Monday, May 20, 2013

THE ADAMTS FAMILY!

PLAY WITH THE ADAMTS

ADAMTS1. A disintegrin and metalloproteinase with thrombospondin motifs 1, has anti-angiogenic activity. The expression of this gene may be associated with various inflammatory processes as well as development of cancer cachexia. This gene is likely to be necessary for normal growth, fertility, and organ morphology and function.[2]ADAMTS1 has been shown to interact with Vascular endothelial growth factor A.[3]

ADAMTS2. procollagen I N-proteinase (PC I-NP) is an enzyme[ 
Ehlers-Danlos syndrome, dermatosparaxis type is caused by mutations in the ADAMTS2 gene.

 3.The protein encoded by this gene is the major procollagen II N-propeptidase. A deficiency of this protein may be responsible for dermatosparaxis, a genetic defect of connective tissues. [provided by RefSeq, Jul 2008

4.The enzyme encoded by this gene lacks a C-terminal TS motif. It is responsible for the degradation of aggrecan, a major proteoglycan of cartilage, and brevican, a brain-specific extracellular matrix protein. The cleavage of aggrecan and brevican suggests key roles of this enzyme in arthritic disease and in the central nervous system, potentially, in the progression of glioma.[2]
5.The enzyme encoded by this gene contains two C-terminal TS motifs and functions as aggrecanase to cleave aggrecan, a major proteoglycan of cartilage.[3]

Clinical significance

Genetically modified mice in which the catalytic domain of ADAMTS5 was deleted are resistant to cartilage destruction in an experimental model of osteoarthritis.[4] ADAMTS5 is the major aggrecanase in mouse cartilage in a mouse model of inflammatory arthritis.[5]

6.CLEARLY POORLY STUDIED, ?PROHORMONE CONVERTASE

7.ADAMTS-7: a metalloproteinase that directly binds to and degrades cartilage oligomeric matrix protein
Chuan-ju Liu*


IT IS SAID TO BE INCREASED IN RHEUMATOID ARTHRITIS
SO BLOCK METALLOPROTEASE 7, NO MORE DESTRUCTION OF YOUR KNEES!

8.A number of disorders have been mapped in the vicinity of this gene, most notably lung neoplasms.[2]

 ADAMTS-8 indicated promoter hypermethylation in one out of 24 brain tumours (a metastasis) and three out of four glioma cell lines suggesting an alternative mechanism of downregulation. These data suggest a role for ADAMTS-8 in brain tumorigenesis, warranting further investigation into its role in regulation of tumour angiogenesis and local invasion.

Expression of ADAMTS-8, a secreted protease with antiangiogenic properties, is downregulated in brain tumours

J R Dunn,1,*ET AL.

?PROGNOSTIC VALUE IN BRAIN TUMOR OR RESISTANCE TO AVASTIN INDICATOR?

AND YOU CAN PLAY THIS GAME ALL DAY
(TO BE CONTINUED)
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