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Cartilage intermediate layer protein, nucleotide pyrophosphohydrolase

CILP, Cartilage intermediate layer protein
Major alterations in the composition of the cartilage extracellular matrix occur in joint disease, such as osteoarthrosis. This gene encodes the cartilage intermediate layer protein (CILP), which increases in early osteoarthrosis cartilage. The encoded protein was thought to encode a protein precursor for two different proteins; an N-terminal CILP and a C-terminal homolog of NTPPHase, however, later studies identified no nucleotide pyrophosphatase phosphodiesterase (NPP) activity. The full-length and the N-terminal domain of this protein was shown to function as an IGF-1 antagonist. An allelic variant of this gene has been associated with lumbar disc disease. [provided by RefSeq, Sep 2010] (from NCBI)
Top mentioned proteins: AGE, fibrillin-1, CAN, fibronectin, Comp
Papers on CILP
CD36 Is a Matrix Metalloproteinase-9 Substrate that Stimulates Neutrophil Apoptosis and Removal during Cardiac Remodeling.
New
Lindsey et al., Jackson, United States. In Circ Cardiovasc Genet, Dec 2015
Cartilage intermediate layer protein (CILP) and platelet glycoprotein 4 (CD36) were identified as having the highest fold increase in MMP-9 null mice.
Fibrotic-like changes in degenerate human intervertebral discs revealed by quantitative proteomic analysis.
New
Chan et al., Hong Kong, Hong Kong. In Osteoarthritis Cartilage, Nov 2015
RESULTS: In the AF, quantitative analysis revealed increased levels of HTRA1, COMP and CILP in degeneration when compared with samples from older individuals.
Label-free relative quantification applied to LC-MALDI acquisition for rapid analysis of chondrocyte secretion modulation.
New
Vincourt et al., Vandœuvre-lès-Nancy, France. In J Proteomics, Mar 2015
Novel targets of TGFβ1 were evidenced, such as pro-collagen C-proteinase enhancer protein 1, Metalloproteinase inhibitor 1, Fibulin-3, Tetranectin and Cartilage Intermediate Layer Protein 1, while others match previous findings.
Cartilage intermediate layer protein promotes lumbar disc degeneration.
Kimura et al., Toyama, Japan. In Biochem Biophys Res Commun, 2014
CILP encodes cartilage intermediate layer protein, which is highly associated with LDD.
Cartilage Intermediate Layer Protein and Asporin Polymorphisms Are Independent Risk Factors of Lumbar Disc Degeneration in Male Collegiate Athletes.
Hiranuma et al., Tokyo, Japan. In Cartilage, 2014
DESIGN: We investigated two susceptibility genes for LDDG-cartilage intermediate layer protein (CILP) and asporin (ASPN)-in 516 collegiate athletes and genotyped the risk allele of CILP (1184T/C) and ASPN (D14).
Genetic polymorphisms associated with intervertebral disc degeneration.
Review
Hecht et al., New York City, United States. In Spine J, 2013
RESULTS: Genetic polymorphisms in 20 genes have been analyzed in association with DD, including vitamin D receptor, growth differentiation factor 5 (GDF5), aggrecan, collagen Types I, IX, and XI, fibronectin, hyaluronan and proteoglycan link protein 1 (HAPLN1), thrombospondin, cartilage intermediate layer protein (CILP), asporin, MMP1, 2, and 3, parkinson protein 2, E3 ubiquitin protein ligase (PARK2), proteosome subunit β type 9 (PSMB9), tissue inhibitor of metalloproteinase (TIMP), cyclooxygenase-2 (COX2), and IL1α, IL1β, and IL6.
Quantitative proteomic analysis of eight cartilaginous tissues reveals characteristic differences as well as similarities between subgroups.
Heinegård et al., Lund, Sweden. In J Biol Chem, 2012
asporin, CILP, and COMP, indicating cross-linking.
Cartilage intermediate layer protein (CILP) regulation in intervertebral discs. The effect of age, degeneration, and bone morphogenetic protein-2.
