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GRAP2 — MMP10

Text-mined interactions from Literome

Montero et al., J Am Coll Cardiol 2006 (Atherosclerosis...) : C-reactive protein stimulation also increased MMP-1 and -10 protein in conditioned culture medium ( p < 0.001 ), as well as MMP activity ( p = 0.001 ). Specific inhibition of p38 or MEK abolished the CRP induction of the MMP-1, whereas MMP-10 induction blockade required the simultaneous inhibition of p38 and Jun N-terminal kinase pathways. Subjects with CRP values > 3 mg/l ( n = 37 ) had increased plasma MMP-1 and -10 ( p < 0.05 ), the association being significant after adjustment for confounding variables ( p = 0.04 and p = 0.008, respectively )
Cheung et al., Cancer Res 2006 (Neoplasm Invasiveness...) : In addition, we showed that the c-Jun NH ( 2 ) -terminal kinase, but not extracellular signal regulated kinase 1/2 or p38 mitogen activated protein kinase, signaling pathway was critical for GnRH mediated up-regulation of MMP , cell invasion, and motility
Sanka et al., Invest Ophthalmol Vis Sci 2007 : Primary human TM ( HTM ) cells treated with different actin cytoskeleton interfering agents, including cytochalasin D, latrunculin A, ethacrynic acid ( ECA ), a Rho kinase inhibitor ( Y-27632 ), and H-7 ( serine/threonine kinase inhibitor ), were examined for changes in actin cytoskeletal organization by phalloidin staining, MMP-2 activation by gelatin zymography, expression of MT1-MMP by quantitative real-time PCR analysis, levels of tissue inhibitor of metalloproteinases ( TIMP-1 and TIMP-2 ), and activation of p38 mitogen activated protein kinase ( p38 MAPK ) and extracellular signal regulated protein kinase ( ERK ) by immunoblotting