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Rabbit Anti-Human Von Willebrand Factor Polyclonal Antibody, HRP Conjugated

RRID:AB_579516

Antibody ID

AB_579516

Target Antigen

Human Von Willebrand Factor human

Proper Citation

(Agilent Cat# P022602, RRID:AB_579516)

Clonality

polyclonal antibody

Comments

Applications: ELISA, Western Blot, Blot,ELISA. Original Manufacturer: Dako. Now part of Agilent.

Host Organism

rabbit

Vendor

Agilent

Cat Num

P022602

Publications that use this research resource

Elucidation of the anti-autophagy mechanism of the Legionella effector RavZ using semisynthetic LC3 proteins.

  • Yang A
  • Elife
  • 2017 Apr 11

Literature context: P022602, RRID:AB_579516) and anti-


Abstract:

Autophagy is a conserved cellular process involved in the elimination of proteins and organelles. It is also used to combat infection with pathogenic microbes. The intracellular pathogen Legionella pneumophila manipulates autophagy by delivering the effector protein RavZ to deconjugate Atg8/LC3 proteins coupled to phosphatidylethanolamine (PE) on autophagosomal membranes. To understand how RavZ recognizes and deconjugates LC3-PE, we prepared semisynthetic LC3 proteins and elucidated the structures of the RavZ:LC3 interaction. Semisynthetic LC3 proteins allowed the analysis of structure-function relationships. RavZ extracts LC3-PE from the membrane before deconjugation. RavZ initially recognizes the LC3 molecule on membranes via its N-terminal LC3-interacting region (LIR) motif. The RavZ ╬▒3 helix is involved in extraction of the PE moiety and docking of the acyl chains into the lipid-binding site of RavZ that is related in structure to that of the phospholipid transfer protein Sec14. Thus, Legionella has evolved a novel mechanism to specifically evade host autophagy.

Abnormal hemostatic function one year after orthotopic liver transplantation can be fully attributed to endothelial cell activation.

  • Arshad F
  • F1000Res
  • 2014 Oct 8

Literature context: of A0082 (RRID:AB_579516), DAKO, Gl


Abstract:

BACKGROUND: The long-term risk of thrombotic and vascular complications is elevated in liver transplant recipients compared to the general population. Patients with cirrhosis are in a hypercoagulable status during and directly after orthotopic liver transplantation, but it is unclear whether this hypercoagulability persists over time. AIM: We aimed to investigate the hemostatic status of liver transplant recipients one year after transplantation. METHODS: We prospectively collected blood samples of 15 patients with a functioning graft one year after orthotopic liver transplantation and compared the hemostatic status of these patients with that of 30 healthy individuals. RESULTS: Patients one year after liver transplantation had significantly elevated plasma levels of von Willebrand factor (VWF). Thrombin generation, as assessed by the endogenous thrombin potential, was decreased in patients, which was associated with increased plasma levels of the natural anticoagulants antithrombin and tissue factor pathway inhibitor.  Plasma fibrinolytic potential was significantly decreased in patients and correlated inversely with levels of plasminogen activator inhibitor-1. CONCLUSION: One year after liver transplantation, liver graft recipients have a dysregulated hemostatic system characterised by elevation of plasma levels of endothelial-derived proteins. Increased levels of von Willebrand factor and decreased fibrinolytic potential may (in part) be responsible for the increased risk for vascular disease seen in liver transplant recipients.