Готові списки джерел за темами / DGKκ

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Добірка наукової літератури з теми "DGKκ"

Автор: Grafiati

Опубліковано: 2 листопада 2024

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Статті в журналах з теми "DGKκ"

Gravina, Teresa, Chiara Maria Teresa Boggio, Elisa Gorla, Luisa Racca, Silvia Polidoro, Sara Centonze, Daniela Ferrante, et al. "Role of Diacylglycerol Kinases in Acute Myeloid Leukemia." Biomedicines 11, no. 7 (July 1, 2023): 1877. http://dx.doi.org/10.3390/biomedicines11071877.

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Diacylglycerol kinases (DGKs) play dual roles in cell transformation and immunosurveillance. According to cancer expression databases, acute myeloid leukemia (AML) exhibits significant overexpression of multiple DGK isoforms, including DGKA, DGKD and DGKG, without a precise correlation with specific AML subtypes. In the TGCA database, high DGKA expression negatively correlates with survival, while high DGKG expression is associated with a more favorable prognosis. DGKA and DGKG also feature different patterns of co-expressed genes. Conversely, the BeatAML and TARGET databases show that high DGKH expression is correlated with shorter survival. To assess the suitability of DGKs as therapeutic targets, we treated HL-60 and HEL cells with DGK inhibitors and compared cell growth and survival with those of untransformed lymphocytes. We observed a specific sensitivity to R59022 and R59949, two poorly selective inhibitors, which promoted cytotoxicity and cell accumulation in the S phase in both cell lines. Conversely, the DGKA-specific inhibitors CU-3 and AMB639752 showed poor efficacy. These findings underscore the pivotal and isoform-specific involvement of DGKs in AML, offering a promising pathway for the identification of potential therapeutic targets. Notably, the DGKA and DGKH isoforms emerge as relevant players in AML pathogenesis, albeit DGKA inhibition alone seems insufficient to impair AML cell viability.

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Tabet, Ricardos, Enora Moutin, Jérôme A. J. Becker, Dimitri Heintz, Laetitia Fouillen, Eric Flatter, Wojciech Krężel, et al. "Fragile X Mental Retardation Protein (FMRP) controls diacylglycerol kinase activity in neurons." Proceedings of the National Academy of Sciences 113, no. 26 (May 27, 2016): E3619—E3628. http://dx.doi.org/10.1073/pnas.1522631113.

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Fragile X syndrome (FXS) is caused by the absence of the Fragile X Mental Retardation Protein (FMRP) in neurons. In the mouse, the lack of FMRP is associated with an excessive translation of hundreds of neuronal proteins, notably including postsynaptic proteins. This local protein synthesis deregulation is proposed to underlie the observed defects of glutamatergic synapse maturation and function and to affect preferentially the hundreds of mRNA species that were reported to bind to FMRP. How FMRP impacts synaptic protein translation and which mRNAs are most important for the pathology remain unclear. Here we show by cross-linking immunoprecipitation in cortical neurons that FMRP is mostly associated with one unique mRNA: diacylglycerol kinase kappa (Dgkκ), a master regulator that controls the switch between diacylglycerol and phosphatidic acid signaling pathways. The absence of FMRP in neurons abolishes group 1 metabotropic glutamate receptor-dependent DGK activity combined with a loss of Dgkκ expression. The reduction of Dgkκ in neurons is sufficient to cause dendritic spine abnormalities, synaptic plasticity alterations, and behavior disorders similar to those observed in the FXS mouse model. Overexpression of Dgkκ in neurons is able to rescue the dendritic spine defects of the Fragile X Mental Retardation 1 gene KO neurons. Together, these data suggest that Dgkκ deregulation contributes to FXS pathology and support a model where FMRP, by controlling the translation of Dgkκ, indirectly controls synaptic proteins translation and membrane properties by impacting lipid signaling in dendritic spine.

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YAMADA, Keiko, Fumio SAKANE, Norio MATSUSHIMA та Hideo KANOH. "EF-hand motifs of α, β and γ isoforms of diacylglycerol kinase bind calcium with different affinities and conformational changes". Biochemical Journal 321, № 1 (1 січня 1997): 59–64. http://dx.doi.org/10.1042/bj3210059.

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The three diacylglycerol kinase isoenzymes (DGKα, DGKβ and DGKγ) cloned so far contain in common a tandem repeat of EF-hand motifs. However, the Ca2+ dependences of the DGK activities are known to be variable between isoenzymes, and the Ca2+-binding activities of these motifs have not been tested except for those present in DGKα. We therefore attempted to define the intrinsic properties of EF-hands occurring in the DGK isoenzymes. For this purpose we bacterially expressed and purified the EF-hand motifs (termed DKE forms) of the three DGKs. Equilibrium dialysis with the purified DKE forms showed that all of the expressed proteins could bind approx. 2 mol of Ca2+ per mol. However, the apparent dissociation constant (Kd) for calcium binding to α-DKE (9.9 µM) was an order of magnitude greater than those estimated for β-DKE (0.89 µM) and γ-DKE (0.40 µM). Experiments with 2-p-toluidinylnaphthalene 6-sulphonate, a probe for hydrophobic regions of proteins, showed that the binding of Ca2+ to β-DKE resulted in the exposure of hydrophobic amino acids, whereas hydrophobic regions of α-DKE and γ-DKE were masked by the addition of Ca2+. Taken together, these results indicate that DGKα, DGKβ and DGKγ possess EF-hand structures with intrinsic properties different from each other with respect to affinities for Ca2+ and Ca2+-induced conformational changes.

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Baldanzi, Gianluca, та Mario Malerba. "DGKα in Neutrophil Biology and Its Implications for Respiratory Diseases". International Journal of Molecular Sciences 20, № 22 (13 листопада 2019): 5673. http://dx.doi.org/10.3390/ijms20225673.

