Department of Internal Medicine, Wake Forest University School of Medicine, Medical Center BLV, Winston-Salem, NC 27157, USA.
Published: December 2006
AI Article Synopsis
Article Abstract
To improve production of functional fully gamma-carboxylated recombinant human clotting factor IX (r-hFIX), cell lines stably overexpressing r-hFIX have been engineered to also overexpress proteins of the gamma-carboxylation system. Here we demonstrate that siRNA silencing of calumenin, an inhibitor of the gamma-carboxylation system, enhances production of functional r-hFIX produced by engineered BHK21 cells. The production yield of functional r-hFIX was 80% in engineered cells where calumenin had been silenced 78%. We propose that this high-yield expression system can easily be adapted to overproduce functional forms of all members of the vitamin K-dependent protein family.
Introduction: The use of cardiopulmonary bypass (CPB) can induce sterile systemic inflammation that contributes to morbidity and mortality, especially in children. Patients have been found to have increased expression of cytokines and transmigration of leukocytes during and after CPB. Previous work has demonstrated that the supraphysiologic shear stresses existing during CPB are sufficient to induce proinflammatory behavior in non-adherent monocytes.
Argonaute proteins are active throughout the lifetime in a variety of organisms and they bind to small RNAs (sRNAs) to regulate gene expression. The Argonaute proteins of vertebrates can be classified into two clades: the Ago clade and the Piwi clade. Both clades have N, L1, L2, PAZ, MID and PIWI domains.
Schwann cells (SCs) are necessary for peripheral nerve regeneration due to their plasticity and trophic supply after sciatic nerve injury (SNI). However, the multiple adaptations of SCs are still poorly understood. This study explored the effects of transient axonal glycoprotein type-1 (TAG-1) on cell migration and neuropilin1 (NRP1) expression in SCs and examined the impact of TAG-1 on nerve regeneration in rats with SNI.
The Hippo pathway plays a tumorigenic role in highly angiogenic glioblastoma (GBM), whereas little is known about clinically relevant Hippo pathway inhibitors' ability to target adaptive mechanisms involved in GBM chemoresistance. Their molecular impact was investigated here in vitro against an alternative process to tumour angiogenesis termed vasculogenic mimicry (VM) in GBM-derived cell models. In silico analysis of the downstream Hippo signalling members YAP1, TAZ and TEAD1 transcript levels in low-grade glioblastoma (LGG) and GBM tumour tissues was performed using GEPIA.
Introduction: The plasma membrane-bound protein, multi-drug resistance-associated protein 4 (), has gained attention for its pivotal role in facilitating the efflux of a wide range of endogenous and xenobiotic molecules. Its significance in adipogenesis and fatty acid metabolism has been brought to light by recent studies. Notably, research on knockout ( ) mice has established a link between the absence of and the development of obesity and diabetes.
