Inhibition of Mitogen Activated Protein Kinase Activated Protein Kinase II with MMI-0100 reduces intimal hyperplasia ex vivo and in vivo.

[1]  A. Barbul,et al.  Peptide inhibitors of MK2 show promise for inhibition of abdominal adhesions. , 2011, The Journal of surgical research.

[2]  T. Nishibe,et al.  Eph-B4 prevents venous adaptive remodeling in the adult arterial environment , 2011, The Journal of experimental medicine.

[3]  C. Flynn,et al.  A novel cell permeant peptide inhibitor of MAPKAP kinase II inhibits intimal hyperplasia in a human saphenous vein organ culture model. , 2010, Journal of vascular surgery.

[4]  Yibin Wang,et al.  MAPK-Activated Protein Kinase-2 in Cardiac Hypertrophy and Cyclooxygenase-2 Regulation in Heart , 2010, Circulation research.

[5]  A. Panitch,et al.  Design of a bioactive cell‐penetrating peptide: when a transduction domain does more than transduce , 2009, Journal of peptide science : an official publication of the European Peptide Society.

[6]  A. Barbul,et al.  MK2 inhibitor peptide reduces adhesion formation without affecting colonic anastomotic healing , 2009 .

[7]  C. Flynn,et al.  Inhibition of HSP27 phosphorylation by a cell-permeant MAPKAP Kinase 2 inhibitor. , 2009, Biochemical and biophysical research communications.

[8]  B. Bibby,et al.  Reduced oxazolone-induced skin inflammation in MAPKAP kinase 2 knockout mice. , 2009, The Journal of investigative dermatology.

[9]  In vivo modulation of Nogo-B attenuates neointima formation. , 2008, Molecular therapy : the journal of the American Society of Gene Therapy.

[10]  E. Edelman,et al.  Innate immunity has a dual effect on vascular healing: suppression and aggravation of neointimal formation and remodeling post-endotoxin challenge. , 2008, Atherosclerosis.

[11]  M. Gaestel,et al.  MAPKAP kinase 2‐deficiency prevents neurons from cell death by reducing neuroinflammation – relevance in a mouse model of Parkinson’s disease , 2008, Journal of neurochemistry.

[12]  G. Stoecklin,et al.  Control of mRNA decay by phosphorylation of tristetraprolin. , 2008, Biochemical Society transactions.

[13]  J. Hagood,et al.  Muscle fatigue: MK2 signaling and myofibroblast differentiation. , 2007, American journal of respiratory cell and molecular biology.

[14]  D. Corradi,et al.  Functional effects of nitric oxide-releasing aspirin on vein conduits of diabetic patients undergoing CABG. , 2007, International journal of cardiology.

[15]  Tiegang Liu,et al.  Smooth muscle α‐actin expression and myofibroblast differentiation by TGFβ are dependent upon MK2 , 2007 .

[16]  M. Dashwood,et al.  Surgical damage of the saphenous vein and graft patency. , 2007, The Journal of thoracic and cardiovascular surgery.

[17]  G. Owens,et al.  Excitation–Transcription Coupling in Arterial Smooth Muscle , 2006, Circulation research.

[18]  Scott A Berceli,et al.  Results of PREVENT III: a multicenter, randomized trial of edifoligide for the prevention of vein graft failure in lower extremity bypass surgery. , 2006, Journal of vascular surgery.

[19]  Prevent Iv Investigators.  Efficacy and safety of edifoligide, an E2F transcription factor decoy, for prevention of vein graft failure following coronary artery bypass graft surgery: PREVENT IV: a randomized controlled trial. , 2005 .

[20]  P. Cohen,et al.  Nogo-B is a new physiological substrate for MAPKAP-K2. , 2005, The Biochemical journal.

[21]  M. Birnbaum,et al.  Akt1/protein kinase Bα is critical for ischemic and VEGF-mediated angiogenesis , 2005 .

[22]  M. Birnbaum,et al.  Akt1/protein kinase Balpha is critical for ischemic and VEGF-mediated angiogenesis. , 2005, The Journal of clinical investigation.

[23]  M. Dashwood,et al.  Surgical Trauma and Vein Graft Failure: Further Evidence for a Role of ET-1 in Graft Occlusion , 2004, Journal of cardiovascular pharmacology.

