Academic literature on the topic 'GFOGER'

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Journal articles on the topic "GFOGER"

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Pugh, Nicholas, Anna M. C. Simpson, Peter A. Smethurst, Philip G. de Groot, Nicolas Raynal, and Richard W. Farndale. "Synergism between platelet collagen receptors defined using receptor-specific collagen-mimetic peptide substrata in flowing blood." Blood 115, no. 24 (2010): 5069–79. http://dx.doi.org/10.1182/blood-2010-01-260778.

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AbstractExposed subendothelial collagen acts as a substrate for platelet adhesion and thrombus formation after vascular injury. Synthetic collagen-derived triple-helical peptides, designated collagen-related peptide (CRP), GFOGER, and VWF-III, can specifically engage the platelet collagen receptors, glycoprotein VI and integrin α2β1, and plasma von Willebrand factor (VWF), respectively. Hitherto, the role of these 3 collagen-binding axes has been studied indirectly. Use of these uniform peptide substrates, rather than collagen fibers, provides independent control of each axis. Here, we use con
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Zhang, Wan-Ming, Jarmo Käpylä, J. Santeri Puranen та ін. "α11β1Integrin Recognizes the GFOGER Sequence in Interstitial Collagens". Journal of Biological Chemistry 278, № 9 (2002): 7270–77. http://dx.doi.org/10.1074/jbc.m210313200.

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Elton, Catherine, Peter Smethurst, Paul Eggleton та Rich Farndalerd. "Physical and Functional Interaction Between Cell-Surface Calreticulin and the Collagen Receptors Integrin α2β1 and Glycoprotein VI in Human Platelets". Thrombosis and Haemostasis 88, № 10 (2002): 648–54. http://dx.doi.org/10.1055/s-0037-1613270.

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SummaryCalreticulin is an abundant protein in the endoplasmic reticulum of most cells. In this study, flow cytometry and immunoprecipitation from surface-biotinylated platelets each provided direct evidence that calreticulin is also expressed on the surface of human platelets. Anti-calreticulin antibodies caused platelet activation, inducing Fc RIIa-independent platelet aggregation. In addition, these antibodies inhibited platelet adhesion to the integrin α2β1-specific ligands, GFOGER-GPP and monomeric collagen I, and to the glycoprotein VI-specific ligand, CRP. Inhibition of platelet adhesion
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SLATTER, D. A., and R. W. FARNDALE. "Platelet Adhesion to Glycated GFOGER Peptide and Bovine Serum Albumin." Annals of the New York Academy of Sciences 1043, no. 1 (2005): 930. http://dx.doi.org/10.1196/annals.1333.144.

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Gigout, Anne, Mario Jolicoeur, Monica Nelea, Nicolas Raynal, Richard Farndale та Michael D. Buschmann. "Chondrocyte Aggregation in Suspension Culture Is GFOGER-GPP- and β1 Integrin-dependent". Journal of Biological Chemistry 283, № 46 (2008): 31522–30. http://dx.doi.org/10.1074/jbc.m804234200.

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Wojtowicz, Abigail M., Asha Shekaran, Megan E. Oest, et al. "Coating of biomaterial scaffolds with the collagen-mimetic peptide GFOGER for bone defect repair." Biomaterials 31, no. 9 (2010): 2574–82. http://dx.doi.org/10.1016/j.biomaterials.2009.12.008.

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Mhanna, Rami, Ece Öztürk, Queralt Vallmajo-Martin, Christopher Millan, Michael Müller, and Marcy Zenobi-Wong. "GFOGER-Modified MMP-Sensitive Polyethylene Glycol Hydrogels Induce Chondrogenic Differentiation of Human Mesenchymal Stem Cells." Tissue Engineering Part A 20, no. 7-8 (2014): 1165–74. http://dx.doi.org/10.1089/ten.tea.2013.0519.