Yoon et al., Atlanta, United States. In Spine (phila Pa 1976), 2012
OBJECTIVE: To evaluate the effects of disc degeneration, age, and bone morphogenetic proteins-2 (BMP-2) on cartilage intermediate layer protein (CILP) expression and elucidate the molecular mechanism by which BMP-2 regulates CILP expression.
Changes in the chondrocyte and extracellular matrix proteome during post-natal mouse cartilage development.
Bateman et al., Melbourne, Australia. In Mol Cell Proteomics, 2012
Proteomics 9, 1296-1313) identified components involved in both systems, such as Urb, and components with specific roles in vivo, including vitrin and CILP-2 (cartilage intermediate layer protein-2).
Cartilage intermediate layer protein 2 (CILP-2) is expressed in articular and meniscal cartilage and down-regulated in experimental osteoarthritis.
Bateman et al., Melbourne, Australia. In J Biol Chem, 2011
CILP-2 is highly homologous to CILP-1 (cartilage intermediate layer protein 1), which is expressed in the intermediate zone of articular cartilage and has been linked to cartilage degenerative diseases.
High throughput proteomic analysis of the secretome in an explant model of articular cartilage inflammation.
Mobasheri et al., Nottingham, United Kingdom. In J Proteomics, 2011
Tryptic peptides originating from aggrecan core protein, cartilage oligomeric matrix protein (COMP), fibronectin, fibromodulin, thrombospondin-1 (TSP-1), clusterin (CLU), cartilage intermediate layer protein-1 (CILP-1), chondroadherin (CHAD) and matrix metalloproteinases MMP-1 and MMP-3 were detected.
Genetic susceptibility of intervertebral disc degeneration among young Finnish adults.
GeneRIF
Männikkö et al., Oulu, Finland. In Bmc Med Genet, 2010
CILP is involved in the etiology of intervertebral disc degeneration among young adults.
Cartilage intermediate layer protein gene is associated with lumbar disc degeneration in male, but not female, collegiate athletes.
GeneRIF
Hiranuma et al., Tokyo, Japan. In Am J Sports Med, 2010
The researchers found that the single nucleotide polymorphism (1184T/C) of the CILP gene is associated an increased risk of lumbar disc degeneration in male athletes.
The cartilage intermediate layer protein gene is associated with lumbar disc degeneration in collegiate judokas.
GeneRIF
Hiranuma et al., Tokyo, Japan. In Int J Sports Med, 2009
the CILP gene 1184T/C polymorphism is a significant risk factor for lumbar disc degeneration occurrence in Japanese collegiate judo athletes
The genetics of intervertebral disc degeneration. Associated genes.
Review
Hunter et al., Boston, United States. In Joint Bone Spine, 2008
RESULTS AND CONCLUSIONS: There are a number of genes that have been associated with intervertebral disk degeneration in humans, including genes coding for collagen I, collagen IX (COL9A2 and COL9A3), collagen XI (COL11A2), IL-1, aggrecan, vitamin D receptor, MMP-3, and CILP.
Phenotypic and population differences in the association between CILP and lumbar disc disease.
GeneRIF
Chan et al., In J Med Genet, 2007
SNP analysis suggested that the CILP gene is not a major risk factor for symptoms of lumbar disc disease in Finnish or Chinese populations.
Transcriptional regulation of the cartilage intermediate layer protein (CILP) gene.
GeneRIF
Ikegawa et al., Tokyo, Japan. In Biochem Biophys Res Commun, 2006
These observations, together with the finding that CILP protein binds and inhibits TGF-beta1, suggest that CILP and TGF-beta1 may form a functional feedback loop that controls chondrocyte metabolism.
A functional SNP in CILP, encoding cartilage intermediate layer protein, is associated with susceptibility to lumbar disc disease.
Impact
GeneRIF
Ikegawa et al., Tokyo, Japan. In Nat Genet, 2005
CILP regulates TGF-beta signaling and that this regulation has a crucial role in the etiology and pathogenesis of LDD.
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