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Статті в журналах з теми "Tyrosine protein phosphatase non-receptor type 11"
Becker, Helen M., Barbara Schnell, Joba M. Arikkat, Markus Schuppler, Martin J. Loessner, Michael Fried, Gerhard Rogler, and Michael Scharl. "Protein Tyrosine Phosphatase Non-Receptor Type 2 Regulates NLRP3 Inflammasome Activation." Gastroenterology 140, no. 5 (May 2011): S—633. http://dx.doi.org/10.1016/s0016-5085(11)62618-8.
Повний текст джерелаScharl, Michael, Kacper A. Wojtal, Helen M. Becker, Anne Fischbeck, Joba M. Arikkat, Theresa Pesch, Silvia Kellermeier, et al. "Protein Tyrosine Phosphatase Non-Receptor Type 2 is a Regulator of Authophagosome Function." Gastroenterology 140, no. 5 (May 2011): S—172. http://dx.doi.org/10.1016/s0016-5085(11)60696-3.
Повний текст джерелаSahu, Mahadev, Armiya Sultan, and Manas Ranjan Barik. "Molecular docking and high throughput screening of designed potent inhibitor to PTPN11 involved in Peptic Ulcer." South Asian Journal of Experimental Biology 6, no. 4 (December 23, 2016): 124–30. http://dx.doi.org/10.38150/sajeb.6(4).p124-130.
Повний текст джерелаKang, J., P. Posner, and C. Sumners. "Angiotensin II type 2 receptor stimulation of neuronal K+ currents involves an inhibitory GTP binding protein." American Journal of Physiology-Cell Physiology 267, no. 5 (November 1, 1994): C1389—C1397. http://dx.doi.org/10.1152/ajpcell.1994.267.5.c1389.
Повний текст джерелаHEINRICH, Peter C., Iris BEHRMANN, Gerhard MÜLLER-NEWEN, Fred SCHAPER, and Lutz GRAEVE. "Interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway1." Biochemical Journal 334, no. 2 (September 1, 1998): 297–314. http://dx.doi.org/10.1042/bj3340297.
Повний текст джерелаIdrees, Muhammad, Lianguang Xu, Seok-Hwan Song, Myeong-Don Joo, Kyeong-Lim Lee, Tahir Muhammad, Marwa El Sheikh, Tabinda Sidrat, and Il-Keun Kong. "PTPN11 (SHP2) Is Indispensable for Growth Factors and Cytokine Signal Transduction During Bovine Oocyte Maturation and Blastocyst Development." Cells 8, no. 10 (October 18, 2019): 1272. http://dx.doi.org/10.3390/cells8101272.
Повний текст джерелаHonda, H., J. Inazawa, J. Nishida, Y. Yazaki, and H. Hirai. "Molecular cloning, characterization, and chromosomal localization of a novel protein-tyrosine phosphatase, HPTP eta." Blood 84, no. 12 (December 15, 1994): 4186–94. http://dx.doi.org/10.1182/blood.v84.12.4186.bloodjournal84124186.
Повний текст джерелаScharl, Michael, Kacper A. Wojtal, Helen M. Becker, Anne Fischbeck, Joba M. Arikkat, Theresa Pesch, Silvia Kellermeier, et al. "The Crohn's Disease Associated Variant of the Protein Tyrosine Phosphatase Non-Receptor Type 2 Gene Affects Cellular Responses to Invading Listeria Monocytogenes." Gastroenterology 140, no. 5 (May 2011): S—496. http://dx.doi.org/10.1016/s0016-5085(11)62052-0.
Повний текст джерелаG, Bhusnure Omprakash. "In-silico exploration of piperine for invent proton pump and protein phosphatase non-receptor Inhibitors in gastric and peptic ulcer." Journal of medical pharmaceutical and allied sciences 11, no. 6 (December 31, 2022): 5334–38. http://dx.doi.org/10.55522/jmpas.v11i6.1865.
