Добірка наукової літератури з теми "TGFbeta pathway"
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Статті в журналах з теми "TGFbeta pathway"
Verma, Amit. "Presentation name: TGFbeta pathway targeting." Leukemia Research 108 (September 2021): 106682.8. http://dx.doi.org/10.1016/j.leukres.2021.106682.8.
Повний текст джерелаWeiss, Alexander, and Liliana Attisano. "The TGFbeta Superfamily Signaling Pathway." Wiley Interdisciplinary Reviews: Developmental Biology 2, no. 1 (October 5, 2012): 47–63. http://dx.doi.org/10.1002/wdev.86.
Повний текст джерелаKrishna, S., L. L. Maduzia, and R. W. Padgett. "Specificity of TGFbeta signaling is conferred by distinct type I receptors and their associated SMAD proteins in Caenorhabditis elegans." Development 126, no. 2 (January 15, 1999): 251–60. http://dx.doi.org/10.1242/dev.126.2.251.
Повний текст джерелаTran, Dat Q., Ellen Regalado, and Dianna Milewicz. "Immune Perturbation In Patients With Tgfbeta Pathway Defects." Journal of Allergy and Clinical Immunology 133, no. 2 (February 2014): AB248. http://dx.doi.org/10.1016/j.jaci.2013.12.881.
Повний текст джерелаWang, ZacK Z., Hao Bai, Melanie Arzigian, Yong-Xing Gao, and Wen-Shu Wu. "BMP4 and TGFbeta Differentially Regulate CD34+ Progenitor Development in Human Embryonic Stem Cells through SMAD-Dependent Pathway." Blood 112, no. 11 (November 16, 2008): 889. http://dx.doi.org/10.1182/blood.v112.11.889.889.
Повний текст джерелаFrench, Deborah, Francesca Belleudi, Maria Mauro, Francesca Mazzetta, Salvatore Raffa, Vincenza Fabiano, Antonio Frega, and Maria Torrisi. "Expression of HPV16 E5 down-modulates the TGFbeta signaling pathway." Molecular Cancer 12, no. 1 (2013): 38. http://dx.doi.org/10.1186/1476-4598-12-38.
Повний текст джерелаTran, Dat, Ellen Regalado, and Dianna Milewicz. "Immune perturbation in patients with TGFbeta pathway defects (LYM7P.729)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 193.17. http://dx.doi.org/10.4049/jimmunol.192.supp.193.17.
Повний текст джерелаTervonen, Topi A., Denis Belitškin, Pauliina Munne, Shishir M. Pant, Ilida Suleymanova, Kati Belitškina, Jeroen Pouwels, and Juha Klefström. "Abstract 834: Serine protease hepsin regulates tumor growth via TGFbeta-EGFR signaling axis." Cancer Research 82, no. 12_Supplement (June 15, 2022): 834. http://dx.doi.org/10.1158/1538-7445.am2022-834.
Повний текст джерелаTang, S. J., P. A. Hoodless, Z. Lu, M. L. Breitman, R. R. McInnes, J. L. Wrana, and M. Buchwald. "The Tlx-2 homeobox gene is a downstream target of BMP signalling and is required for mouse mesoderm development." Development 125, no. 10 (May 15, 1998): 1877–87. http://dx.doi.org/10.1242/dev.125.10.1877.
Повний текст джерелаThatcher, J. D., C. Haun, and P. G. Okkema. "The DAF-3 Smad binds DNA and represses gene expression in the Caenorhabditis elegans pharynx." Development 126, no. 1 (January 1, 1999): 97–107. http://dx.doi.org/10.1242/dev.126.1.97.
Повний текст джерелаДисертації з теми "TGFbeta pathway"
Raja, Erna. "Cross-regulation between TGFβ/BMP Signalling and the metabolic LKB1 pathway". Doctoral thesis, Ludwig Institute for Cancer Research, Faculty of Medicine, Uppsala University, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-178181.
Повний текст джерелаGirardi, Francesco. "TGFbeta signalling pathway in muscle regeneration : an important regulator of muscle cell fusion." Electronic Thesis or Diss., Sorbonne université, 2019. http://www.theses.fr/2019SORUS114.
Повний текст джерелаMuscle regeneration relies on a pool of muscle-resident stem cells called satellite cells (MuSCs). MuSCs are quiescent and can activate following muscle injury to give rise to transient amplifying progenitors (myoblasts) that will differentiate and finally fuse together to form new myofibers. During this process, a complex network of signalling pathways is involved, among which, Transforming Growth Factor beta (TGFβ) signalling cascade plays a fundamental role. Previous reports proposed several functions for TGFβ signalling in muscle cells including quiescence, activation and differentiation. However, the impact of TGFβ on myoblast fusion has never been investigated. In this study, we show that TGFβ signalling reduces muscle cell fusion independently of the differentiation step. In contrast, inhibition of TGFβ signalling enhances cell fusion and promotes branching between myotubes. Pharmacological modulation of the pathway in vivo perturbs muscle regeneration after injury. Exogenous addition of TGFβ protein results in a loss of muscle function while inhibition of the TGFβ pathway induces the formation of giant myofibres. Transcriptome analyses and functional assays revealed that TGFβ acts on actin dynamics to reduce cell spreading through modulation of actin-based protrusions. Together our results reveal a signalling pathway that limits mammalian myoblast fusion and add a new level of understanding to the molecular regulation of myogenesis
CITRON, FRANCESCA. "An integrated approach identifies mediators of local recurrence in head and neck squamous cell carcinoma." Doctoral thesis, Università degli Studi di Trieste, 2018. http://hdl.handle.net/11368/2924765.
