The pathology of bone tissue during peri-implantitis.
Göttingen, Germany. In J Dent Res, Feb 2015
The levels of typical bone matrix molecules, including SPP1, BGLAP, and COL9A1, in patients with peri-implantitis were reduced, while the inflammation marker interleukin 8 (IL8) was highly expressed.
Differentiation of stem cells from human infrapatellar fat pad: characterization of cells undergoing chondrogenesis.
Melbourne, Australia. In Tissue Eng Part A, 2014
Normalized microarray highlighted 608 differentially expressed genes; 10 chondrogenic genes were upregulated (2- to 87-fold), including COL2A1, COL10A1, COL9A1, COL11A1, COL9A2, COL11A2, COL1A1, COMP, SOX9, and COL3A1.
Enhanced tissue regeneration potential of juvenile articular cartilage.
Austin, United States. In Am J Sports Med, 2013
The genes mostly involved in cartilage growth and expansion, such as COL2A1, COL9A1, MMP2, MMP14, and TGFB3, were upregulated in juvenile cartilage, whereas the genes primarily responsible for structural integrity, such as COMP, FN1, TIMP2, TIMP3, and BMP2, were upregulated in adult cartilage.
Multiple Epiphyseal Dysplasia, Autosomal Dominant
Seattle, United States. In Unknown Journal, 2003
CLINICAL CHARACTERISTICS: Autosomal dominant multiple epiphyseal dysplasia (MED) presents in early childhood, usually with pain in the hips and/or knees after exercise.
Pseudoachondroplasia and multiple epiphyseal dysplasia: mutation review, molecular interactions, and genotype to phenotype correlations.
Manchester, United Kingdom. In Hum Mutat, 2002
PSACH is almost exclusively caused by mutations in cartilage oligomeric matrix protein (COMP) whereas various forms of MED are caused by mutations in the genes encoding COMP, type IX collagen (COL9A1, COL9A2, and COL9A3), matrilin-3 (MATN3), and solute carrier member 26, member 2 gene (SLC26A2).
Identification of a novel common genetic risk factor for lumbar disk disease.
Oulu, Finland. In Jama, 2001
MAIN OUTCOME MEASURES: Frequencies of sequence variations covering the entire coding sequences and exon boundaries of the collagen IX genes, COL9A1, COL9A2, and COL9A3, which code for the alpha1, alpha2, and alpha3 chains of the protein, detected by conformation-sensitive gel electrophoresis and confirmed by sequencing, compared between individuals with and without LDD.
Seattle, United States. In Unknown Journal, 2000
Pathogenic variants in one of six genes (COL2A1, COL11A1, COL11A2, COL9A1, COL9A2, COL9A3) have been associated with Stickler syndrome; because a few families with features of Stickler syndrome are not linked to any of these six loci, mutation of other genes may also cause the disorder.