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Diacylglycerol kinases (DGKs) play a key role in phosphoinositide signaling by removing diacylglycerol and generating phosphatidic acid. Besides the well-documented role of DGKα and DGKζ as negative regulators of lymphocyte responses, a robust body of literature points to those enzymes, and specifically DGKα, as crucial regulators of leukocyte function. Upon neutrophil stimulation, DGKα activation is necessary for migration and a productive response. The role of DGKα in neutrophils is evidenced by its aberrant behavior in juvenile periodontitis patients, which express an inactive DGKα transcript. Together with in vitro experiments, this suggests that DGKs may represent potential therapeutic targets for disorders where inflammation, and neutrophils in particular, plays a major role. In this paper we focus on obstructive respiratory diseases, including asthma and chronic obstructive pulmonary disease (COPD), but also rare genetic diseases such as alpha-1-antitrypsin deficiency. Indeed, the biological role of DGKα is understudied outside the T lymphocyte field. The recent wave of research aiming to develop novel and specific inhibitors as well as KO mice will allow a better understanding of DGK’s role in neutrophilic inflammation. Better knowledge and pharmacologic tools may also allow DGK to move from the laboratory bench to clinical trials.

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Gharbi, Severine I., Esther Rincón, Antonia Avila-Flores, Pedro Torres-Ayuso, María Almena, María Angeles Cobos, Juan Pablo Albar та Isabel Mérida. "Diacylglycerol kinase ζ controls diacylglycerol metabolism at the immunological synapse". Molecular Biology of the Cell 22, № 22 (15 листопада 2011): 4406–14. http://dx.doi.org/10.1091/mbc.e11-03-0247.

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Diacylglycerol (DAG) generation at the T cell immunological synapse (IS) determines the correct activation of antigen-specific immune responses. DAG kinases (DGKs) α and ζ act as negative regulators of DAG-mediated signals by catalyzing DAG conversion to phosphatidic acid (PA). Nonetheless, the specific input of each enzyme and their spatial regulation during IS formation remain uncharacterized. Here we report recruitment of endogenous DGKα and DGKζ to the T cell receptor (TCR) complex following TCR/CD28 engagement. Specific DGK gene silencing shows that PA production at the activated complex depends mainly on DGKζ, indicating functional differences between these proteins. DGKζ kinase activity at the TCR is enhanced by phorbol-12-myristate-13-acetate cotreatment, suggesting DAG-mediated regulation of DGKζ responsiveness. We used GFP-DGKζ and -DGKα chimeras to assess translocation dynamics during IS formation. Only GFP-DGKζ translocated rapidly to the plasma membrane at early stages of IS formation, independent of enzyme activity. Finally, use of a fluorescent DAG sensor confirmed rapid, sustained DAG accumulation at the IS and allowed us to directly correlate membrane translocation of active DGKζ with DAG consumption at the IS. This study highlights a DGKζ-specific function for local DAG metabolism at the IS and offers new clues to its mode of regulation.

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Katagiri, Yuji, Tsukasa Ito, Sachiko Saino-Saito, Yasukazu Hozumi, Akira Suwabe, Kazuhisa Otake, Makoto Sata, et al. "Expression and localization of diacylglycerol kinase isozymes and enzymatic features in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 6 (June 2005): L1171—L1178. http://dx.doi.org/10.1152/ajplung.00237.2004.

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Diacylglycerol kinase (DGK) catalyzes phosphorylation of diacylglycerol to generate phosphatidic acid, and both molecules are known to serve as second messengers as well as important intermediates for the synthesis of various lipids. In this study, we investigated the spatiotemporal expression patterns of DGK isozymes together with the developmental changes of the mRNA expression and enzymatic property in rat lung. Northern blot and RT-PCR analyses showed that mRNAs for DGKα, -ε, and -ζ were detected in the lung. By immunohistochemical examination, DGKα and -ζ were shown to be coexpressed in alveolar type II cells and macrophages. Interestingly, these isozymes were localized at distinct subcellular locations, i.e., DGKα in the cytoplasm and DGKζ in the nucleus, suggesting different roles for these isozymes. In the developing lung, the expression for DGKα and -ζ was transiently elevated on embryonic day 21 (E21) to levels approximately two- to threefold higher than on postnatal day 0 (P0). On the other hand, the expression for DGKε was inversely elevated approximately twofold on P0 compared with that on E21. These unique changes in the expression pattern during the perinatal period suggest that each isozyme may play a distinct role in the adaptation of the lung to air or oxygen breathing at birth.

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Topham, Matthew K., та Stephen M. Prescott. "Diacylglycerol Kinase ζ Regulates Ras Activation by a Novel Mechanism". Journal of Cell Biology 152, № 6 (12 березня 2001): 1135–44. http://dx.doi.org/10.1083/jcb.152.6.1135.

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Guanine nucleotide exchange factors (GEFs) activate Ras by facilitating its GTP binding. Ras guanyl nucleotide-releasing protein (GRP) was recently identified as a Ras GEF that has a diacylglycerol (DAG)-binding C1 domain. Its exchange factor activity is regulated by local availability of signaling DAG. DAG kinases (DGKs) metabolize DAG by converting it to phosphatidic acid. Because they can attenuate local accumulation of signaling DAG, DGKs may regulate RasGRP activity and, consequently, activation of Ras. DGKζ, but not other DGKs, completely eliminated Ras activation induced by RasGRP, and DGK activity was required for this mechanism. DGKζ also coimmunoprecipitated and colocalized with RasGRP, indicating that these proteins associate in a signaling complex. Coimmunoprecipitation of DGKζ and RasGRP was enhanced in the presence of phorbol esters, which are DAG analogues that cannot be metabolized by DGKs, suggesting that DAG signaling can induce their interaction. Finally, overexpression of kinase-dead DGKζ in Jurkat cells prolonged Ras activation after ligation of the T cell receptor. Thus, we have identified a novel way to regulate Ras activation: through DGKζ, which controls local accumulation of DAG that would otherwise activate RasGRP.

