Auswahl der wissenschaftlichen Literatur zum Thema „Fusicoccin-A (FC-A)“
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Zeitschriftenartikel zum Thema "Fusicoccin-A (FC-A)"
Bock, FD, A. Fer und G. Marigo. „Effect of Fusicoccin on Sucrose Exchanges Between a Host, Pelargonium zonale, and a Higher Parasitic Plant, Cuscuta reflexa“. Functional Plant Biology 22, Nr. 4 (1995): 553. http://dx.doi.org/10.1071/pp9950553.
Der volle Inhalt der QuelleKenmoku, Hiromichi, Hiroyuki Tada, Megumi Oogushi, Tomoyuki Esumi, Hironobu Takahashi, Masaaki Noji, Takeshi Sassa, Masao Toyota und Yoshinori Asakawa. „Seed Dormancy Breaking Diterpenoids from the Liverwort Plagiochila sciophila and their Differentiation Inducing Activity in Human Promyelocytic Leukemia HL-60 Cells“. Natural Product Communications 9, Nr. 7 (Juli 2014): 1934578X1400900. http://dx.doi.org/10.1177/1934578x1400900708.
Der volle Inhalt der QuelleTognoli, L., und R. Colombo. „Protein phosphorylation in intact cultured sycamore (Acer pseudoplatanus) cells and its response to fusicoccin“. Biochemical Journal 235, Nr. 1 (01.04.1986): 45–48. http://dx.doi.org/10.1042/bj2350045.
Der volle Inhalt der QuelleNelson, J. M., und G. C. Sharples. „Emergence at High Temperature and Seedling Growth Following Pretreatment of Lettuce Seeds with Fusicoccin and Other Growth Regulators“. Journal of the American Society for Horticultural Science 111, Nr. 4 (Juli 1986): 484–87. http://dx.doi.org/10.21273/jashs.111.4.484.
Der volle Inhalt der QuelleMarra, Mauro, Lorenzo Camoni, Sabina Visconti, Anna Fiorillo und Antonio Evidente. „The Surprising Story of Fusicoccin: A Wilt-Inducing Phytotoxin, a Tool in Plant Physiology and a 14-3-3-Targeted Drug“. Biomolecules 11, Nr. 9 (21.09.2021): 1393. http://dx.doi.org/10.3390/biom11091393.
Der volle Inhalt der QuelleMalerba, Massimo, und Raffaella Cerana. „Possible Role of Peroxynitrite in the Responses Induced by Fusicoccin in Plant Cultured Cells“. Plants 10, Nr. 1 (19.01.2021): 182. http://dx.doi.org/10.3390/plants10010182.
Der volle Inhalt der QuelleShe, Xiao-Ping, Jin Li, Ai-Xia Huang und Xi-Zhu Han. „Fusicoccin inhibits dark-induced stomatal closure by reducing nitric oxide in the guard cells of broad bean“. Australian Journal of Botany 58, Nr. 2 (2010): 81. http://dx.doi.org/10.1071/bt09182.
Der volle Inhalt der Quellevan der Meulen, René M., Gerda E. M. Lamers, Martien P. M. Caspers, Jolanda C. Heistek, Albertus H. de Boer, Bert van Duijn und Mei Wang. „Effects of fusicoccin and gibberellic acid on the germination of embryos from dormant barley grains: roles of starch degradation and external pH“. Seed Science Research 10, Nr. 2 (Juni 2000): 171–82. http://dx.doi.org/10.1017/s0960258500000180.
Der volle Inhalt der QuelleBlanchard, Lisa M., und Thomas Björkman. „The Role of Auxin in Enhanced Root Growth of Trichodermacolonized Sweet Corn“. HortScience 31, Nr. 4 (August 1996): 688c—688. http://dx.doi.org/10.21273/hortsci.31.4.688c.
Der volle Inhalt der QuelleSeo, Ye-Eun, Xin Yan, Doil Choi und Hyunggon Mang. „Phytophthora infestans RxLR effector PITG06478 hijacks 14-3-3 to suppress PMA activity leading to necrotrophic cell death“. Molecular Plant-Microbe Interactions®, 22.11.2022. http://dx.doi.org/10.1094/mpmi-06-22-0135-r.
Der volle Inhalt der QuelleDissertationen zum Thema "Fusicoccin-A (FC-A)"
Alleman, Cécile. „Accès synthétique au châssis [5-8-5] de la fusicoccine-A pour la synthèse d’analogues simplifiés en vue d'étudier les interactions protéine-protéine“. Electronic Thesis or Diss., Université de Rennes (2023-....), 2023. http://www.theses.fr/2023URENS090.
Der volle Inhalt der QuelleIn biological media, protein-protein interactions (PPI) are of huge importance, as they allow the regulation of many cellular events. PPI classically involve two partners: an adapter protein and its effector protein(s) regulated either in a positive or a negative manner. Inhibition of PPI has thus been considered as a solid therapeutic approach. On the other hand, stabilization of PPI remains scarcely investigated, but may lead to new promising approaches. This project focuses on the 14-3-3 family adapter protein which interacts with more than 200 protein partners. Among them, p53 protein is subjected to a lot of studies as this tumor suppressor protein regulates multiple biological processes (DNA repair, apoptosis). However, those major functions appear to be silenced in most cancer cases, thus allowing tumor cells proliferation. Some studies have shown that stabilization of the 14-3-3/p53 pair with the help of a molecular glue permitted to restore tumor suppressor activity of p53. Among the examined molecular glues, the fusicoccin-A (FC-A) natural product is shown to lodge in the valley formed by 14-3-3 and increases stabilization of the 14-3-3/p53 interaction. In this context, to enlarge the p53/14-3-3 molecular glue library, this project focuses on the access to simplified FC-A analogs through the synthesis of tricyclic scaffold. [6-8-5] analogs from an aromatic substrate are envisaged, as well as [5-8-5] analogs from a cyclopentane derivative, closer to the target structure. Various strategies have been explored in order to access these analogs
DI, LUCENTE CRISTINA. „The phytotoxin fusicoccin: a regulator of multiple 14-3-3 targets“. Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/202271.
Der volle Inhalt der QuelleThe fungal toxin fusicoccin induces plant wilting by affecting ion transport across the plasma membrane of plant cell. The activity of this toxin is so far unknown in humans. In this work, we show that fusicoccin is able to affect the platelet aggregation process. The toxin associates to platelet intracellular binding sites and induces aggregation in platelet-rich plasma in a dose-dependent manner. We identified the adhesion receptor glycoprotein Ib-IX-V as fusicoccin target. The toxin promotes the binding of the regulatory 14-3-3 proteins to glycoprotein Ibα and hampers that to glycoprotein Ibβ subunit. As a result, platelet adhesion to von Willebrand Factor is stimulated, leading to platelet spreading and integrin αIIbβ3 activation. We anticipate our study to be a starting point for future therapeutic use of fusicoccin in genetic bleeding diseases characterized by qualitative or quantitative abnormalities of the platelet membrane adhesion receptors. Furthermore, we demonstrated that fusicoccin action can be widen also to other 14-3-3 clients, provided that a mode III motif with an appropriate C terminal amino acid is present. Results obtained suggest also the rationale for fusicoccin inability to promote 14-3-3 binding to targets with a mode I consensus sequence. In addition, the availability of a large number of fusicoccin derivatives and analogues made possible a detailed analysis of the relationship between activity and chemical structure. The activity of these fusicoccin-related compounds has been tested either in vivo and in vitro.