Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0065-2571(02)00028-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Apolipoprotein-L Functions in Membrane Remodeling.
Cells
December 2024
Laboratory of Molecular Parasitology, Institut de Biologie et de Médecine Moléculaires (IBMM), Université Libre de Bruxelles, 6041 Gosselies, Belgium.
The mammalian Apolipoprotein-L families (APOLs) contain several isoforms of membrane-interacting proteins, some of which are involved in the control of membrane dynamics (traffic, fission and fusion). Specifically, human APOL1 and APOL3 appear to control membrane remodeling linked to pathogen infection. Through its association with Non-Muscular Myosin-2A (NM2A), APOL1 controls Golgi-derived trafficking of vesicles carrying the lipid scramblase Autophagy-9A (ATG9A).
View Article and Find Full Text PDFMeasurement of ORP10-Mediated Lipid Countertransport at ER-Endosome Membrane Contact Sites via a Chemically Induced Dimerization Strategy.
Methods Mol Biol
December 2024
Department of Neurochemistry and Molecular Cell Biology, Niigata University School of Medicine and Graduate School of Medical/Dental Sciences, Niigata, Japan.
Oxysterol-binding protein (OSBP)-related proteins (ORPs) are a large family of lipid transfer proteins (LTPs) in mammals. ORPs mediate the countertransport of two distinct lipids at membrane contact sites (MCSs). ORP10 is localized via binding to ORP9 at the endoplasmic reticulum (ER)-endosome MCSs, where it mediates countertransport of phosphatidylinositol 4-phosphate (PI4P) and phosphatidylserine (PS).
View Article and Find Full Text PDFDysregulation of PI4P in the trans Golgi regions activates the mammalian Golgi stress response.
J Biol Chem
December 2024
Department of Molecular Biochemistry, Graduate School of Science, University of Hyogo, Ako, Hyogo, Japan. Electronic address:
The Golgi stress response is an important cytoprotective system that enhances Golgi function in response to cellular demand, while cells damaged by prolonged Golgi stress undergo cell death. OSW-1, a natural compound with anticancer activity, potently inhibits OSBP that transports cholesterol and phosphatidylinositol-4-phosphate (PI4P) at contact sites between the endoplasmic reticulum and the Golgi apparatus. Previously, we reported that OSW-1 induces the Golgi stress response, resulting in Golgi stress-induced transcription and cell death.
View Article and Find Full Text PDFARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network.
Nat Commun
November 2024
Division of Neurosciences and Cellular Structure, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
ARL5 is a member of the ARF family of small GTPases that is recruited to the trans-Golgi network (TGN) by another ARF-family member, ARFRP1, in complex with the transmembrane protein SYS1. ARL5 recruits its effector, the multisubunit tethering complex GARP, to promote SNARE-dependent fusion of endosome-derived retrograde transport carriers with the TGN. To further investigate the function of ARL5, we sought to identify additional effectors.
View Article and Find Full Text PDFPck2 association with the plasma membrane and efficient response of the cell integrity pathway require regulation of PI4P homeostasis by exomer.
Open Biol
November 2024
Departamento de Microbiología y Genética, Universidad de Salamanca, Salamanca 37007, Spain.
Exomer is a protein complex that facilitates trafficking between the Golgi and the plasma membrane (PM). exomer is composed of Cfr1 and Bch1, and we have found that full activation of the cell integrity pathway (CIP) in response to osmotic stress requires exomer. In the wild-type, the CIP activators Rgf1 (Rho1 GEF) and Pck2 (PKC homologue) and the MEK kinase Mkh1 localize in the PM, internalize after osmotic shock and re-localize after adaptation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!