Gotowa bibliografia na temat „BMP/TGFbeta pathway”
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Artykuły w czasopismach na temat "BMP/TGFbeta pathway"
Tang, S. J., P. A. Hoodless, Z. Lu, M. L. Breitman, R. R. McInnes, J. L. Wrana i M. Buchwald. "The Tlx-2 homeobox gene is a downstream target of BMP signalling and is required for mouse mesoderm development". Development 125, nr 10 (15.05.1998): 1877–87. http://dx.doi.org/10.1242/dev.125.10.1877.
Pełny tekst źródłaWang, ZacK Z., Hao Bai, Melanie Arzigian, Yong-Xing Gao i Wen-Shu Wu. "BMP4 and TGFbeta Differentially Regulate CD34+ Progenitor Development in Human Embryonic Stem Cells through SMAD-Dependent Pathway". Blood 112, nr 11 (16.11.2008): 889. http://dx.doi.org/10.1182/blood.v112.11.889.889.
Pełny tekst źródłaYokouchi, Y., J. Sakiyama, T. Kameda, H. Iba, A. Suzuki, N. Ueno i A. Kuroiwa. "BMP-2/-4 mediate programmed cell death in chicken limb buds". Development 122, nr 12 (1.12.1996): 3725–34. http://dx.doi.org/10.1242/dev.122.12.3725.
Pełny tekst źródłaMintzer, K. A., M. A. Lee, G. Runke, J. Trout, M. Whitman i M. C. Mullins. "Lost-a-fin encodes a type I BMP receptor, Alk8, acting maternally and zygotically in dorsoventral pattern formation". Development 128, nr 6 (15.03.2001): 859–69. http://dx.doi.org/10.1242/dev.128.6.859.
Pełny tekst źródłaKoromila, T., Z. Dailiana, S. Samara, C. Chassanidis, V. Aleporou - Marinou i P. Kollia. "TGFbeta-BMP signaling pathway gene expression in osteoporotic postmenopausal women by DNA microarrays". Bone 48 (maj 2011): S159. http://dx.doi.org/10.1016/j.bone.2011.03.350.
Pełny tekst źródłaPostigo, A. A. "Opposing functions of ZEB proteins in the regulation of the TGFbeta/BMP signaling pathway". EMBO Journal 22, nr 10 (15.05.2003): 2443–52. http://dx.doi.org/10.1093/emboj/cdg225.
Pełny tekst źródłaBaron, Margaret H., Stephen Willey, Kenneth Sahr, Hailan Zhang, Kevin Balbi, Michael A. Dyer i Matthew Adlam. "Induction and Patterning of Pre-Hemato-Vascular Mesoderm by the Mouse Mix Homeodomain Protein." Blood 104, nr 11 (16.11.2004): 565. http://dx.doi.org/10.1182/blood.v104.11.565.565.
Pełny tekst źródłaFaure, S., M. A. Lee, T. Keller, P. ten Dijke i M. Whitman. "Endogenous patterns of TGFbeta superfamily signaling during early Xenopus development". Development 127, nr 13 (1.07.2000): 2917–31. http://dx.doi.org/10.1242/dev.127.13.2917.
Pełny tekst źródłaFrisch, A., i C. V. Wright. "XBMPRII, a novel Xenopus type II receptor mediating BMP signaling in embryonic tissues". Development 125, nr 3 (1.02.1998): 431–42. http://dx.doi.org/10.1242/dev.125.3.431.
Pełny tekst źródłaWharton, Natalia, Alyson Parris, Amy Reynolds, Esther M. Mitchell, Anastasia Sobolewski, Ahmed El Hadi, Michael P. Lewis i in. "Su1734 Canonical Wnt Signals Combined With Suppressed TGFbeta/BMP Pathways Promote Renewal of the Native Human Colonic Epithelium". Gastroenterology 144, nr 5 (maj 2013): S—463. http://dx.doi.org/10.1016/s0016-5085(13)61712-6.
Pełny tekst źródłaRozprawy doktorskie na temat "BMP/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.
Pełny tekst źródłaLauraine, 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.
Pełny tekst źródłaSpondyloarthritis (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
Nasim, Md Talat, T. Ogo, H. M. Chowdhury, L. Zhao, C.-n. Chen, C. Rhodes i 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.
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