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ROCHE, Marc A. de la, Janet L. SMITH, Maribel RICO, Silvia CARRASCO, Isabel MERIDA, Lucila LICATE, Graham P. CÔTÉ та Thomas T. EGELHOFF. "Dictyostelium discoideum has a single diacylglycerol kinase gene with similarity to mammalian θ isoforms". Biochemical Journal 368, № 3 (15 грудня 2002): 809–15. http://dx.doi.org/10.1042/bj20021027.

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Diacylglycerol kinases (DGKs) phosphorylate the neutral lipid diacylglycerol (DG) to produce phosphatidic acid (PA). In mammalian systems DGKs are a complex family of at least nine isoforms that are thought to participate in down-regulation of DG-based signalling pathways and perhaps activation of PA-stimulated signalling events. We report here that the simple protozoan amoeba Dictyostelium discoideum appears to contain a single gene encoding a DGK enzyme. This gene, dgkA, encodes a deduced protein that contains three C1-type cysteine-rich repeats, a DGK catalytic domain most closely related to the θ subtype of mammalian DGKs and a C-terminal segment containing a proline/glutamine-rich region and a large aspargine-repeat region. This gene corresponds to a previously reported myosin II heavy chain kinase designated myosin heavy chain-protein kinase C (MHC-PKC), but our analysis clearly demonstrates that this protein does not, as suggested by earlier data, contain a protein kinase catalytic domain. A FLAG-tagged version of DgkA expressed in Dictyostelium displayed robust DGK activity. Earlier studies indicating that disruption of this locus alters myosin II assembly levels in Dictyostelium raise the intriguing possibility that DG and/or PA metabolism may play a role in controlling myosin II assembly in this system.

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DU, Xiangnan, Ying JIANG, Weijun QIAN, Xiaolan LU та James P. WALSH. "Fatty acids inhibit growth-factor-induced diacylglycerol kinase α activation in vascular smooth-muscle cells". Biochemical Journal 357, № 1 (25 червня 2001): 275–82. http://dx.doi.org/10.1042/bj3570275.

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We have previously shown that unsaturated fatty acids amplify platelet-derived-growth-factor (PDGF)-induced protein kinase C (PKC) activation in vascular smooth-muscle cells (VSMCs). Diacylglycerol-induced PKC activation is normally terminated by diacylglycerol kinases (DGKs). We thus hypothesized that fatty acids act by inhibiting a DGK. Fractionation of VSMC extracts demonstrated that the DGK α isoform was the major DGK activity present. PDGF markedly increased the DGK activity of cultured cells. An inhibitor selective for the DGK α isoform,R59949[3-{2-[4-(bis-(4-fluorophenyl)methylene]piperidin-1-yl)ethyl}-2,3-dihydro-2-thioxo-4(1H)-quinazolinone], abolished the growth-factor-induced increase in DGK activity, but had little effect on basal activity. PDGF thus selectively activates DGKα. Epidermal growth factor and α-thrombin stimulated total DGK activity similarly to PDGF. Activation by epidermal growth factor was sensitive to R59949, again suggesting involvement of DGKα. However, the α-thrombin-induced activity was unaffected by this agent. Unsaturated fatty acids inhibited growth-factor-induced DGKα activation, but had no effect on basal activity. Fatty acids also amplified the PDGF-induced increase in cell diacylglycerol content. These results indicate that inhibition of DGKα contributes to fatty-acid-induced amplification of PKC activation. Increased levels of fatty acids in diabetes may thus contribute to chronic PKC activation associated with this disorder.

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Dougan, Stephanie K. "Abstract SY12-04: Lowering the TCR signaling threshold with a DGKa/z dual inhibitor potentiates anti-tumor immunity." Cancer Research 83, no. 7_Supplement (April 4, 2023): SY12–04—SY12–04. http://dx.doi.org/10.1158/1538-7445.am2023-sy12-04.

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Abstract Checkpoint blockade immunotherapies expand neoantigen- or virus-specific T cells, and poor responsiveness to immunotherapy is associated with lower mutational burden in tumors of non-viral origin. Although mouse models demonstrate that lower affinity T cells recognizing self-antigens can contribute to tumor control if sufficiently activated, therapeutic options for enhancing T cell priming are limited. Diacylglycerol kinases (DGKs) suppress DAG signaling by converting DAG to phosphatidic acid, thereby attenuating pathways downstream of TCR signaling. Using a novel dual DGKa/z inhibitor (DGKi), tumor-specific CD8 T cells with different affinities (TRP1high and TRP1low), and a series of altered peptide ligands, we demonstrate that inhibition of DGKa/z can lower the signaling threshold for T cell priming. TRP1high and TRP1low CD8 T cells produced more IL-2 and IFNγ in the presence of cognate antigen and DGKi. Effector TRP1high- and TRP1low-mediated cytolysis of tumor cells with low antigen load was MHC-restricted, mediated by IFNg and augmented by DGKi. Adoptive T cell transfer into mice bearing pancreatic or melanoma tumors synergized with single-agent DGKi or DGKi and αPD1, with increased expansion of low affinity T cells and increased cytokine production observed in tumor infiltrates of treated mice. Collectively, our findings highlight DGKa/z as therapeutic targets for augmenting tumor-specific CD8 T cell function. Citation Format: Stephanie K. Dougan. Lowering the TCR signaling threshold with a DGKa/z dual inhibitor potentiates anti-tumor immunity. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr SY12-04.

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Дисертації з теми "DGKκ"

Çakil, Oktay. "Regulation of the diacylglycerol kinase kappa (DGKk) by FMRP and its dysregulation in Fragile X Syndrome." Electronic Thesis or Diss., Strasbourg, 2024. http://www.theses.fr/2024STRAJ031.

