Research Topics
Genomes and Genes
| James L DanielSummaryAffiliation: Temple University Country: USA Publications
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Detail Information
Publications
Cbl-b is a novel physiologic regulator of glycoprotein VI-dependent platelet activationJames L Daniel
Department of Anatomy, Sol Sherry Thrombosis Research Center, Temple University, Philadelphia, Pennsylvania 19140, USA
J Biol Chem 285:17282-91. 2010..These data indicate that Cbl-b plays a positive modulatory role in GPVI-dependent platelet signaling, which translates to an important regulatory role in hemostasis and thrombosis in vivo...- RhoA downstream of G(q) and G(12/13) pathways regulates protease-activated receptor-mediated dense granule release in plateletsJianguo Jin
Department of Physiology, Temple University School of Medicine, Philadelphia, PA, USA
Biochem Pharmacol 77:835-44. 2009..We conclude that G(12/13) pathways, through RhoA, regulate dense granule release and fibrinogen receptor activation in platelets... - Role of phosphoinositide 3-kinase beta in glycoprotein VI-mediated Akt activation in plateletsSoochong Kim
Department of Physiology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
J Biol Chem 284:33763-72. 2009..In addition, a significant portion of GPVI-dependent, ADP-independent Akt activation also exists, and PI3Kbeta plays an essential role in GPVI-mediated platelet aggregation and Akt activation... - Rapid ubiquitination of Syk following GPVI activation in plateletsCarol A Dangelmaier
Department of Pharmacology, Temple University School of Medicine, 3420 N Broad St, Philadelphia, PA 19140, USA
Blood 105:3918-24. 2005..Furthermore, Syk is not dephosphorylated in these mice. We propose that c-Cbl plays a regulatory role in glycoprotein VI (GPVI)/Fc receptor gamma (FcRgamma)-chain-dependent platelet activation through its interaction with Syk... - A novel histidine tyrosine phosphatase, TULA-2, associates with Syk and negatively regulates GPVI signaling in plateletsDafydd H Thomas
Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Blood 116:2570-8. 2010..We therefore propose that TULA-2 is the primary tyrosine phosphatase mediating the dephosphorylation of Syk and thus functions as a negative regulator of GPVI signaling in platelets... - Lyn, PKC-delta, SHIP-1 interactions regulate GPVI-mediated platelet-dense granule secretionRamya Chari
Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Blood 114:3056-63. 2009..Therefore, we conclude that Lyn-mediated phosphorylations of PKC-delta and SHIP-1 and their associations negatively regulate GPVI-mediated dense granule secretion in platelets... - Evaluation of [3-(1-methyl-1H-indol-3-yl-methylene)-2-oxo-2, 3-dihydro-1H-indole-5-sulfonamide] (OXSI-2), as a Syk-selective inhibitor in plateletsKamala Bhavaraju
Department of Physiology, Temple University, School of Medicine, Philadelphia, PA, USA
Eur J Pharmacol 580:285-90. 2008..In contrast, OXSI-2, unlike PKC inhibitors, did not inhibit secretion. Therefore, we conclude that OXSI-2 is not a Syk-selective inhibitor in platelets because of its unexplained non-specific effects... 
Curcumin inhibits GPVI-mediated platelet activation by interfering with the kinase activity of Syk and the subsequent activation of PLCgamma2Azad Mayanglambam
Department of Physiology, Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA
Platelets 21:211-20. 2010..We conclude that curcumin inhibits platelet activation induced by GPVI agonists through interfering with the kinase activity of Syk and the subsequent activation of PLCgamma2...- Hematopoietic lineage cell specific protein 1 (HS1) is a functionally important signaling molecule in platelet activationBryan N Kahner
Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Blood 110:2449-56. 2007..These results demonstrate that phosphorylation of the HS1 protein occurs downstream of GPVI stimulation and that HS1 plays a significant functional role in platelet activation downstream of GPVI and PARs... 
Dynamic regulation of microtubule coils in ADP-induced platelet shape change by p160ROCK (Rho-kinase)Benjamin Z S Paul
Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Platelets 14:159-69. 2003..Continued disruption of the cytoskeletal microtubule ring, appears to be a Rhokinase-dependent event involved in the transformation of discoid platelets into spheres...- Expression of enzymatically-active phospholipase Cgamma2 in E. coliFatih Ozdener
Department of Pharmacology, Temple University Medical School, Philadelphia, PA, USA
J Biochem Mol Biol 35:508-12. 2002..Similar to previous reports on PLCgamma2 that is isolated from mammalian tissue, the recombinant enzyme was Ca2+ dependent with optimal activity at 1-10 microM Ca2+... - Regulation of plasmin-induced protease-activated receptor 4 activation in plateletsYingying Mao
Department of Physiology, Temple University School of Medicine, Philadelphia, PA, USA
Platelets 20:191-8. 2009..In contrast to thrombin-dependent activation of platelets, wherein PAR3 acts as a co-receptor, mPAR3 inhibits plasmin-induced PAR4 activation... - Activation of phospholipase Cgamma2 by tyrosine phosphorylationFatih Ozdener
Department of Pharmacology, Temple University Medical School, Philadelphia, Pennsylvania 19140, USA
Mol Pharmacol 62:672-9. 2002..These studies demonstrate the importance of these two tyrosine residues in regulating the activity of PLCgamma2... - Glycoprotein VI-mediated platelet fibrinogen receptor activation occurs through calcium-sensitive and PKC-sensitive pathways without a requirement for secreted ADPTodd M Quinton
Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Blood 99:3228-34. 2002..Furthermore, protein kinase C- and calcium-regulated pathways independently contribute to GPVI-mediated platelet aggregation...