Human MutY homolog, a DNA glycosylase involved in base excision repair, physically and functionally interacts with mismatch repair proteins human MutS homolog 2/human MutS homolog 6.
Authors Gu Yesong; Parker Antony; Wilson Teresa M; Bai Haibo; Chang Dau-Yin; Lu A-Lien;
JournalJ Biol Chem
PubMed ID11801590
Adenines mismatched with guanines or 7,8-dihydro-8-oxo-deoxyguanines that arise through DNA replication errors can be repaired by either base excision repair or mismatch repair. The human MutY homolog (hMYH), a DNA glycosylase, removes adenines from these mismatches. Human MutS homologs, hMSH2/hMSH6 (hMutSalpha), bind to the mismatches and initiate the repair on ... More
Stimulation of neuronal neurite outgrowth using functionalized carbon nanotubes.
AuthorsMatsumoto K, Sato C, Naka Y, Whitby R, Shimizu N
JournalNanotechnology
PubMed ID20173239
Low concentrations (0.11-1.7 microg ml(-1)) of functionalized carbon nanotubes (CNTs), which are multi-walled CNTs modified by amino groups, when added with nerve growth factor (NGF), promoted outgrowth of neuronal neurites in dorsal root ganglion (DRG) neurons and rat pheochromocytoma cell line PC12h cells in culture media. The quantity of active ... More
Dystrophin deficiency markedly increases enterovirus-induced cardiomyopathy: a genetic predisposition to viral heart disease.
Authors Xiong Dingding; Lee Gil-Hwan; Badorff Cornel; Dorner Andrea; Lee Sang; Wolf Paul; Knowlton Kirk U;
JournalNat Med
PubMed ID12118246
Both enteroviral infection of the heart and mutations in the dystrophin gene can cause cardiomyopathy. Little is known, however, about the interaction between genetic and acquired forms of cardiomyopathy. We previously demonstrated that the enteroviral protease 2A cleaves dystrophin; therefore, we hypothesized that dystrophin deficiency would predispose to enterovirus-induced cardiomyopathy. ... More
The Slp homology domain of synaptotagmin-like proteins 1-4 and Slac2 functions as a novel Rab27A binding domain.
rab27A, which encodes a small GTP-binding protein, was recently identified as a gene in which mutations caused human hemophagocytic syndrome (Griscelli syndrome) and ashen mice, which exhibit defects in melanosome transport as well as in regulated granule exocytosis in cytotoxic T lymphocytes. However, little is known about the molecular mechanism ... More
Role for 18:1 lysophosphatidic acid as an autocrine mediator in prostate cancer cells.
AuthorsXie Y, Gibbs TC, Mukhin YV, Meier KE.
JournalJ Biol Chem
PubMed ID12084719
Lysophosphatidic acid (LPA) is a lipid mediator that may play an important role in growth and survival of carcinomas. In this study, LPA production and response were characterized in two human prostate cancer (CaP) cell lines: PC-3 and Du145. Bombesin, a neuroendocrine peptide that is mitogenic for CaP cells, stimulated ... More