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Le syndrome de l'X fragile (FXS) est la principale cause familiale de déficience intellectuelle et d'autisme. Le FXS résulte de la perte d’expression de la protéine de liaison aux ARN, FMRP. L’équipe a précédemment découvert que l'ARNm de la diacylglycérol kinase kappa (DGKκ) est une cible principale de FMRP. DGKκ est une enzyme régulatrice de la signalisation lipidique dont la perte d’expression dans le FXS pourrait expliquer les phénotypes observés. Nous avons démontré que la réexpression de DGKκ dans le cerveau de souris Fmr1-KO à l'aide d’un vecteur viral adéno-associé corrige à long terme les principaux phénotypes du FXS. Par ailleurs, nous avons identifié le site de liaison de FMRP sur l'ARNm de DGKκ et déterminé la contribution des modifications m6A dans la liaison de FMRP et le contrôle traductionnel de DGKκ. De plus, nous avons mis en évidence les fonctions neurologiques de DGKκ grâce à la caractérisation du modèle murin Dgkk-KO qui reproduit des phénotypes de type FXS. Ainsi, cette étude démontre le rôle crucial de DGKκ dans le cerveau et sa contribution dans FXS, et permet de proposer un nouveau modèle par lequel FMRP contrôle l'expression d’une cible d'ARNm
Fragile X syndrome (FXS) is the main cause of inherited intellectual disability and autism. FXS results from the lack of FMRP that leads to aberrant neuronal protein synthesis associated with neurological alterations. The team found that diacylglycerol kinase kappa (DGKκ) is a primary mRNA target of FMRP in cortical neurons. DGKκ is an enzyme regulating lipid signaling whose downregulation upon loss of FMRP could account for several main alterations observed in FXS. We demonstrated that the reexpression of DGKκ into the brains of Fmr1-KO mice using adeno-associated viral vectors provides long-term correction of the core FXS phenotypes. We identified the binding site of FMRP on DGKκ mRNA and underscored the contribution of m6A RNA modifications in FMRP binding to DGKκ mRNA and its translational control. Additionally, we evidenced the contribution of DGKκ to neurological functions by the characterization of the Dgkk-KO mouse model that recapitulates hallmarks of FXS phenotypes. Overall, this study demonstrates the pivotal role of DGKκ in brain functions and its contributions to FXS, and proposes a novel model by which FMRP controls the expression of an mRNA target

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Yellenki, Vaibhav. "Role of Diacylglycerol kinase alpha (DGKA) as a therapeutic target in Glioblastoma (GB)." Doctoral thesis, Università del Piemonte Orientale, 2020. http://hdl.handle.net/11579/115034.

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Glioblastoma (GB) is the most common high-grade fatal brain tumor. The standard of care treatment is surgery, followed by radiotherapy and chemotherapy. Despite decades of research, the median life expectancy of patients is still between 12 to 15 months. The activation of multiple receptor tyrosine kinases (RTKs) and/or downstream tumour-intrinsic mutations provide oncogenic stimuli to GB progression and accounts for resistance to current therapies. Identifying a target that is capable of simultaneously disabling of multiple, parallel oncogenic signals can represent an effective therapy. Mounting reports indicate DGKα relevance as a therapeutic target across multiple cancers, given its role in different aspects of tumour biology. DGKα phosphorylates diacylglycerol (DG) resulting in the production of phosphatidic acid (PA). Both DG and PA are membrane bound secondary messengers that regulate signalling molecules involved in cancer. DGKs act simultaneously as both terminators and activators of DG- and PA-mediated signalling. In order to exploit DGKα as a therapeutic target we investigated the role of DGKα in GB biology and signalling. Our results show that DGKα is required for GB stem-like cell long term viability and stemness maintenance and sensitize tumor cells to temozolomide. Inhibition of DGKα strongly impairs NF-κB transcriptional activity and analysis of the TNFR signalling showed that DGKα is necessary for FAK and AKT activation downstream TNFa stimulation. Taken together, the results of this study strongly suggest that DGKα plays a key role in stemness maintenance contributing FAK, Akt and NF-kB activation upon TNF stimulation and for this reason DGKa might represent a targetable oncogene that links inﬂammation and tumor growth and progression.

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Velnati, Suresh. "Development of novel DGKα inhibitors for the treatment of XLP1 and metastatic tumours". Doctoral thesis, Università del Piemonte Orientale, 2020. http://hdl.handle.net/11579/115022.

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Heil, Alexandra [Verfasser], and Andreas [Gutachter] Reif. "Assoziation einer DGKH-Risikogenvariante mit phänotypischen Merkmalen bei bipolar-affektiv erkrankten Patienten / Alexandra Heil ; Gutachter: Andreas Reif." Würzburg : Universität Würzburg, 2016. http://d-nb.info/1117477266/34.

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Fagundes, Gabriela Xavier. "Imunolocalização de células positivas para a enzima diacilglicerol quinase α (DGKα) em polpas de ratos expostas à contaminação". Pontifícia Universidade Católica do Rio Grande do Sul, 2014. http://hdl.handle.net/10923/6678.

