Poly (ADP-ribose) polymerase inhibitors selectively induce cytotoxicity in TCF3-HLF-positive leukemic cells.

Poly (ADP-ribose) polymerase (PARP) is an indispensable component of the DNA repair machinery. PARP inhibitors are used as cutting-edge treatments for patients with homologous recombination repair (HRR)-defective breast cancers harboring mutations in BRCA1 or BRCA2. Other tumors defective in HRR, including some hematological malignancies, are predicted to be good candidates for treatment with PARP inhibitors.

Estimation of conditions evoking fracture in finger bones under pinch loading based on finite element analysis.

A finger finite element (FE) model was created from CT images of a Japanese male in order to obtain a shape-biofidelic model. Material properties and articulation characteristics of the model were taken from the literature. To predict bone fracture and realistically represent the fracture pattern under various loading conditions, the ESI-Wilkins-Kamoulakos rupture model in PAM-CRASH (ESI Group S.

Caspase-mediated protein kinase C-delta cleavage is necessary for apoptosis of vascular smooth muscle cells.

Apoptotic death of vascular smooth muscle cells (SMCs) is a prominent feature of blood vessel remodeling and various vascular diseases. We have previously shown that protein kinase C-delta (PKC-delta) plays a critical role in SMC apoptosis. In this study, we tested the importance of PKC-delta proteolytic cleavage and tyrosine phosphorylation within the apoptosis pathway.

Protein kinase C delta activated adhesion regulates vascular smooth muscle cell migration.

Background: Vascular smooth muscle cell (VSMC) migration, fundamental in the pathophysiology of atherogenesis and restenosis, is a coordinated process governed by the formation and disassembly of focal adhesions. Previous studies have demonstrated that VSMC migration is regulated via a signaling network involving protein kinase C delta (PKCdelta). In these studies, we test the hypothesis that PKCdelta regulates VSMC migration through modulation of cell adhesion.

Phosphorylation of the cyclic AMP response element binding protein mediates transforming growth factor beta-induced downregulation of cyclin A in vascular smooth muscle cells.

Transforming growth factor beta (TGFbeta), a multifunctional cytokine associated with vascular injury, is a potent inhibitor of cell proliferation. The current results demonstrate that the TGFbeta-induced growth arrest of vascular smooth muscle cells (VSMCs) is associated with cyclin A downregulation. TGFbeta represses the cyclin A gene through a cyclic AMP (cAMP) response element, which complexes with the cAMP response element binding protein (CREB).

Protein kinase C-delta regulates migration and proliferation of vascular smooth muscle cells through the extracellular signal-regulated kinase 1/2.

Background: Smooth muscle cell (SMC) migration and proliferation are early and crucial events in the pathogenesis of intimal hyperplasia, the primary cause of restenosis after vascular intervention. We tested the hypothesis that protein kinase C-delta (PKCdelta), a ubiquitously expressed intracellular protein kinase, regulates vascular SMC proliferation and migration.

Methods: Exogenous PKCdelta was expressed in cultured SMCs via stable transfection or adenovirus-mediated gene transfer.

Dwarfism and cytochrome P450-mediated C-6 oxidation of plant steroid hormones.

BRs (brassinosteroids) are plant steroid hormones that are essential for normal plant development. The dramatic dwarfism exhibited by mutants in the CYP (cytochrome P450) enzymes involved in BR biosynthesis indicates a role for these hormones in plant growth and development. Since the mid-1990s, collaborative research has been geared towards developing a better understanding of the CYP85 class of CYPs involved in BR biosynthesis in both Arabidopsis and tomato.