|1.||Fosang, Amanda J: 12 articles (01/2015 - 04/2005)|
|2.||Glant, Tibor T: 12 articles (04/2013 - 01/2003)|
|3.||Mikecz, Katalin: 12 articles (04/2013 - 01/2003)|
|4.||Glant, T T: 10 articles (01/2014 - 04/2000)|
|5.||Struglics, André: 8 articles (12/2015 - 01/2009)|
|6.||Nagase, Hideaki: 8 articles (11/2015 - 01/2003)|
|7.||Mikecz, K: 8 articles (01/2014 - 04/2000)|
|8.||Little, Christopher B: 7 articles (12/2014 - 04/2005)|
|9.||Lohmander, L S: 7 articles (02/2014 - 02/2006)|
|10.||Sandy, John D: 7 articles (07/2011 - 09/2005)|
10/01/2006 - "Aggrecan core protein of a certain length is protective against hand osteoarthritis."
10/01/2006 - "To study the contribution of aggrecan VNTR (variable number of tandem repeats) polymorphism to clinically differing manifestations of hand osteoarthritis (OA). "
10/01/1998 - "Further studies on aggrecan will lead to prophylaxis and treatment of joint destructive diseases such as osteoarthrosis and to elucidation of cartilage development, which is essential for skeletal formation."
08/13/2015 - "The aggrecan degrading metalloprotease ADAMTS-4 has been identified as a novel therapeutic target for osteoarthritis. "
01/02/2015 - "High-bandwidth AFM-based rheology is a sensitive indicator of early cartilage aggrecan degradation relevant to mouse models of osteoarthritis."
02/01/2015 - "Plasma KS level in JIA patients, reflecting the aggrecan structure, indicates that treatment that modifies inflammation simultaneously does not contribute to total regeneration of articular matrix components and signalizes the need for further treatment."
01/01/2013 - "Taken together our observations indicate aggrecan CLD as one factor involved in the sustained inflammation of the joint."
01/01/2013 - "Herein, we postulated that chronic low-level inflammation may also contribute to OA progression by promoting regulatory mechanisms in early CS biosynthesis that yield incomplete linkage structures on aggrecan. "
06/01/2011 - "Since aggrecan accumulation is a major feature of incomplete healing in tendon and skin of the ADAMTS5 knockout mouse, we propose that ligament failure in DSLD results from a process involving tissue inflammation and the complexation of ADAMTS5."
01/01/2010 - "Aggrecan, a well-known component of cartilage matrix, is increased in CSF from cases of neural damage and inflammation of the spinal cord. "
11/15/1999 - "Directly increasing integrin expression by adenoviral infection is sufficient to eliminate the inhibitory effects of aggrecan, indicating that upregulation of integrin receptors may promote neuronal regeneration in the presence of inhibitory matrix components."
08/01/2008 - "2) The mRNA expression of aggrecan, type I collagen, type II collagen, LMP-1, BMP-2, and BMP-7 is increased in both AF cells and chondrocytes in 20 MOI AdLMP1-GFP infection. "
10/01/2001 - "We showed that infection of migratory CNCC with adenovirus Msx2 mutants accelerated the rate and extent of chondrogenesis, as indicated by the expression level of type II collagen and aggrecan, and the amount of alcian blue staining. "
06/01/2001 - "Infection of C3HIOT1/2 cells with this retroviral construct resulted in an infection efficiency of 90-95% and was highly effective in converting cells in micromass culture to a chondrocyte phenotype, as assessed by positive Alcian blue staining for extracellular matrix proteoglycans, increased sulfate incorporation, increased expression of the cartilage marker genes collagen type II and aggrecan, and decreased expression of collagen type I. Interestingly, BMP-2 expression in the micromass cultures also induced the expression of the cell cycle inhibitory protein/differentiation factor p21/WAF1, suggesting its functional involvement in chondrogenesis. "
01/01/2014 - "Fifteen proteins were differentially expressed at all time points, among which eight proteins related to pathologies in higher animals were shown to be down-regulated after V. splendidus infection: paxillin, fascin-2, aggrecan, ololfactomedin-1, nesprin-3, a disintegrin-like and metallopeptidase with thrombospondin type 1 motif (Adamts7), C-type lectin domain family 4 (Clec4g) and n-myc downstream regulated gene 1 (Ndrg1). "
04/15/1998 - "These studies reveal that a T cell line specific to an epitope on the G1 domain of aggrecan, also recognizing a corresponding mouse G1 epitope, can induce arthritis by adoptive transfer and homing to the intraarticular epitope, thereby implicating T cells in arthritis development caused by immunity to the G1 domain of aggrecan. "
05/01/1995 - "These studies demonstrate for the first time the MMP-dependent catabolism of aggrecan at sites of chondrodestruction during inflammatory arthritis."
02/01/2013 - "Thus, Sp1 could be potentially targeted to reduce arthritis-associated cartilage aggrecan loss."
04/01/2009 - "Compared to the reference, the acute arthritis and acute joint injury groups had a 30-fold elevated concentration of ARGS fragments, and both groups had a higher proportion of the aggrecan in joint fluid as ARGS fragments compared to the other groups. "
06/01/2007 - "Aggrecan loss from cartilage in arthritis is mediated by aggrecanases. "
02/10/1995 - "A rat chondrosarcoma cell line and primary bovine chondrocytes have been used to study cell-mediated aggrecan catabolism. "
12/01/2014 - "The Acan KO cell lines also provided a tool for characterizing the response of chondrocytes to aggrecan loss and the role of aggrecan in chondrosarcoma development. "
03/01/2001 - "Soluble CD44-IgG and CD44(+) cells bound to aggrecan from rat chondrosarcoma and bovine cartilage, immobilized on microtiter plates. "
05/15/2012 - "No studies have examined the roles of versican in chondrosarcoma nor compared them to those of aggrecan. "
07/01/2014 - "The system is based on co-transfection of candidate enhancer elements and reporter constructs into Swarm rat chondrosarcoma chondrocytes that retain a high level of aggrecan expression. "
|1.||Collagen Type II (Type II Collagen)
|2.||Biological Markers (Surrogate Marker)
|4.||Collagen Type I (Type I Collagen)
|8.||Matrix Metalloproteinase 13
|2.||Deep Brain Stimulation
|4.||Tissue Therapy (Cell Therapy)