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Made available in DSpace on 2014-07-08T02:01:24Z (GMT). No. of bitstreams: 1 000459063-Texto+Completo-0.pdf: 1347092 bytes, checksum: 2e34761fdd59a6506f5f964b304ec24c (MD5) Previous issue date: 2014
Introduction: Dental pulp is composed of loose connective tissue, which reacts when facing a pathogenic agent, and the inflammation is the first response. DGKα is one of the key enzymes involved on inflammations cellular events. It participates on the neutrophils recruiting to the injury site and on the regulation of superoxide production. The aim of this study was to evaluate the localization of the DGKα in healthy and inflamed/infected dental pulp of rats.Methods: Were used eighteen (18) male Wistar rats. The animals were divided into three groups of six rats each. In Group 1 (control group), no cavity opening was performed. In Groups 2 and 3 dental pulp of the left first molars was exposed to oral environment for 24hours and 7 days respectively. Euthanasia was performed after the experimental periods and the jaws were dissected for histological evaluation and immunodetection of DGKα enzyme.Results: Histological analysis of the dental pulp showed that tissue exposure led to inflammatory and degenerative events, which varied in their extension according to the experimental period of time. In groups 2 and 3, DGKα immunolabeling was observed in neutrophils and abscessed areas, being detected on a greater amplitude of pulp tissue in the 24 hour period.Conclusions: DGKα is expressed on the initial stages of pulp inflammation, although there is no relation with its extent. The understanding of the DGKα role in the pathways of pulp inflammation can help the development of new therapeutic strategies to promote pulp repair.
Introdução: A polpa dentária é formada por um tecido conjuntivo frouxo, que reage frente a um agente agressor patogênico, sendo a inflamação uma de suas manifestações iniciais. A DGKα é uma das enzimas-chave envolvida em eventos celulares da inflamação. A mesma participa do recrutamento de neutrófilos para o local da injúria e da regulação da produção de superóxido. O objetivo deste estudo foi avaliar, em ratos, a localização da DGKα em polpas saudáveis e em polpas inflamadas/infectadas.Metodologia: Foram utilizados dezoito (18) ratos machos Wistar. Os animais foram divididos em três grupos de seis animais cada. No grupo 1 (grupo controle), não foi realizado nenhum procedimento. Nos grupos 2 e 3, a polpa dentária dos primeiros molares do lado esquerdo foi exposta ao meio bucal por 24horas e por 7 dias, respectivamente. A eutanásia foi realizada após os períodos experimentais, e as mandíbulas foram dissecadas para análise histológica e imunolocalização da enzima DGKα.Resultados: A avaliação histológica da polpa dentária mostrou que a exposição tecidual levou a eventos inflamatórios e degenerativos, que variaram de acordo com o período de tempo. Nos grupos 2 e 3, houve marcação da DGKα em neutrófilos e áreas próximas a abscessos, sendo detectada em uma maior amplitude no período de 24 horas.Conclusões: A DGKα é expressa em estágios iniciais da inflamação, não sendo relacionada com a extensão da inflamação pulpar. O entendimento do papel da DGKα na cascata de eventos da inflamação pulpar pode trazer informações para o desenvolvimento de novas estratégias terapêuticas que promovam o reparo pulpar.

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Fagundes, Gabriela Xavier. "Imunolocaliza??o de c?lulas positivas para a enzima diacilglicerol quinase ? (DGK?) em polpas de ratos expostas ? contamina??o." Pontif?cia Universidade Cat?lica do Rio Grande do Sul, 2014. http://tede2.pucrs.br/tede2/handle/tede/1257.

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Анотація:

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Introduction: Dental pulp is composed of loose connective tissue, which reacts when facing a pathogenic agent, and the inflammation is the first response. DGK? is one of the key enzymes involved on inflammations cellular events. It participates on the neutrophils recruiting to the injury site and on the regulation of superoxide production. The aim of this study was to evaluate the localization of the DGK? in healthy and inflamed/infected dental pulp of rats. Methods: Were used eighteen (18) male Wistar rats. The animals were divided into three groups of six rats each. In Group 1 (control group), no cavity opening was performed. In Groups 2 and 3 dental pulp of the left first molars was exposed to oral environment for 24hours and 7 days respectively. Euthanasia was performed after the experimental periods and the jaws were dissected for histological evaluation and immunodetection of DGK? enzyme. Results: Histological analysis of the dental pulp showed that tissue exposure led to inflammatory and degenerative events, which varied in their extension according to the experimental period of time. In groups 2 and 3, DGK? immunolabeling was observed in neutrophils and abscessed areas, being detected on a greater amplitude of pulp tissue in the 24 hour period. Conclusions: DGK? is expressed on the initial stages of pulp inflammation, although there is no relation with its extent. The understanding of the DGK? role in the pathways of pulp inflammation can help the development of new therapeutic strategies to promote pulp repair.
Introdu??o: A polpa dent?ria ? formada por um tecido conjuntivo frouxo, que reage frente a um agente agressor patog?nico, sendo a inflama??o uma de suas manifesta??es iniciais. A DGK? ? uma das enzimas-chave envolvida em eventos celulares da inflama??o. A mesma participa do recrutamento de neutr?filos para o local da inj?ria e da regula??o da produ??o de super?xido. O objetivo deste estudo foi avaliar, em ratos, a localiza??o da DGK? em polpas saud?veis e em polpas inflamadas/infectadas. Metodologia: Foram utilizados dezoito (18) ratos machos Wistar. Os animais foram divididos em tr?s grupos de seis animais cada. No grupo 1 (grupo controle), n?o foi realizado nenhum procedimento. Nos grupos 2 e 3, a polpa dent?ria dos primeiros molares do lado esquerdo foi exposta ao meio bucal por 24horas e por 7 dias, respectivamente. A eutan?sia foi realizada ap?s os per?odos experimentais, e as mand?bulas foram dissecadas para an?lise histol?gica e imunolocaliza??o da enzima DGK?. Resultados: A avalia??o histol?gica da polpa dent?ria mostrou que a exposi??o tecidual levou a eventos inflamat?rios e degenerativos, que variaram de acordo com o per?odo de tempo. Nos grupos 2 e 3, houve marca??o da DGK? em neutr?filos e ?reas pr?ximas a abscessos, sendo detectada em uma maior amplitude no per?odo de 24 horas. Conclus?es: A DGK? ? expressa em est?gios iniciais da inflama??o, n?o sendo relacionada com a extens?o da inflama??o pulpar. O entendimento do papel da DGK? na cascata de eventos da inflama??o pulpar pode trazer informa??es para o desenvolvimento de novas estrat?gias terap?uticas que promovam o reparo pulpar.

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Kang, Kiho Paul. "Commandes robustes d'un actionneur synchrone." Grenoble INPG, 1996. http://www.theses.fr/1996INPG0097.