Повний текст джерелаScharl, Michael, Kacper A. Wojtal, Anne Fischbeck, Joba M. Arikkat, Theresa Pesch, Silvia Kellermeier, Stephan R. Vavricka, Michael Fried, Declan F. McCole, and Gerhard Rogler. "The Crohn's Disease Candidate Gene, Protein Tyrosine Phosphatase Non-Receptor Type 2, Regulates Muramyldipetide-Induced NOD2-Dependent Effects in Human Monocytes and Fibroblasts." Gastroenterology 140, no. 5 (May 2011): S—487. http://dx.doi.org/10.1016/s0016-5085(11)62007-6.
Повний текст джерелаДисертації з теми "Tyrosine protein phosphatase non-receptor type 11"
Fourmentraux, Emmanuelle. "Modulation de l'activité lymphocytaire T CD4⁺ par le récepteur inhibiteur KIR2DL1." Paris 7, 2009. http://www.theses.fr/2009PA077022.
Повний текст джерелаThe functional activity of immune cells is controlled by a balance between activators and inhibitors signals. The Inhibitory killer Ig-like receptors (KIR) expressed on NK cells and memory effectors T-cell recognize the CMH-I molecules and inhibit cellular activation by SHP-1 recruitment. To better understand the fonction of KIR receptors on CD4⁺ T-cells, KIR2DL1 transfectants were obtained from human T-cell line and from primary CD4⁺ T-cells. Following TCR stimulation, IL-2 production is increased in CD4+ T cells transfected by KIR2DL1 independently of its engagement. When KIR2DL1 is engaged by its cognate ligand the TCR activation is inhibited. Co-stimulation of the TCR signaling by KIR2DL1 requires intact ITIM and their phosphorylation. It induces a subséquent SHP-2 recruitment and an increased of PKCθ and ERK phosphorylation. Synapses leading to activation are characterized by an increase in the recruitment of p-Tyr, SHP-2, and p-PKCθ. Interaction of KIR2DL1 with its ligand leads to a strong synaptic KIR2DL1 accumulation and SHP-1/SHP-2 recruitment resulting in the inhibition of TCR-induced IL-2 production. These data reveal that KIR2DL1 may induce two opposite signaling outputs in CD4⁺ T cells, depending on whether the KIR receptor is bound to its ligand. The unexpected results observed on the regulation of CD4⁺ T cells by KIR2DL1 receptors, through the functional duality of ITIM, is fundamental to determine the immune System capacity to develop an adapted answer, i. E. To maintain the balance between tolerance and immunity
Medina-Pérez, Paula Andrea. "Functional characterization of cancer- and RASopathies-associated SHP2 and BRAF mutations." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17420.
Повний текст джерелаDeregulation of the Ras/MAPK signaling is implicated in a variety of human diseases, including cancer and developmental disorders. The RASopathies are characterized by an overlapping phenotype in patients and result from germline mutations in key regulators of the MAPK signaling cascade. Although the incidence of solid tumors is rather low, reports on different leukemia forms have increased. In this work, a group of mutations in the genes PTPN11 and BRAF were selected for expression in cell lines for a comprehensive molecular and phenotypic characterization. Non-tumorigenic human cell lines and the rat 208F fibroblasts were transduced with lentiviral particles with SHP2/BRAF wildtype (wt), Noonan (NS)-, NS- and leukemia- or LS–associated SHP2 mutations (mut) and CFC-associated BRAF mutations to identify their potential roles in neoplastic transformation. Mutations in both genes promoted cell morphology alterations, cell proliferation, density- and anchorage-independent growth in rat fibroblasts. These results suggested that RASopathies-associated mutations in both genes confer a transformation phenotype in vitro similar to the classical oncogenes. To investigate whether mutations in SHP2 contribute to tumor growth in vivo, 208F cells expressing wt/mut SHP2 were injected in nude mice. Both wt/mut SHP2 expressing cells promoted tumor growth. Additionally, RASopathies-associated mutant SHP2 and BRAF proteins constitutively activate the MAPK signaling in a moderate manner compared to oncogenic BRAF. To identify modifications in the protein interaction of mut-SHP2, TAP assays were performed. Mut-SHP2 proteins showed an increased binding strength to GAB1 compared to wt. Finally, a microarray analysis revealed a gene cluster commonly regulated in both RASopathies and the oncogenic BRAF. The findings of this work might be useful for a better understanding of the downstream mechanisms of RASopathies-related signaling and their involvement in cancer progression.
