| Identification of Mep1a as a susceptibility gene for atherosclerosis in mice. | Identification of Mep1a as a susceptibility gene for atherosclerosis in mice.
Grainger AT, Pilar N, Li J, Chen MH, Abramson AM, Becker-Pauly C, Shi W., Free PMC Article | 02/19/2022 |
| Mep1a contributes to Ang II-induced cardiac remodeling by promoting cardiac hypertrophy, fibrosis and inflammation. | Mep1a contributes to Ang II-induced cardiac remodeling by promoting cardiac hypertrophy, fibrosis and inflammation.
Ge W, Hou C, Zhang W, Guo X, Gao P, Song X, Gao R, Liu Y, Guo W, Li B, Zhao H, Wang J. | 11/27/2021 |
| this study shows that docking of meprin alpha to heparan sulphate protects the endothelium from inflammatory cell extravasation | Docking of Meprin α to Heparan Sulphate Protects the Endothelium from Inflammatory Cell Extravasation.
Biasin V, Wygrecka M, Bärnthaler T, Jandl K, Jain PP, Bálint Z, Kovacs G, Leitinger G, Kolb-Lenz D, Kornmueller K, Peters F, Sinn K, Klepetko W, Heinemann A, Olschewski A, Becker-Pauly C, Kwapiszewska G. | 01/19/2019 |
| no significant dentin malformation was observed in Mep1b (-/-) or Mep1a (-/-) deficient mice. | Deficiency of the DSPP-cleaving enzymes meprin α and meprin β does not result in dentin malformation in mice.
Arnold P, Koopmann L, Peters F, Birkenfeld F, Goff SV, Damm T, Qin C, Moali C, Lucius R, Becker-Pauly C. | 06/3/2017 |
| meprin alpha and meprin beta join the modulators of Reelin signalling as they cleave Reelin at a specific site and are upregulated under specific pathological conditions. | Determination of cleavage site of Reelin between its sixth and seventh repeat and contribution of meprin metalloproteases to the cleavage.
Sato Y, Kobayashi D, Kohno T, Kidani Y, Prox J, Becker-Pauly C, Hattori M. | 09/3/2016 |
| While meprin A only cleaved protein kinase A (PKA) catalytic subunit beta1, meprin B cleaved all three PKA catalytic isoforms. | Isoform-specific interactions between meprin metalloproteases and the catalytic subunit of protein kinase A: significance in acute and chronic kidney injury.
Niyitegeka JM, Bastidas AC, Newman RH, Taylor SS, Ongeri EM., Free PMC Article | 03/21/2015 |
| meprin alpha and meprin beta are unique in their ability to process and release both C- and N-propeptides from type I procollagen in vitro and in vivo | Metalloproteases meprin α and meprin β are C- and N-procollagen proteinases important for collagen assembly and tensile strength.
Broder C, Arnold P, Vadon-Le Goff S, Konerding MA, Bahr K, Müller S, Overall CM, Bond JS, Koudelka T, Tholey A, Hulmes DJ, Moali C, Becker-Pauly C., Free PMC Article | 11/23/2013 |
| the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to ischemia/reperfusion injury on kidney transplantation and hemorrhagic shock | Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.
Hirano M, Ma BY, Kawasaki N, Oka S, Kawasaki T. | 03/31/2012 |
| Absence of meprin A aggravates chronic inflammation and lack of meprin B affords some protection from injury. Manipulation of expression of meprin gene products may have therapeutic potential. | Balance of meprin A and B in mice affects the progression of experimental inflammatory bowel disease.
Banerjee S, Jin G, Bradley SG, Matters GL, Gailey RD, Crisman JM, Bond JS., Free PMC Article | 03/19/2011 |
| MEP1A is a UC susceptibility gene and indicate that decreased meprin-alpha expression is associated with intestinal inflammation in IBD patients and in a mouse experimental model of IBD. | MEP1A allele for meprin A metalloprotease is a susceptibility gene for inflammatory bowel disease.
Banerjee S, Oneda B, Yap LM, Jewell DP, Matters GL, Fitzpatrick LR, Seibold F, Sterchi EE, Ahmad T, Lottaz D, Bond JS., Free PMC Article | 01/21/2010 |
| meprin alpha/beta null (alpha(-/-)/beta(-/-)) mice had decreased prevalence of resident monocytes and natural killer (NK) cells in blood, with a concomitant accumulation of inflammatory monocytes and NK cells in bone marrow. | Disruption of the meprin alpha and beta genes in mice alters homeostasis of monocytes and natural killer cells.
Sun Q, Jin HJ, Bond JS., Free PMC Article | 01/21/2010 |
| Meprin A contributes to the renal and urogenital pathogenesis of endotoxicity. | Meprin A metalloproteases enhance renal damage and bladder inflammation after LPS challenge.
Yura RE, Bradley SG, Ramesh G, Reeves WB, Bond JS., Free PMC Article | 01/21/2010 |
| meprin A, a multimeric metalloprotease expressed in the brush borders of kidney proximal tubules initially truncates mouse BNP in the N terminus to mBNP7-32 | Successive action of meprin A and neprilysin catabolizes B-type natriuretic peptide.
Pankow K, Wang Y, Gembardt F, Krause E, Sun X, Krause G, Schultheiss HP, Siems WE, Walther T. | 01/21/2010 |
| Meprin A appears to be an important therapeutic target and urinary excretion appears to be a potential biomarker of acute kidney injury. | Role of meprin A in renal tubular epithelial cell injury.
Herzog C, Seth R, Shah SV, Kaushal GP. | 01/21/2010 |
| conserved sequences essential for zinc binding and enzymatic activity were determined by site-directed mutagenesis | Zinc ligands in an astacin family metalloprotease meprin A.
Doll BA, Villa JP, Ishmael FT, Bond JS. | 01/21/2010 |
| determined the sites of glycan attachment and assessed their ability to affect the formation and stability of the homo-oligomer | Protease domain glycans affect oligomerization, disulfide bond formation, and stability of the meprin A metalloprotease homo-oligomer.
Ishmael SS, Ishmael FT, Jones AD, Bond JS. | 01/21/2010 |
| meprin-alpha may play a role in the pathogenesis of diabetic nephropathy and the benefits of ACE inhibitor therapy | Meprin-alpha in chronic diabetic nephropathy: interaction with the renin-angiotensin axis.
Mathew R, Futterweit S, Valderrama E, Tarectecan AA, Bylander JE, Bond JS, Trachtman H. | 01/21/2010 |