Search Results

You are looking at 1 - 10 of 2,591 items :

Clear All

[1] Lemanske RF, Busse WW (2010) Asthma: clinical expression and molecular mechanisms. J Allergy Clin Immunol 125(2 Suppl 2):S95–102 http://dx.doi.org/10.1016/j.jaci.2009.10.047 [2] Kumar A, Ghosh B (2009) Genetics of asthma: a molecular biologist perspective. Clin Mol Allergy 7:7 http://dx.doi.org/10.1186/1476-7961-7-7 [3] Groneberg DA, Witt H, Adcock IM, Hansen G, Springer J (2004) Smads as intracellular mediators of airway inflammation. Exp Lung Res 30(3):223–250 http://dx.doi.org/10.1080/01902140490276320 [4] Hahn SA, Schutte M, Hoque AT, Moskaluk CA, da

Die Sowjetische Militäradministration in Deutschland 1945-1949

Introduction Transforming growth factor-β (TGFβ) signaling pathway distortion often leads to a variety of diseases, especially cancer ( Pickup et al., 2013 ; Kleczko and Heasley, 2018 ; Tauriello et al., 2018 ). The most important signal transducers of TGFβ intracellular signaling are SMADs. A TGFβ ligand binds and brings together the type I and II serine/threonine kinase receptors (TGFβ-R1, TGFβ-R2) at the cell membrane to form a ligand-receptor complex, which allows TGFβ-R2 to phosphorylate TGFβ-R1. Upon activation, TGFβ-R1 subsequently phosphorylates

Oxana Kosenko SMAD-Dokumente Probleme der Archivierung und der Verteilung in den Archiven der UdSSR und der Russischen Föderation 1. Die Archivierung der SMAD-Akten Die archivalische Hinterlassenschaft der SMAD besitzt trotz ihres lücken- haften Charakters ein hohes Informationspotential. Die in den Akten ent- haltenen Angaben erhellen verschiedene Fa cetten der sowjetischen Besat- zungspolitik in Deutschland. Der SMAD-Dokumen ten kom plex, den die Historikerinnen und Historiker heute kennen und benutzen, bildete sich wie je ner Teil, zu dem sie immer noch

[1] Feng X.-H., Derynck R., Specificity and versatility in TGF-b signaling through Smads, Annu. Rev. Cell Dev. Biol., 2005, 21, 659–693 http://dx.doi.org/10.1146/annurev.cellbio.21.022404.142018 [2] Siegel P.M., Massague J., Cytostatic and apoptotic actions of TGF-beta in homeostasis and cancer, Nat. Rev. Cancer, 2003, 3, 807–820 http://dx.doi.org/10.1038/nrc1208 [3] Goumans M.J., Mummery C., Functional analysis of the TGFbeta receptor/Smad pathway through gene ablation in mice, Int. J. Dev. Biol., 2000, 44, 253–265 [4] Witze E.S., Old W.M., Resing K.A., Ahn N

[1] Clarke, D.C. and Liu, X. Decoding the quantitative nature of TGFbeta/Smad signaling. Trends Cell Biol. 18 (2008) 430–442. http://dx.doi.org/10.1016/j.tcb.2008.06.006 [2] Feng, X.H. and Derynck, R. Specificity and versatility in tgf-beta signaling through Smads. Ann. Rev. Cell Dev. Biol. 21 (2005) 659–693. http://dx.doi.org/10.1146/annurev.cellbio.21.022404.142018 [3] Massague, J. TGF-beta in cancer. Cell 134 (2008) 215–230. http://dx.doi.org/10.1016/j

promoter in the later stages of carcinogenesis [ 15 , 16 ]. TGF-β/SMAD signaling pathway is believed to play a major role in EMT. In this pathway, the activated complex SMAD2/SMAD3 binds the mediator SMAD4 and is translocated to the nucleus, where it further binds regulatory elements and induce the transcription of key genes associated with EMT, such as Snail1, ZEB1/2, and Twist. Despite the importance of TGF-β/SMAD pathway in EMT, the roles of TGF-β and SMAD4 in tumor progression remain controversial. Consistent with the role of TGF-β as a tumor suppressor is the

trans-membrane serine/threonine kinase receptors, which leads to the phosphorylation of SMAD2 and3. This in association with SMAD4 subsequently translocates into the nucleus, finally leading to transcriptional activations of downstream targets [ 7 - 8 ]. The tumor suppressor role of TGF-β in many cell types is mediated by downregulation of c-myc oncogene expression in a SMAD-dependent manner, and by upregulation of p15 INK4B and p21 CIP1 . This further leads to cyclin-dependent kinases (CDKs) inhibition [ 9 , 10 ]. Epithelial-to-mesenchymal transition (EMT) is a

to a tetramer of two type I and two type II receptors (Greenwald et al., 2003; Keller et al., 2004; Ehrlich et al., 2012). The kinase of the type II receptor is constitutively active independent of ligand binding and phosphorylates the GS domain of the type I receptor ( Figure 3 ). The receptor complex activates downstream signaling components including Smads, p38 mitogen-activated protein (MAP) kinase and phosphoinositide 3 kinase ( Figure 3 ) (Hassel et al., 2003; Nohe et al., 2004). FKBP12, a binding partner of the immunosuppressant FK506, has been shown to

. ( Robson et al., 2009 ); Li et al., 2013 ; Qi et al., 2017 ; Ma et al., 2019 ). As a member of the innate immune cells, NK cells have the ability to kill target cells naturally and secrete a large number of cytokines, such as interferon (IFN)-γ, IL-2, IL-10, etc., and also are the first immune defense line for the body to eliminate malignant cells ( Seif et al., 2009 ); Vanherberghen et al., 2013 ; Handgretinger et al., 2016 ). Recent studies have reported that activin receptors and their downstream signaling molecules Smads are expressed in human and mouse