Добірка наукової літератури з теми "PTPN11, tyrosine protein phosphatase non-receptor type 11"
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Статті в журналах з теми "PTPN11, tyrosine protein phosphatase non-receptor type 11"
Sahu, 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 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 джерелаNoordam, C., P. G. M. Peer, I. Francois, J. De Schepper, I. van den Burgt, and B. J. Otten. "Long-term GH treatment improves adult height in children with Noonan syndrome with and without mutations in protein tyrosine phosphatase, non-receptor-type 11." European Journal of Endocrinology 159, no. 3 (September 2008): 203–8. http://dx.doi.org/10.1530/eje-08-0413.
Повний текст джерелаFobare, Sydney, Jessica Kohlschmidt, Hatice Gulcin Ozer, Krzysztof Mrózek, Deedra Nicolet, Alice S. Mims, Ramiro Garzon, et al. "Molecular, clinical, and prognostic implications of PTPN11 mutations in acute myeloid leukemia." Blood Advances 6, no. 5 (February 25, 2022): 1371–80. http://dx.doi.org/10.1182/bloodadvances.2021006242.
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 джерелаLi, Kang, Luobu Gesang, Zeng Dan, and Lamu Gusang. "Genome-Wide Transcriptional Analysis Reveals the Protection against Hypoxia-Induced Oxidative Injury in the Intestine of Tibetans via the Inhibition of GRB2/EGFR/PTPN11 Pathways." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/6967396.
Повний текст джерелаBinder, G., K. Neuer, M. B. Ranke, and N. E. Wittekindt. "PTPN11 Mutations Are Associated with Mild Growth Hormone Resistance in Individuals with Noonan Syndrome." Journal of Clinical Endocrinology & Metabolism 90, no. 9 (September 1, 2005): 5377–81. http://dx.doi.org/10.1210/jc.2005-0995.
Повний текст джерелаStevens, Brett M., Courtney L. Jones, Amanda Winters, James Dugan, Diana Abbott, Michael R. Savona, Stephen W. Fesik, Daniel A. Pollyea, and Craig T. Jordan. "PTPN11 Mutations Confer Unique Metabolic Properties and Increase Resistance to Venetoclax and Azacitidine in Acute Myelogenous Leukemia." Blood 132, Supplement 1 (November 29, 2018): 909. http://dx.doi.org/10.1182/blood-2018-99-119806.
Повний текст джерелаShafaee, Maryam Nemati, Kristen Otte, Nicholas J. Neill, Kent C. Osborne, Thomas F. Westbrook, Susan Hilseneck, and Matthew J. Ellis. "Abstract OT2-28-01: A phase 2 study of sitravatinib in metastatic, pre-treated, triple negative breast cancer, NCT # 04123704." Cancer Research 82, no. 4_Supplement (February 15, 2022): OT2–28–01—OT2–28–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-ot2-28-01.
Повний текст джерелаKim, Jin Soo, Ok Ran Shin, Hyung Keun Kim, Young Seok Cho, Chang Hyeok An, Keun Woo Lim, and Sung Soo Kim. "Overexpression of Protein Phosphatase Non-receptor Type 11 (PTPN11) in Gastric Carcinomas." Digestive Diseases and Sciences 55, no. 6 (August 19, 2009): 1565–69. http://dx.doi.org/10.1007/s10620-009-0924-z.
Повний текст джерелаДисертації з теми "PTPN11, 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.
Частини книг з теми "PTPN11, 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 джерела