Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg, Würzburg, Germany.
Published: November 2009
AI Article Synopsis
Article Abstract
Proteins of the Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) family link signal transduction pathways to actin cytoskeleton dynamics. VASP is substrate of cAMP-dependent, cGMP-dependent and AMP-activated protein kinases that primarily phosphorylate the sites S157, S239 and T278, respectively. Here, we systematically analyzed functions of VASP phosphorylation patterns for actin assembly and subcellular targeting in vivo and compared the phosphorylation effects of Ena/VASP family members. Methods used were the reconstitution of VASP-null cells with ;locked' phosphomimetic VASP mutants, actin polymerization of VASP mutants in vitro and in living cells, site-specific kinase-mediated VASP phosphorylation, and analysis of the endogenous protein with phosphorylation-status-specific antibodies. Phosphorylation at S157 influenced VASP localization, but had a minor impact on F-actin assembly. Phosphorylation of the S157-equivalent site in the Ena/VASP family members Mena and EVL had no effect on the ratio of cellular F-actin to G-actin. By contrast, VASP phosphorylation at S239 (and the equivalent site in Mena) or T278 impaired VASP-driven actin filament formation. The data show that VASP functions are precisely regulated by differential phosphorylation and provide new insights into cytoskeletal control by serine/threonine kinase-dependent signaling pathways.
UCD School of Medicine, UCD Conway Institute, University College Dublin, Dublin 4, Belfield, Ireland; Irish Centre for Vascular Biology, Royal College of Surgeons in Ireland, 123 St Stephen's Green, Dublin D02 YN77, Ireland. Electronic address:
Hypochlorous acid (HOCl), made by neutrophil-derived myeloperoxidase, has been suggested to inhibit platelets, however, the mechanisms involved have not been described. Here we confirm that HOCl exposure changes platelet morphology and inhibits platelet spreading and aggregation. HOCl effects could be reversed by glutathione suggesting a role for cysteine oxidation.
Purpose: Exercise has been shown to reduce platelet reactivity and increase platelet sensitivity to prostacyclin, an endothelium-derived inhibitor of platelet activation, in middle-aged men and women. It is currently unknown if these beneficial effects can also be observed in young women and the intracellular mechanisms involved have not been identified. In this study, the feasibility of detecting changes in platelet reactivity, prostacyclin sensitivity and cAMP signalling were tested.
Rhodium(III) complexes have gained attention for their anticancer potential. In this study, we investigated a rhodium(III) bipyridylsulfonamide complex () and its ligand () for their effects on breast cancer (SKBr3) and noncancerous mammary cells (HB2). Both compounds significantly reduced oxidative phosphorylation (OXPHOS) and mitochondrial function in SKBr3 cells while sparing HB2 cells.
Background & Aims: Transforming growth factor (TGF)β1 induces plasma membrane (PM) accumulation of glucose transporter 1 (Glut1) required for glycolysis of hepatic stellate cells (HSCs) and HSC activation. This study aimed to understand how Glut1 is anchored/docked onto the PM of HSCs.
Methods: HSC expression of protein kinase M zeta isoform (PKMζ) was detected by reverse transcription polymerase chain reaction (RT-PCR), Western blotting, and immunofluorescence.
Department of Urology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China; Institute of Urology, Anhui Medical University, Hefei, Anhui, China; Anhui Provincial Key Laboratory of Urological and Andrological Diseases Research and Medical Transformation, Hefei, Anhui, China. Electronic address:
This study investigates the role of autophagy-related genes (ARGs) in bladder cancer (BLCA), focusing on the regulator of G protein signaling 19 (RGS19). Using data from The Cancer Genome Atlas (TCGA) and the Human Autophagy Database (HADb), we identified RGS19 as significantly upregulated and linked to poor prognosis in BLCA. Kaplan-Meier survival analysis confirmed its association with increased mortality and.