Hallé, Maxime. "From intracellular localization to proteolytic cleavage : functional significance of protein tyrosine phosphatase PEST regulatory mechanisms." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115683.
Повний текст джерелаHaga, Christopher L. "Analysis of the role of FCRL5 and FIGLERs in B cell development, signaling and malignancy." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008d/haga.pdf.
Повний текст джерелаTchankouo, Nguetcheu Stéphane. "Rôle des kinases LAMMER et des phosphatases PTP1B/PTP61F dans la régulation des voies de signalisation médiées par l'insuline." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T067/document.
Повний текст джерелаType 2 diabetes and cancer represent the major public health problems. One important therapeutic target for these pathologies is the protein tyrosin phosphatase PTP1B. The phosphatase is known to negatively regulates the insulin signaling pathway by dephosphorylating the insulin receptor, IR or the insulin receptor substrate, IRS. However,PTP1B functions and its regulation mechanism remain poorly known. Two studies has notably described opposite effects of PTP1B activity following phosphorylation of its Ser50 residue either by CLK1/CLK2, LAMMER kinases or by AKT. Furthermore, AKT, a main insulin signaling pathway component, has been shown to phosphorylate the LAMMER kinaseCLK1 following insulin stimulation. In addition, the role of PTP1B in the regulation of the RAS/MAPK signaling pathway and hence in cancer is a very controversial subject. The first objective of this work was to analyse, the role of Ptp61F (the Drosophila ortholog of human PTP1B) in the Drosophila insulin pathway, the interaction between the phosphatase and the Drosophila LAMMER kinase gene, Doa, the role of Ptp61F in the RAS/MAPK signaling pathway. To achieve these, we took advantage of the genetic powerful of Drosophila to generate a Ptp61F gene mutant which has been characterized and its role in signaling pathways has been studied. This study showed that Ptp61F interacts with IR like PTP1B in mammals. It shows that Ptp61F regulates key components of insulin signaling pathway Pi3K/Akt. It also shows that Ptp61F is able to regulate the Drosophila LAMMER kinase gene, Doa. Finally, we noted that Ptp61F interacts by inhibiting the activity of severalcomponent of the RAS/MAPK signaling pathway of Drosophila (Egfr, Ras, rl (human ERK)) and conclude that Rl coud be a direct substrate of PTP61F. The data showing that Ptp61F interacts with Akt and the Drosophila LAMMER kinase gene, Doa, were the basis for the second study in order to show the role that the mammal LAMMER kinase CLK2 (Cdc-like kinase 2) could play in the insulin signaling pathway at molecular level using the human neuroblastoma cell line SH-SY5Y. From this second study, we show that CLK2 play an important role in insulin signaling. CLK2 is induced by insulin and its expression increases with time. PTP1B interacts in vivo and in vitro with CLK2. Overexpression of CLK2 impairs AKT phosphorylation by a mechanism which could involved PTP1B, since in vitro, CLK2 phosphorylates PTP1B and the latter interacts withAKT in vivo. It is the Ser50 residue of PTP1B being phosphorylated by CLK2 and this phosphorylation event represses PTP1B activity in vitro. AKT cannot phosphorylates PTP1B in vitro, suggesting that the phosphorylation of PTP1B by AKT could be cellular environment dependant
Santaniemi, M. (Merja). "Genetic and epidemiological studies on the role of adiponectin and PTP1B in the metabolic syndrome." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514261855.