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Le travail présenté dans cette thèse est consacré à la commande robuste d'un axe synchrone. Cet axe est un système qui risque d'être fortement perturbé par le couple de charge et le bruit sur la sortie. Sur le plan théorique, des lois de commande robuste basées sur l'algorithme DGKF et sur l'approche µ, sont développées. Ces lois de commande permettent de contrôler l'axe indifféremment du comportement des deux perturbations seulement si ces dernières peuvent être définies par leurs bornes. Par ailleurs, pour obtenir le modèle nominal, une approche d'identification itérative en boucle fermée est développée et utilisée pour les commandes. Sur le plan expérimental, l'application des lois de commande développées sur un banc d'essais utilisant un processeur de signal montre la faisabilité et l'efficacité de l'approche. De nombreux problèmes de mise en oeuvre lises à l'implantation discrète des lois, à la prise en compte des saturations du variateur et à l'implantation de l'identification en temps réel sont résolus

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Kovalenko, Andrii. "Therapeutic targeting of DGKA-mediated macropinocytosis in lymphangioleiomyomatosis." Thesis, 2020. https://hdl.handle.net/2144/41149.

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BACKGROUND: Lymphangioleiomyomatosis (LAM) is a rare disease characterized by cystic destruction of the lung. It occurs in 80% of people with Tuberous Sclerosis Complex disorder (TSC), a multisystem, autosomal dominant disorder caused by mutations in tumor suppressor genes TSC1 and TSC2. Spontaneous biallelic mutations in these genes can give rise to sporadic LAM. Mammalian target of rapamycin complex I (mTORC1), a master regulator of cellular anabolic metabolism is hyperactivated in LAM cells. Upregulation of protein synthesis and downregulation of autophagy creates a state of starvation stress that upregulates pathways of extracellular nutrient acquisition. Macropinocytosis, a form of clathrin-independent endocytosis, is upregulated in TSC2-deficient cells. We performed a high-throughput compound screen utilizing a repurposing drug library. We identified that ritanserin, a diacylglycerol kinase alpha (DGKA) inhibitor, synergizes with Chloroquine (CQ) to selectively inhibit proliferation of TSC2-deficient mouse embryonic fibroblasts (MEFs) compared to TSC2+/+ MEFs. OBJECTIVE: We hypothesized that TSC2-deficient cells rely on macropinocytosis to support their growth during the periods of stress and starvation and that ritanserin synergizes with CQ to inhibit proliferation in TSC2-deficient cells by inhibiting macropinocytosis. METHODS: Crystal violet-based proliferation assays were used to monitor the effect of pharmacological and genetic inhibition of DGKA on cell proliferation. Immunoblotting was used to measure the expression levels of TSC2, tS6R, pS6R, Cleaved PARP, Cleaved Caspase 3 and Actin. siRNA induced Htr2a knockdown and shRNA induced DGKA knockdown cell culture models were used to define the dual functions of ritanserin and observe their effects on macropinocytosis and cell proliferation. LC/MS was used to measure cell lipid content and how it changes in response to ritanserin. Fluorophore-labeled BSA and 70-kDa Dextran were used to measure macropinocytosis. Lysotracker was used to measure the number of lysosomes, while DQ-BSA was used to measure lysosomal functionality. RESULTS: TSC2-deficient cells express higher levels and show upregulated activity of DGKA. Genetic and pharmacologic inhibition of DGKA prevents TSC2-deficient cells from acquiring nutrients via macropinocytosis. Phospholipid metabolism is altered in TSC2-deficient cells, marked by the accumulation of phosphatidic acid and ceramides. Treatment with ritanserin leads to the accumulation of diacylglycerol and phospholipids, as well as a reduction in phosphatidic acid. CONCLUSIONS: TSC2-deficient cells rely on macropinocytosis to meet their metabolic needs. Diacylglycerol kinase alpha (DGKA) is required for macropinocytic nutrient uptake. Pharmacologic or genetic inhibition of DGKA creates metabolic stress in TSC2-deficient cells, which ultimately leads to increased apoptotic response to treatment with CQ. This project identifies a novel connection between mTOR signaling, lysosome metabolism and macropinocytosis, and a vulnerability that allows the selective targeting of LAM cells.
2021-06-07T00:00:00Z

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Heil, Alexandra. "Assoziation einer DGKH-Risikogenvariante mit phänotypischen Merkmalen bei bipolar-affektiv erkrankten Patienten." Doctoral thesis, 2015. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-139051.

