An H333N mutation conferred resistance to both zinc and nickel, with properties in keeping with the known pH-dependent chelation of these metals by histidine. Biochemical studies demonstrated that zinc strongly inhibits formation of the postfusion E1 trimer in wild-type SFV but not in an H333 mutant. Together our results suggest that zinc acts by blocking the fold-back of DIII via its interaction with H333.”
“Parkin is an ubiquitin-protein ligase (E3), mutations of which cause juvenile onset – autosomal recessive Parkinson’s disease,

and result in reduced enzymic activity. In contrast, increased levels are protective against mitochondrial dysfunction and neurodegeneration, the mechanism of which is largely unknown. In this study, 2-DE and MS proteomic techniques were utilised to investigate the effects of increased Parkin levels on protein expression check details in whole cell lysates using in an inducible Parkin expression system in HEK293 cells, and also to isolate potential interactants Z-VAD-FMK of Parkin using tandem affinity purification and

MS. Nine proteins were significantly differentially expressed (+/- 2-fold change; p < 0.05) using 2-DE analysis. M S revealed the identity of these proteins to be ACAT2, HNRNPK, HSPD1, PGK1, PRDX6, VCL, VIM, TPI1, and IMPDH2. The first seven of these were reduced in expression. Western blot analysis confirmed the reduction in one of these proteins (HNRNPK), and that its levels were dependent on 26S proteasomal activity. Tandem affinity purification/MS revealed 14 potential

interactants of Parkin; CKB, DBT, HSPD1, HSPA9, LRPPRC, NDUFS2, PRDX6, SLC25A5, TPI1, UCHL1, UQCRC1, VCL, YWHAZ, YWHAE. Nine of these are directly involved in mitochondrial energy metabolism and glycolysis; four were also identified in the 2-DE study (HSP60, PRDX6, TPI1, and VCL). This study provides further evidence for a role for Parkin in regulating mitochondrial activity within cells.”
“BACKGROUND AND IMPORTANCE: Most neuroendovascular interventions rely on a transfemoral approach to the intracranial circulation; however, this is sometimes not possible because of complex aortic arch anatomy or femoral arterial disease. Transradial Erlotinib solubility dmso arteriography and intervention are well established in interventional cardiology, and there have been some reports of successful neurointervention using this technique. The incidence of radial artery occlusion or other access site complications after transradial access is directly related to the outer diameter of the sheath used to access the artery. We describe a novel approach to neuroendovascular intervention using a 070 Neuron guide catheter to directly access the radial artery for complex cerebrovascular intervention.

CLINICAL PRESENTATION: We describe a technique to directly access the radial artery with a 070 Neuron catheter, without the need for a large 6-French sheath, for cerebrovascular interventions. Two successful cases are described in which this technique was used.