Повний текст джерелаTiivistelmä Metabolinen oireyhtymä on kertymä tekijöitä, jotka altistavat tyypin 2 diabetekselle ja sydän- ja verisuonitaudeille. Keskivartalolihavuus ja insuliiniresistenssi, eli insuliinin heikentynyt teho, vaikuttavat olevan keskeisiä metabolisessa oireyhtymässä. Kuitenkaan taustalla olevaa syntymekanismia ei täysin tunneta. Väitöskirjatyön tavoitteena oli tutkia PTP1B- ja adiponektiinigeenin muuntelun sekä plasman adiponektiinitason yhteyttä metaboliseen oireyhtymään, sen osatekijöihin ja seurauksiin. PTP1B on insuliinin toimintaa soluissa estävä molekyyli. Ensimmäisessä tutkimuksessa havaittiin että kolme tutkittua PTP1B-geenin nukleotidimuutosta eivät ole vahvasti yhteydessä tyypin 2 diabetekseen. Eräs nukleotidimuutos saattaisi olla lievästi suojaava tyypin 2 diabetesta vastaan, sillä se oli yleisempi terveillä kuin tyypin 2 diabetesta sairastavilla. PTP1B:n ja leptiinireseptorigeenin eräiden alleelien yhdistelmä oli yhteydessä painoindeksiin. Adiponektiini on rasvakudoksen erittämä hormoni, jolla on suotuisia, insuliinin vaikutusta edesauttavia vaikutuksia elimistössä sekä edullisia vaikutuksia verenkiertoelimistössä. Toisessa työssä havaittiin että Amerikan valkoihoisilla, joilla oli eräs harvinainen adiponektiinigeenin alleeli (Tyr111His), oli heikompi insuliinin teho kuin henkilöillä joilla ei ollut kyseistä muutosta. Tämä alleeli oli yleisempi suomalaisilla tyypin 2 diabetesta sairastavilla kuin terveillä, mikä saattaa tarkoittaa että se liittyy suurentuneeseen riskiin tyypin 2 diabetekselle. Afroamerikkalaisilla taas toiset nukleotidimuutokset olivat yhteydessä lihavuuteen ja plasman rasva-arvoihin. Adiponektiinin pitoisuutta plasmassa mitattiin erilaisissa aineistoissa. Kolmannessa tutkimuksessa havaittiin, että matala pitoisuus oli yhteydessä metabolisen oireyhtymän eri osatekijöihin ja pitoisuus oli sitä matalampi, mitä enemmän osatekijöitä henkilöllä on. Neljännessä tutkimuksessa havaittiin että matala plasman adiponektiinipitoisuus oli yhteydessä suurentuneeseen riskiin saada huonontunut glukoosin sietokyky tai tyypin 2 diabetes tulevaisuudessa. Viidennessä tutkimuksessa adiponektiinitaso määritettiin naisilta jotka olivat ohittaneet vaihdevuodet ja saivat estrogeenikorvaushoitoa. Havaittiin että plasman adiponektiinitaso laski niillä naisilla, jotka saivat korvaushoitoa suun kautta. Tämä saattaisi osittain selittää suun kautta annettavan estrogeenikorvaushoidon epäedullista vaikutusta sydän ja -verisuonitautien riskitekijöihin. Tutkimus vahvistaa edelleen adiponektiinin merkitystä lihavuuteen liittyvissä sairauksissa ja tuo uutta tietoa adiponektiini- ja PTP1B-geenien muuntelun merkityksestä eri väestöissä
Carmona, Sylvie. "Un analogue de synthèse de la squalamine, NV669, comme nouvel inhibiteur de la protéine Tyrosine Phosphatase 1B (PTP1B) : étude de ses effets in vitro et in vivo sur la croissance des tumeurs pancréatiques et hépatiques." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0616.