Повний текст джерелаLauraine, Marc. "Effets d'HLA-B27 sur la voie BMP/TGFbeta dans les lymphocytes T CD4+, dans le contexte de la spondyloarthrite." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL130.
Повний текст джерелаSpondyloarthritis (SpA) is a common chronic inflammatory disease. In human, the association between the HLA-B27 allele of the class-I major histocompatibility complex (MHC-I) and the development of this disease was demonstrated 50 years ago, with 70-90% of SpA patients carrying this allele. However, the exact role of HLA-B27 in the pathophysiology of SpA remains unknown. The model of rat transgenic for HLA-B27 and the human β2-microglobulin (hβ2m) (B27 rat), which develops manifestations similar to the human disease, has shed light on certain aspects of the question. In particular, the involvement of CD4+ T lymphocytes in SpA has been demonstrated. In the B27 rat, regulatory CD4+ T lymphocytes (Treg) exhibit an imbalance of the interleukin-10/interleukin-17 (IL-10/IL-17) ratio, which are anti-inflammatory and pro-inflammatory, respectively. On the other hand, an expansion of the sub-population of pro-inflammatory CD4+ T helper 17 (lymphocytes Th17), which produce IL-17, was observed in both B27 rats and SpA patients. To study the non-canonical effects of HLA-B27, a Drosophila melanogaster model transgenic for HLA-B27 and hβ2m was developed and demonstrated that an interaction between HLA-B27 and type I receptors of the BMP/TGFβ pathway (BMPR1s) altered the formation of the wing transverse veins. In this model, an interaction between HLA-B27 and the Saxophone (Sax) receptor has previously been shown to lead to increased BMP signalling. Our study complemented these results by showing that aberrant signaling via the BMPR1 Baboon (Babo) of the activin/TGFβ pathway also contributed to the abnormal phenotype induced by HLA-B27 expression. In an attempt to extrapolate these results to a mechanism of HLA-B27 pathogenicity in SpA, we first demonstrated that there was a specific interaction between HLA-B27 and activin receptor-like kinase 2 (ALK2), the orthologue of Sax, and also with ALK5, the type 1 receptor for TGFβ orthologue of Babo, in rat B27 lymphocytes. Study of SMAD2/3, the main transducer of the TGFβ signal, in T lymphocytes from B27 and nontransgenic rats revealed a lower basal phosphorylation and a higher amplitude of phosphorylation after stimulation by TGFβ1. Concordantly, we observed that several genes induced by TGFβ signaling and involved in Treg and Th17 differentiation (Foxp3, Rorc, Runx1) had increased expression in naive CD4+ T lymphocytes (Tn) from B27 rats. Taken together, these results indicate a possible early activation of the TGFβ pathway in B27 rat Tn followed by a negative feedback loop. Interestingly, the Tgfb1 gene itself was decreased. Given the importance of autocrine TGFβ1 produced by T lymphocytes in preventing chronic inflammation, these observations open up prospects for a better understanding of the role of HLA-B27 in the development of SpA. In particular, we propose to study in greater depth the response of Tn from B27 rats to TGFβ1 using multi-omics methods (transciptomic, phosphoproteomic, proteomic). Finally, given the essential role of autocrine TGFβ1 in the maintenance of Treg and Th17 profiles, a study of the plasticity of Treg and Th17 in B27 rat would be relevant to a better understanding of the pathophysiology of SpA
Labbe, Etienne. "Transcriptional cooperation by the TGFbeta and Wnt signalling pathways in development and cancer." 2007. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=742435&T=F.
Повний текст джерелаNasim, Md Talat, T. Ogo, H. M. Chowdhury, L. Zhao, C.-n. Chen, C. Rhodes, and R. C. Trembath. "BMPR-II deficiency elicits pro-proliferative and anti-apoptotic responses through the activation of TGFbeta-TAK1-MAPK pathways in PAH." 2012. http://hdl.handle.net/10454/6115.
Повний текст джерелаТези доповідей конференцій з теми "TGFbeta pathway"
Gharibi, Armen, Sa La Kim, Daniel Brambilla, Yvess Adamian, Malachia Hoover, Joy Lin, Megan Agajanian, Laurelin Wolfenden, and Jonathan A. Kelber. "Abstract 4426: The PEAK1/ZEB1/ITGA1 pathway mediates survival, stemness and TGFbeta-induced EMT in pancreatic cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4426.
Повний текст джерелаЗвіти організацій з теми "TGFbeta pathway"
Matusik, Robert J. The Role of the TGFbeta Pathway in Prostate Cancer Progression to an Androgen-Independent Disease. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada406869.
Повний текст джерелаO'Neill, Peter, and Jennifer Anderson. Systems Biology Model of Interactions Between Tissue Growth Factors and DNA Damage Pathways: Low Dose Response and Cross-Talk in TGFbeta and ATM Signaling. Office of Scientific and Technical Information (OSTI), October 2014. http://dx.doi.org/10.2172/1158919.
Повний текст джерела