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Die Tatsache, dass sich DGKH-GAT in einer vorausgehenden Studie als ein krankheitsübergreifender Risiko-Haplotyp für verschiedene Stimmungserkrankungen herausstellte, legte für uns den Schluss nahe, dass dieser Einfluss auf psychiatrische Symptome haben könnte, die typischerweise mit Stimmungsschwankungen einhergehen. In Anlehnung an das Endophänotypenkonzept vermuteten wir, dass wir über die Symptomebene möglicherweise Parameter definieren könnten, die enger mit DGKH-GAT assoziiert sind als die bipolar-affektive Erkrankung selbst. Ziel dieser Doktorarbeit war es daher, den Einfluss von DGKH-GAT auf klinische Symptome in einer bipolaren Stichprobe darzustellen, wobei wir insbesondere eine Assoziation mit der Dimension „Erregung“, in welcher typische manische Symptome zusammengefasst sind, und der Dimension „Depression“, die typische depressive Symptome umfasst, vermuteten. Zur Erfassung der psychiatrischen Symptome verwendeten wir den OPCRIT (McGuffin et al., 1991; Farmer et al., 1992), eine Checkliste von 90 Items, die Psychopathologie und sozio-demographische Hintergrundinformation erfasst. Um die so erhobenen Daten statistisch sinnvoll auswerten zu können, war eine Zusammenfassung der Items in Dimensionen notwendig. In der Vergangenheit waren zahlreiche Faktorenmodelle für den OPCRIT berechnet worden. Wir entschlossen uns, das 9-Faktorenmodell von Maciukiewicz et al. (2012) zu übernehmen. Als Dimensionen wurden somit „Depression“, „atypische Depression“, „Desorganisation“, „soziales Funktionsniveau“, „Erregung“, „Positiv“, „Psychotisch“, „Substanzgebrauch“ und „Negativ“ definiert. In dieser Arbeit wurde nun für 186 bipolare Patienten die klinische Symptomatik über die gesamte Lebenszeit mittels OPCRIT erfasst. Das Sample setzte sich aus 106 GAT-Trägern und 80 Nicht-Trägern zusammen. Eine signifikante Assoziation mit dem Vorhandensein von DGKH-GAT konnte lediglich für die Dimension „Substanzgebrauch“ ermittelt werden. Da jedoch zwischen Frauen und Männern ein signifikanter Unterschied für diese Dimension bestand und die Merkmale Geschlecht und Vorhandensein von DGKH-GAT statistisch voneinander abhängig waren (t (108) = 3,7; p = 0,000), wurden die Geschlechter nochmals getrennt voneinander berechnet. Hierbei stellte sich heraus, dass bei den Frauen keine Assoziation von DGKH-GAT mit einer OPCRIT-Dimension mehr nachgewiesen werden, wohingegen die signifikante Assoziation zwischen DGKH-GAT und „Substanzgebrauch“ bei den männlichen Probanden weiterhin bestand (t (56,4) = -3,56; p = 0.01). DGKH-GAT zeigte entgegen unserer Erwartung keine Assoziation mit den Stimmungsdimensionen „Depression“ und „Erregung“. Diese Arbeit legt also nahe, dass DGKH-GAT keinen Einfluss auf die Ausprägung von Stimmungssymptomen hat. Möglicherweise lässt sich dieses Ergebnis dadurch erklären, dass, wenn man von einem polygenen Vererbungsmuster mit kleinen Effektstärkten eines einzelnen Haplotyps wie DGKH-GAT auf die klinische Ausprägung von psychiatrischen Symptomen ausgeht, unsere Samplegröße von 186 Patienten für den untersuchten genetischen Zusammenhang zu gering war. Damit wären weitere Untersuchungen mit größeren Kollektiven notwendig, um den Einfluss von DGKH-GAT sicher beurteilen zu können. Es erscheint auch denkbar, dass klinische Symptomkomplexe grundsätzlich nicht geeignet sind, um die Auswirkungen einer genetischen Risikovariante zuverlässig abzubilden, da sie zeitlich nicht stabil sind und durch viele Umweltfaktoren beeinflusst werden können. Bisher ist die exakte Rolle, die das von DGKH kodierte Enzym in der Pathophysiologie der bipolar-affektiven Erkrankung spielt, noch nicht vollständig aufgeklärt worden. Da DGKH am lithiumregulierten Signalweg beteiligt ist, könnte man spekulieren, dass es auf einer ähnlichen Ebene wirkt wie Lithium. Das Medikament übt keinen großen Einfluss auf den Phänotyp aus, sondern verhindert das „Kippen“ in eine Krankheitsphase. Möglicherweise wirkt der Risiko-Haplotyp DGKH-GAT entgegengesetzt, indem er die Erkrankung „anstößt“, wohingegen der Verlauf und die Ausprägung der klinischen Symptomatik durch andere Faktoren beeinflusst wird
A previous study suggested that haplotyp DGKH-GAT can be seen as common risk factor for mood disorders (bipolar disorder, unipolar depression and aADHD). Our aim was to show associations between haplotyp DGKH-GAT and mood symptoms as well as other psychiatric symptoms. We could not find any associations between DGKH-GAT and clinical symptoms

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Dias, Sara Melo. "Characterization of a chromosome rearrangement associated with cardiopathy and autism." Master's thesis, 2017. http://hdl.handle.net/10362/27627.

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Chromosomal rearrangements have been associated with multiple congenital abnormalities, including malformative syndromes and global developmental delay. The aim of this study was identification of candidate genes for a complex phenotype characterized by cardiopathy and autism, identified in an individual with a chromosome translocation t(4;7)(q21.1;p21.2). Since classical and molecular cytogenetic analyses have low resolutions, large-insert whole-genome sequencing (liWGS) was applied for identification and mapping of structural chromosomal alterations. By this approach, the 4q21.1 breakpoint was identified between genomic positions chr4:73,918,924-74,049,529 on 4q13.3, whereas the 7p21.2 breakpoint between chr7:13,184,731-14,536,001 [GRCh38/hg38]; suggesting the occurrence of deletions at both breakpoints. Additionally, a 473Kb deletion on 2p16.3 was also identified in the proband. Nucleotide-level resolution of the breakpoints and familial segregation analysis were carried out by amplification of the junction fragments and Sanger sequencing. At the 4q13.3 breakpoint, the 130Kb deletion erases four genes PF4, PPBP, CXCL5 and CXCL3, whereas at 7p21.2, the 1351Kb deletion removes the entire ETV1 and disrupts DGKB and the long non-coding intergenic (Linc) RNA AC011288.2. Furthermore, at this breakpoint region, genomic array analysis identified in the proband’s father a 742Kb deletion comprising DGKB and ETV but not the LincRNA AC011288.2. The maternally inherited 473Kb deletion on 2p16.3 removes the first 5 exons of NRXN1, a gene associated with Pitt-Hopkins like syndrome (OMIM #614325), susceptibility to schizophrenia and chromosome 2p16.3 deletion (OMIM #614332). Similar deletions have been reported with incomplete penetrance and variable expressivity. Several genes from the 7p21.2 breakpoint region and especially those affected by the deletion, DGKB, ETV1 and LincRNA AC011288.2, have been linked with cognitive, speech, language and auditory disorders. In conclusion, coinheritance of the maternally derived deletion on 2p16.3 and the deletion at the breakpoint of the der(7) on 7p21.2 appear to be the most contributively alterations for the proband’s phenotype. At the time, NRXN1, DGKB, ETV1 and LincRNA AC011288.2 are the most likely genes to be responsible for the proband’s phenotype, being those mainly characterised by cardiopathy and autism.