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Kunicki, Thomas J., Daniel Diaz, Shirley A. Williams, Richard W. Farndale та Diane J. Nugent. "The Integrin α2 Dimorphism E534K Modulates Platelet Binding to Decorin but Not Collagen I",. Blood 118, № 21 (2011): 3256. http://dx.doi.org/10.1182/blood.v118.21.3256.3256.

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Abstract Abstract 3256 Background. Integrin a2b1-mediated adhesion to collagens supports cellular attachment, while decorin binding by a2b1 often attenuates adhesion. Collagen I binds to the a2 I-domain via the triple-helical sequence GFOGER, but the decorin binding site is not within the a2 I-domain and has not yet been identified. A single nucleotide polymorphism in the a2 gene ITGA2 (rs1801106) (G1600A) resulting in the amino acid substitution glutamate-534 to lysine-534 (E534K) is the basis for one of the most important human platelet alloantigen (HPA) systems, HPA-5, yet HPA-5 alleles do
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Lahti, Matti, Jyrki Heino та Jarmo Käpylä. "Leukocyte integrins αLβ2, αMβ2 and αXβ2 as collagen receptors—Receptor activation and recognition of GFOGER motif". International Journal of Biochemistry & Cell Biology 45, № 7 (2013): 1204–11. http://dx.doi.org/10.1016/j.biocel.2013.03.016.

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Farndale, Richard W., Pia R. Siljander, David J. Onley, Pavithra Sundaresan, C. Graham Knight, and Michael J. Barnes. "Collagen-platelet interactions: recognition and signalling." Biochemical Society Symposia 70 (September 1, 2003): 81–94. http://dx.doi.org/10.1042/bss0700081.

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The collagen-platelet interaction is central to haemostasis and may be a critical determinant of arterial thrombosis, where subendothelium is exposed after rupture of atherosclerotic plaque. Recent research has capitalized on the cloning of an important signalling receptor for collagen, glycoprotein VI, which is expressed only on platelets, and on the use of collagen-mimetic peptides as specific tools for both glycoprotein VI and integrin α2ϐ1. We have identified sequences, GPO and GFOGER (where O denotes hydroxyproline), within collagen that are recognized by the collagen receptors glycoprote
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Dissertations / Theses on the topic "GFOGER"

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Mansour, Ali. "Mécanismes physiopathologiques de la calcification vasculaire : les vésicules extracellulaires comme cible thérapeutique potentielle." Thesis, Amiens, 2020. http://www.theses.fr/2020AMIE0029.

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Les maladies cardiovasculaires (MCV) sont classées en tête de liste parmi les principales causes de décès dans le monde. La calcification de la paroi vasculaire entraîne diverses conséquences cardiovasculaires critiques et explique les taux de mortalité élevés chez les patients atteints de nombreuses maladies comme le diabète, l'athérosclérose et la maladie rénale chronique (IRC). VC est un processus actif avec des caractéristiques de la physiologie osseuse et il est régulé par des processus inductifs et inhibiteurs multifactoriels. Au cours du processus de calcification, les cellules musculai
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Wojtowicz, Abigail M. "Genetically-engineered bone marrow stromal cells and collagen mimetic scaffold modification for healing critically-sized bone defects." Diss., Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/34705.

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Non-healing bone defects have a significant socioeconomic impact in the U.S. with approximately 600,000 bone grafting procedures performed annually. Autografts and allografts are clinically the most common treatments; however, autologous donor bone is in limited supply, and allografts often have poor mechanical properties. Therefore, tissue engineering and regenerative medicine strategies are being developed to address issues with clinical bone grafting. The overall objective of this work was to develop bone tissue engineering strategies that enhance healing of orthotopic defects by targeti
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Book chapters on the topic "GFOGER"

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"HO U S IN GFOR PE OPLEWITH SP ECIAL NE EDS." In Housing Policy in the United States. Routledge, 2013. http://dx.doi.org/10.4324/9780203860021-17.

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