Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Maya Breitman"'
Autor:
Maya Breitman, Tracey L. Bonfield, Arnold I. Caplan, Hillard M. Lazarus, Maricela Haghiac, Susan LaSalvia, Jane Reese‐Koc, Nora G. Singer
Publikováno v:
ACR Open Rheumatology, Vol 4, Iss 2, Pp 152-160 (2022)
Objective Seropositive rheumatoid arthritis (RA) is a chronic autoimmune disease that is rarely “cured.” Human mesenchymal stem cells (hMSCs) are known to reduce inflammation and restore immune homeostasis. However, methods for predicting therape
Externí odkaz:
https://doaj.org/article/a7bd0d1395f0457a964cc475331d0a16
Autor:
Sergio Coffa, Maya Breitman, Susan M Hanson, Kari Callaway, Seunghyi Kook, Kevin N Dalby, Vsevolod V Gurevich
Publikováno v:
PLoS ONE, Vol 6, Iss 12, p e28723 (2011)
Arrestins are multifunctional signaling adaptors originally discovered as proteins that "arrest" G protein activation by G protein-coupled receptors (GPCRs). Recently GPCR complexes with arrestins have been proposed to activate G protein-independent
Externí odkaz:
https://doaj.org/article/fb428791600a42a187f3913576941165
Autor:
Maricela Haghiac, Tracey L. Bonfield, Hillard M. Lazarus, Jane Reese-Koc, Arnold I. Caplan, Susan LaSalvia, Maya Breitman, Nora G. Singer
Publikováno v:
ACR Open Rheumatology, Vol 4, Iss 2, Pp 152-160 (2022)
Objective Seropositive rheumatoid arthritis (RA) is a chronic autoimmune disease that is rarely "cured." Human mesenchymal stem cells (hMSCs) are known to reduce inflammation and restore immune homeostasis. However, methods for predicting therapeutic
Autor:
Tracey L. Bonfield, Hillard M. Lazarus, Arnold I. Caplan, Susan Lasalvia, Maya Breitman, Nora G. Singer
Publikováno v:
SATURDAY, 15 JUNE 2019.
Background: Rheumatoid Arthritis (RA) is an autoimmune disease in which early treatment prevents joint damage. Autoantibodies such as rheumatoid factors (RF) and anti-citrullinated peptide antibodies (APCA) define a subset of RA patients at the highe
Publikováno v:
Abstracts Accepted for Publication.
Background: The Wnt–β-catenin pathway may play a critical role in new bone formation in ankylosing spondylitis. Wnt–β-catenin signaling depends primarily on the activity of glycogen synthase kinase-3β (GSK3β) that plays a key role in controll
Autor:
David C. Soler, Anthony E. Ting, Thomas S. McCormick, Maya Breitman, Hillard M. Lazarus, Emma Barnboym, Nicholas Lehman, Nora G. Singer, Arnold I. Caplan, Donald D. Anthony, Gali Shalev-Malul
Publikováno v:
Stem Cells Translational Medicine
This study tested the hypothesis that an ex vivo T-cell suppression assay could estimate response to novel cell-based therapy for rheumatoid arthritis (RA). Results showed multipotent adult progenitor cell products suppressed RA effector T cells. The
Autor:
Brian M. Cartwright, Hui Tang, Ji Liu, Antonio E. Rusiñol, Benjamin Hilton, Phillip R. Musich, Youjie Wang, Rowdy Jones, Yiyong Liu, Yue Zou, Maya Breitman
Publikováno v:
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 31(9)
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder that is caused by a point mutation in the LMNA gene, resulting in production of a truncated farnesylated-prelamin A protein (progerin). We previously reported that XPA mislocalize
Autor:
Seunghyi Kook, Luis E. Gimenez, Vsevolod V. Gurevich, Maria C. Palazzo, Eugenia V. Gurevich, Britney N. Lizama, Maya Breitman
Publikováno v:
Journal of Biological Chemistry. 287:19653-19664
We established a new in vivo arrestin-3-JNK3 interaction assay based on bioluminescence resonance energy transfer (BRET) between JNK3-luciferase and Venus-arrestins. We tested the ability of WT arrestin-3 and its 3A mutant that readily binds β2-adre
Publikováno v:
Journal of Biological Chemistry. 286:27894-27901
Arrestins bind active phosphorylated G protein-coupled receptors, blocking G protein activation and channeling the signaling to G protein-independent pathways. Free arrestin-3 and receptor-bound arrestin-3 scaffold the ASK1-MKK4-JNK3 module, promotin
Publikováno v:
Biochemistry. 50:6951-6958
Arrestins regulate the signaling and trafficking of G protein-coupled receptors (GPCRs). GPCR complexes with both nonvisual arrestins channel signaling to G protein-independent pathways, one of which is the activation of extracellular signal regulate