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant inherited syndrome caused by mutations of the MEN1 gene coding for the protein menin. Although menin is expressed in all tested tissues, its oncosuppressor effect is limited to the endocrine cells. The assumption of my work was that menin interact with specific endocrine functions. To check out this assumption, we selected the β pancreatic cell line INS-1 in which, we analysed the cellular response to glucose stimulation and the regulation of the transcription factor MAFA according to the variation of menin expression. Our results showed that menin inhibition increased BudU incorporation in response to glucose stimulation in INS-1 cells, as well as the expression of several genes involved in the proliferation of these cells. Menin inhibition was associated with a dramatic reduction of MafA expression level, and some of its targeted genes. Interestingly, wild type menin overexpression, but not mutant forms, stimulated MafA expression. Interestingly, modification of MafA expression modified proliferation rate of INS-1 cells. In addition, the in vivo studies, showed a good correlation between menin and MafA expression levels in both rat and human insulinoma. In conclusion, my thesis work results clarified the biological function of menin in β cells, and highlighted the potential implication of MafA factor in insulinoma tumorigenesis
10

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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Book chapters on the topic "Suppressor cells Identification":

1

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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Abstract:
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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Conference papers on the topic "Suppressor cells Identification":

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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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Abstract:
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 means with use of a remote identification methods of high radioactive objects. A distribution of activity along high radiated objects was measured by a collimated radiometer installed on the robot Brokk-90, a gamma image of the object was registered by gammavisor. Spectrum of gamma radiation was measured by a gamma locator and semiconductor detector system. For identification of a presence of uranium isotopes in the HLRW a technique, based on the registration of characteristic radiation of U, was developed. For fragmentation of high radiated objects was used a cold cutting technique and dust suppression system was applied for reduction of volume activity of aerosols in air. The management of HLRW was performed by remote controlled robots Brokk-180 and Brokk-330. They executed sorting, cutting and parking of high radiated part of contaminated equipment. The use of these techniques allowed to reduce individual and collective doses of personal performed the decommissioning. The average individual dose of the personnel was 1,9 mSv/year in 2011, and the collective dose is estimated by 0,0605 man×Sv/year. Use of the remote control machines enables reducing the number of working personal (20 men) and doses. X-ray spectrometric methods enable determination of a presence of the U in high radiated objects and special cans and separation of them for further spent fuel inspection. The sorting of radwaste enabled shipping of the LLRW and ILRW to special repositories and keeping of the HLRW for decay in the Kurchatov institute repository.

Reports on the topic "Suppressor cells Identification":

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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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