Повний текст джерелаNV669 is an aminosterol derived from squalamine found to possess strong antiangiogenic and anticancer effects. The aim of this study was to investigate NV669’s beneficial effects on human pancreatic and hepatic cancer models and to understand the cellular and molecular mechanisms involved in tumor growth decrease upon treatment with NV669.Pancreatic (BxPC3, MiaPaCa-2) and hepatic (HepG2, Huh7) cancer cells were treated with NV669, and the effects on proliferation, on cell cycle and death were determined. The results showed that NV669 inhibited the viability of cancer cells, induced cell cycle arrest through the regulation of G2/M phase via a decrease in the expression of cyclin B1 and phosphorylated Cdk1 and the induction of apoptosis via cleaved caspase-8 and PARP-1 and fragmented DNA. Moreover, in vitro NV669 inhibits PTP1B activity and FAK expression. NV669 impacts on the expression of adhesion molecules CDH-1, -2 and -3 in BxPC3 and Huh7 lines that form cell monolayers. This suggests that NV669 by inhibiting PTP1B would induce apoptosis. Subsequently, our in vivo results showed that NV669 inhibited the growth of pancreatic and hepatic tumor xenografts with a significant decrease in proliferation cell and an increase of tumor cell apoptosis. Therefore, NV669 may serve as an alternative anticancer agent, used alone or in association with other medications, for the treatment of pancreatic adenocarcinoma and hepatocellular carcinoma
Legeay, Samuel. "Physiopathologie de l’endothélium : Applications à l’angiogenèse induite par les répulsifs anti-moustiques à base de DEET et à la dysfonction endothéliale dans le cadre du diabète de type 1 The insect repellent N,N-diethyl-m-toluamide (DEET) induces angiogenesis via allosteric modulation of the M3 muscarinic receptor in endothelial cells." Thesis, Angers, 2016. http://www.theses.fr/2016ANGE0068.
Повний текст джерелаThe endothelium is involved in plenty physiological and pathophysiological process as inflammation, angiogenesis, smooth muscle cell proliferation and metabolism and catabolism of mediators like hormones.The aim of this work was to study the endothelium from two ways: angiogenesis and endothelial dysfunction. Firstly, we evidenced a pro-angiogenic effect in vitro andin vivo of DEET, a mosquito repellent. This effect was associated with an increase of NO production, focal adhesion kinase (FAK) phosphorylation and vascularendothelial growth factor (VEGF) expression leading to an increase of tumor growth in a mouse-xenograft model. In addition, we showed that the effect of DEET was due to both inhibition of the endothelial acetyl cholinesterase and allosteric modulation of the muscarinic type 3 receptor(M3). Secondly, we studied the role of the endoplasmic reticulum stress and the protein-tyrosine phosphatase 1B(PTP1B) in the type 1 diabetes (T1D)-induced endothelial dysfunction. Results allowed us to identify PTP1B as a potential target for the treatment of the endothelial dysfunction in the context of T1D. All these data supply a better understanding of the pathophysiology of the endothelium and consequently provide additional information for the management of pathologies involving endothelium
Govind, Nimmisha Harilall. "The role of the protein tyrosine phosphatase non-receptor type 22 gene polymorphism in disease susceptibility and severity in black South Africans with rheumatoid arthritis." Thesis, 2011. http://hdl.handle.net/10539/10841.
Повний текст джерелаЧастини книг з теми "Tyrosine protein phosphatase non-receptor type 11"
Kotani, Takenori, Yoji Murata, Yasuyuki Saito, and Takashi Matozaki. "Tyrosine-Protein Phosphatase Non-receptor Type 11 (PTPN11)." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101832-1.
Повний текст джерелаDonato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Protein Tyrosine Phosphatase, Non-receptor Type 6 (PTPN6)." In Encyclopedia of Signaling Molecules, 1488. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101107.
Повний текст джерела"PTPN (protein tyrosine phosphatase non-receptor type, PTPN22, 1p13)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1599. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_13802.
Повний текст джерелаBin Huraib, Ghaleb, Fahad Al Harthi, Misbahul Arfin, and Abdulrahman Al-Asmari. "The Protein Tyrosine Phosphatase Non-Receptor Type 22 (PTPN22) Gene Polymorphism and Susceptibility to Autoimmune Diseases." In The Recent Topics in Genetic Polymorphisms. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90836.
Повний текст джерелаТези доповідей конференцій з теми "Tyrosine protein phosphatase non-receptor type 11"
Zhang, Peng, and Zhenghe Wang. "Abstract 229: Identification and functional characterization of p130Cas as a substrate of protein tyrosine phosphatase non-receptor type 14." 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.am2012-229.
Повний текст джерела