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Книги з теми "DGKκ"

Ontario., Ministry of Culture and Communications., Kenora Field Office. Turtles and tourists: Excavations at the Nestor Falls site (DgK1-3) 1989 and 1990. Thunder Bay: Ministry of Culture and Communication, 1992.

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Germany) Symposium der DGK (14th 2001 Hamburg. Innovative Analytik in der Kosmetik: Proceedings : 14. Symposium der DGK Hamburg, 2001, Deutsche Gesellschaft für Wissenschaftliche und Angewandte Kosmetik e.V. Augsburg: Verlag für chemische Industrie, 2001.

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Schmaltz, Achim A. Erwachsene mit angeborenen Herzfehlern (EMAH): S2-Leitlinie der DGK, DGPK und DGTHG zur Diagnostik und Therapie in Klinik und Praxis ; mit 9 Tabellen. [Heidelberg]: Steinkopff, 2008.

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Schmaltz, Achim A. Erwachsene Mit Angeborenen Herzfehlern: S2-Leitlinie der DGK, DGPK und DGTHG Zur Diagnostik und Therapie in Klinik und Praxis. Steinkopff, Dietrich, 2008.

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Частини книг з теми "DGKκ"

Gressner, A. M., and O. A. Gressner. "Klinische(r) Chemiker(in) (DGKL)." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1699-1.

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Gressner, A. M., and O. A. Gressner. "Klinische(r) Chemiker(in) (DGKL)." In Springer Reference Medizin, 1349. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1699.

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Gressner, A. M., and O. A. Gressner. "Deutsche Gesellschaft für Klinische Chemie e.V. (DGKC)." In Springer Reference Medizin, 683–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_863.

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Gressner, A. M., and O. A. Gressner. "Deutsche Gesellschaft für Klinische Chemie e.V. (DGKC)." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_863-1.

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Gressner, A. M., and O. A. Gressner. "Deutsche Gesellschaft für Klinische Chemie und Laboratoriumsmedizin e.V. (DGKL)." In Springer Reference Medizin, 684–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_867.

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Gressner, A. M., and O. A. Gressner. "Deutsche Gesellschaft für Klinische Chemie und Laboratoriumsmedizin e.V. (DGKL)." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_867-1.

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Shirai, Yasuhito, and Naoaki Saito. "Diacylglycerol Kinase (DGK) as a Regulator of PKC." In Protein Kinase Technologies, 259–71. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5_15.

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Schepker, Klaus, and Heiner Fangerau. "Die Gründungsgeschichte der Deutschen Gesellschaft für Kinderpsychiatrie und Heilpädagogik (DGKH) und ihr Wirken." In Kinder- und Jugendpsychiatrie im Nationalsozialismus und in der Nachkriegszeit, 17–186. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49806-4_2.

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Arisz, Steven A., and Teun Munnik. "Distinguishing Phosphatidic Acid Pools from De Novo Synthesis, PLD, and DGK." In Methods in Molecular Biology, 55–62. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-401-2_6.

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"DGKC." In Springer Reference Medizin, 690. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_311015.

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Тези доповідей конференцій з теми "DGKκ"

Schweickert, Patrick G., Gabrielle L. Reiner, Casey G. Mitchell, Dana Piovesan, Cesar Meleza, Juan Jose Fung, Ning Wang та ін. "1385 Dual Inhibition of DGKα and DGKζ increases T cell and NK cell activity". У SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.1385.

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Wee, Susan, Junchen Gu, Cindy Wang, Carolyn Cao, Sandra Holzhauer, Heshani Desilva, Erin Wesley, Susan Tsai, Douglas Evans та Matthew Riese. "Abstract 936: Regulation of CD8+ T-cell function and antitumor activity by DGKα and DGKζ". У Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-936.

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Veugen, Thijs. "Improving the DGK comparison protocol." In 2012 IEEE International Workshop on Information Forensics and Security (WIFS). IEEE, 2012. http://dx.doi.org/10.1109/wifs.2012.6412624.

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Yadav, S., S. S. Shah, S. Pan, B. Singh, T. Kambayashi, and D. A. Deshpande. "Diacylglycerol Kinase (DGK) Regulation of Airway Smooth Muscle Contraction." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4285.

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Wang, Adele, Lance Stapleton, Jean-Philippe Belzie, Weimei Xing, Gladys Muiru, Dmytro Kornyeyev, Edward Hsieh та ін. "1066 Pharmacologic inhibition of DGKα activates T cells and enhances anti-tumor immunity". У SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1066.

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Li, Jie, Chaoyun Pan, Austin C. Boese, Anna Umano, and Sumin Kang. "Abstract 4084: A DGKA-cJUN-WEE1 signaling axis provides platinum resistance in ovarian cancer." 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.am2020-4084.

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Bahadori, Milad, and Kimmo Jarvinen. "A Programmable SoC Implementation of the DGK Cryptosystem for Privacy-Enhancing Technologies." In 2020 23rd Euromicro Conference on Digital System Design (DSD). IEEE, 2020. http://dx.doi.org/10.1109/dsd51259.2020.00049.

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Offringa, Rienk, Catherine Olesch, Frederik Cichon, Mareike Grees, Norbert Schmees, Ulrike Roehn, Florian Prinz, et al. "926 BAY 2965501: a highly selective DGK zeta inhibitor for cancer immunotherapy." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0926.

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Gonzalez, Rachel M., Tianli Qu, Xiaomin Hu, Qi Ren, Qiankun Zhang, Zhaoying Guo, Young-Hwan Kim, Yiran Wang, Xuan Liu, and Wei Fu. "Abstract 4985: PD-L1 and diacylglycerol kinase alpha (DGKA) expression in melanoma, nsclc and bladder cancers." 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.am2020-4985.

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