Zobrazeno 1 - 10
of 38
pro vyhledávání: '"Martyn K Robinson"'
Autor:
Terence H. Rabbitts, Laura Ellen Newnham, Kostas Kostarelos, Alastair D. G. Lawson, Michael J Wright, Martyn K. Robinson, Gill Holdsworth
Publikováno v:
mAbs
The Wnt signaling pathway is of central importance in embryogenesis, development and adult tissue homeostasis, and dysregulation of this pathway is associated with cancer and other diseases. Despite the developmental and potential therapeutic signifi
Autor:
Kevin Greenslade, Joby Jose, Zofia Stencel, Hua Zhu Ke, Hishani Kirby, Martyn K. Robinson, Adrian Moore, Gill Holdsworth
Publikováno v:
Bone. 107
Administration of antibodies to sclerostin (Scl-Ab) has been shown to increase bone mass, bone mineral density (BMD) and bone strength by increasing bone formation and decreasing bone resorption in both animal studies and human clinical trials. In th
Autor:
Alice M. Barkell, Lorna C. Waters, Mark D. Carr, Martyn K. Robinson, Vaclav Veverka, Frederick W. Muskett, Alistair James Henry, Patrick M. Slocombe, Gill Holdsworth
Publikováno v:
Biomolecular NMR Assignments. 9:147-151
A number of proteins have been shown to modulate canonical Wnt signalling at the cell surface, including members of the Dickkopf (Dkk) family (Baron and Rawadi in J Endocrinol 148:2635-2643, 2007; Cruciat and Niehrs in Cold Spring Harb Perspect Biol
Publikováno v:
Drug Discovery Today. 18:637-643
In the 1990s there was a tremendous mood of optimism among pharmaceutical scientists that identification of disease-associated variations in the human genome would result in a surge of new drug targets (the 'gene-to-drug' mantra). To date the expecte
Autor:
David Ke, Joby Jose, Zofia Stencel, Hishani Kirby, Gill Holdsworth, Adrian Moore, Martyn K. Robinson, Kevin Greenslade
Publikováno v:
Bone Abstracts.
Autor:
Adrian Moore, Martyn K. Robinson, Diane Marshall, R. Okoye, K. Greenslade, Massimo Marenzana, A. Eddleston
Publikováno v:
Arthritis & Rheumatism. 63:2385-2395
Objective Exposure to supraphysiologic levels of glucocorticoid drugs is known to have detrimental effects on bone formation and linear growth. Patients with sclerosteosis lack the bone regulatory protein sclerostin, have excessive bone formation, an
Autor:
Adrian Moore, Yongming Gao, Chris Paszty, Fay Vlasseros, Jianhua Gong, Barbara Tipton, Daniel John Lightwood, Alistair James Henry, Jacquelin Jolette, M. D. Hale, Jin Cao, Susan Y. Smith, Michael S. Ominsky, W. Scott Simonet, George Doellgast, David L. Lacey, Jill Cai, Brian Stouch, Rohini Deshpande, Andrew George Popplewell, Lei Zhou, Martyn K. Robinson, Kevin Graham
Publikováno v:
Journal of Bone and Mineral Research. 25:948-959
The development of bone-rebuilding anabolic agents for treating bone-related conditions has been a long-standing goal. Genetic studies in humans and mice have shown that the secreted protein sclerostin is a key negative regulator of bone formation. M
Autor:
Mark D. Carr, Andrew Ventom, Jianhua Gong, Kevin Greenslade, Vaclav Veverka, Chris Paszty, Li Zhang, Martyn K. Robinson, Richard J. K. Taylor, Mariusz Muzylak, Alistair James Henry, Patrick M. Slocombe, Xueming Qian, Adrian Moore, Barbara Mulloy, Frederick W. Muskett
Publikováno v:
Journal of Biological Chemistry. 284:10890-10900
The secreted glycoprotein sclerostin has recently emerged as a key negative regulator of Wnt signaling in bone and has stimulated considerable interest as a potential target for therapeutics designed to treat conditions associated with low bone mass,
Publikováno v:
Immunology. 119:203-211
FOXP3 has been identified as a key regulator of immune homeostasis. Mutations within the FOXP3 gene result in dysregulated CD4+ T-cell function and elevated cytokine production, leading to lymphoproliferative disease. FOXP3 expression in CD4+ T cells
Autor:
Martyn K Robinson, Donald E. Staunton, Revital Shamri, Jean-Marc Gauguet, Waldemar Kolanus, Valentin Grabovsky, Ulrich H. von Andrian, Sara W. Feigelson, Eugenia Manevich, Ronen Alon
Publikováno v:
Nature Immunology. 6:497-506
It is widely believed that rolling lymphocytes require successive chemokine-induced signaling for lymphocyte function-associated antigen 1 (LFA-1) to achieve a threshold avidity that will mediate lymphocyte arrest. Using an in vivo model of lymphocyt