[24]  K. Kent,et al.  Intimal Hyperplasia—Still Here after All These Years! , 2004, Annals of vascular surgery.

[25]  M. Rane,et al.  MAPK-activated protein kinase-2 participates in p38 MAPK-dependent and ERK-dependent functions in human neutrophils. , 2003, Cellular signalling.

[26]  P. Cohen,et al.  Inhibition of SAPK2a/p38 prevents hnRNP A0 phosphorylation by MAPKAP‐K2 and its interaction with cytokine mRNAs , 2002, The EMBO journal.

[27]  M. Gaestel,et al.  Mitogen-activated Protein Kinase-activated Protein (MAPKAP) Kinase 2 Deficiency Protects Brain from Ischemic Injury in Mice* , 2002, The Journal of Biological Chemistry.

[28]  I. Fishbein,et al.  Macrophage Depletion by Clodronate-Containing Liposomes Reduces Neointimal Formation After Balloon Injury in Rats and Rabbits , 2002, Circulation.

[29]  M. Gaestel,et al.  Distinct Cellular Functions of MK2 , 2002, Molecular and Cellular Biology.

[30]  T. Hartung,et al.  Mitogen-Activated Protein Kinase-Activated Protein Kinase 2-Deficient Mice Show Increased Susceptibility to Listeria monocytogenes Infection , 2002, The Journal of Immunology.

[31]  G. Kollias,et al.  MK2 Targets AU-rich Elements and Regulates Biosynthesis of Tumor Necrosis Factor and Interleukin-6 Independently at Different Post-transcriptional Levels* , 2002, The Journal of Biological Chemistry.

[32]  K. Mahtani,et al.  Mitogen-Activated Protein Kinase p38 Controls the Expression and Posttranslational Modification of Tristetraprolin, a Regulator of Tumor Necrosis Factor Alpha mRNA Stability , 2001, Molecular and Cellular Biology.

[33]  R. Passier,et al.  CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo. , 2000, The Journal of clinical investigation.

[34]  Klaus Resch,et al.  The p38 MAP kinase pathway signals for cytokine‐induced mRNA stabilization via MAP kinase‐activated protein kinase 2 and an AU‐rich region‐targeted mechanism , 1999, The EMBO journal.

[35]  M. Gaestel,et al.  Kotlyarov, A. et al. MAPKAP kinase 2 is essential for LPS-induced TNF-alpha biosynthesis. Nat. Cell Biol. 1, 94-97 , 1999 .

[36]  M. Gaestel,et al.  MAPKAP kinase 2 is essential for LPS-induced TNF-alpha biosynthesis. , 1999, Nature cell biology.

[37]  E J Topol,et al.  Aortocoronary saphenous vein graft disease: pathogenesis, predisposition, and prevention. , 1998, Circulation.

[38]  K. Hayess,et al.  Effect of protein kinase inhibitors on activity of mammalian small heat-shock protein (HSP25) kinase. , 1997, Biochemical pharmacology.

[39]  É. Allaire,et al.  Endothelial cell injury in cardiovascular surgery: the intimal hyperplastic response. , 1997, The Annals of thoracic surgery.

[40]  Michael J. O'Donovan,et al.  Neurotrophin and neurotrophin receptors in vascular smooth muscle cells. Regulation of expression in response to injury. , 1995, The American journal of pathology.

[41]  Michel Morange,et al.  A novel kinase cascade triggered by stress and heat shock that stimulates MAPKAP kinase-2 and phosphorylation of the small heat shock proteins , 1994, Cell.

[42]  M. Davies,et al.  Hypercholesterolemia and experimental vein grafts: accelerated development of intimal hyperplasia and an increase in abnormal vasomotor function. , 1993, The Journal of surgical research.

[43]  M. Reidy,et al.  Prevention of stenosis after vascular reconstruction: pharmacologic control of intimal hyperplasia--a review. , 1991, Journal of vascular surgery.

[44]  Julie H. Campbell,et al.  Smooth muscle phenotypic expression in human carotid arteries. I. Comparison of cells from diffuse intimal thickenings adjacent to atheromatous plaques with those of the media. , 1985, Laboratory investigation; a journal of technical methods and pathology.

[45]  W. Quist,et al.  Integrity of vein grafts as a function of initial intimal and medial preservation. , 1983, Circulation.