• The aim of this thesis is to gain deeper insight into the role of TGF-β and its signaling pathway proteins, SMADs, in the pathogenesis of keloids and describe the gene expression profile in different keloid sites in the search for potential target genes for future treatment. (diva-portal.org)
  • Results: While there was a highly significant difference in the protein levels of all three Smads in tumor as compared to normal samples, mRNA levels were significantly different only for Smad4. (bvsalud.org)
  • Protein levels did not correlate significantly with mRNA levels for any of the three Smads. (bvsalud.org)
  • Like the other members of the TGF-β family, AMH transduces its effects through two transmembrane serine/threonine kinase receptors type I and II, and two types of cytoplasmic effectors, specific Smads (R-Smads), and a Smad protein common to all ligands, Smad4 [ 5 ]. (ijbs.com)
  • The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-β level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-β mRNA by immunoblotting and RT-PCR. (biomedcentral.com)
  • Heterozygous, damaging mutations in SMAD6 are the most frequent genetic cause of non-syndromic craniosynostosis identified to date. (wikipedia.org)
  • Amir RE, Van den Veyver IB, Wan M et al (1999) Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2. (springer.com)
  • In the presence of increased Runx2 protein levels, CHIP expression decreases, whereas the expression of other E3 ligases involved in Runx2 degradation, such as Smurf1 or WWP1, remains constant or increases during osteoblast differentiation. (rupress.org)
  • as Smad6 interacts with Runx2 and TNF promotes the expression of Smurf1 expression in osteoblasts. (rupress.org)
  • The protein-protein interactions are mapped onto this pathway. (wikipathways.org)
  • Furthermore, based on genetic interactions with the DPP-binding protein Crossveinless 2 and biochemical interactions with the glypican Dally-like, we propose that LTL acts in the extracellular space where it completes a novel auto-regulatory loop that modulates BMP activity. (biologists.org)
  • The pathway maps illustrate protein interactions and regulation to provide a comprehensive picture of signaling and disease processes. (bio-rad.com)
  • By their targeting of short, linear motif type of interactions, peptide aptamers have joined nucleic acid aptamers for use in signaling studies because of their ease of production, their stability, their high specificity and affinity for individual target proteins, and their use in high-throughput screening protocols. (mdpi.com)
  • Quantitative phosphoproteomic analysis of T cell receptor signaling reveals system-wide modulation of protein-protein interactions. (univ-amu.fr)
  • the RPS2P8 (ribosomal protein S2 pseudogene 8) sequence maps to the minus strand of the RNF11 gene in opposite transcriptional orientation. (atlasgeneticsoncology.org)
  • For visual control of rAAV-mediated BMP (v-BMP) expression we fused the secreted morphogenic polypeptides and the fluorescent reporter protein Venus via the 'ribosomal skip' promoting 2A peptide-bridge. (biomedcentral.com)
  • Recombination rate and linkage disequilibrium with SMAD6 rs12438941 (red diamond) shown for chromosome 15 using SNP Annotation and Proxy Search. (cdc.gov)
  • Members of this gene family;typically encode proteins that contain a paired box domain, an octapeptide, and a paired-type homeodomain. (creativebiomart.net)
  • Like other cAMP-dependent protein kinases, the inactive holoenzyme is probably composed of 2 PRKX catalytic subunits and a dimer of regulatory subunits. (genecards.org)
  • Currently, the therapeutic benefits of MSCs are in part explained by the cells being activated by signals from injured tissues to express an anti-inflammatory protein, tumor-necrosis-factor- α -induced protein 6. (hindawi.com)
  • Many recent studies have suggested that the therapeutic benefits of MSCs are in part explained by the cells being activated by signals from injured tissues to express an anti-inflammatory protein, tumor necrosis factor- (TNF-) α -induced protein (TNAIP)6, or TNF- α -stimulated gene- (TSG-) 6 [ 20 , 28 - 31 ]. (hindawi.com)
  • Together, these events lead to a hypophosphorylated, activated state of the pRB tumor suppressor protein, and thereby to the arrest of the cell cycle in G1. (biomedcentral.com)