Connection

Announcement

You can now add alternative names! Click here to add other names that you've published under.

Search Results to Vladimir Lupashin

This is a "connection" page, showing the details of why an item matched the keywords from your search.

Search Results

Lupashin, Vladimir

One or more keywords matched the following properties of Lupashin, Vladimir

Property

Value

overview

Our laboratory is interested in understanding the molecular mechanisms responsible for the generation and maintenance of intra-cellular membrane-bounded compartments. In all eukaryotic cells intracellular membrane trafficking is critical for a range of important cellular functions including protein secretion, post-translational modifications, cell signalling, cell polarization, and cell maintenance. Defects in membrane trafficking can underline, or even exacerbate, a number of human diseases including cancer, diabetes mellitus, Alzheimer’s, cystic fibrosis, Hermansky-Pudlak syndrome and Congenital Disorders of Glycosylation. Our research directed towards the understanding of the basic mechanisms of intracellular vesicular trafficking using both yeast and mammalian tissue culture cell model systems. Our lab played a principal role in the discovery of a novel vesicle tethering factors, published more than 60 original papers in high-profile journals, including Journal of Cell Biology, PNAS, Science, Journal of Neuroscience, Molecular Biology of Cell and Nature Communications. My current research has been continuously supported by grants from both NSF and NIH. We have pioneered the functional analysis of the Conserved Oligomeric Golgi (COG), an evolutionarily conserved complex of eight gene products, each of which is critical for the membrane trafficking and protein modifications in the Golgi apparatus. The COG complex interacts with core fusion machinery components including SNAREs, SM proteins, Rabs, coiled-coil tethers and COPI coat to organize specific docking and fusion of transport intermediates with their acceptor membrane. By using state of the art biochemical, genetic and microscopy approaches (including mass-spectrometry, electron and super-resolution microscopy, CRISPR directed gene editing techniques) we would like to determine how the key components of intracellular membrane trafficking machinery work together to direct efficient protein trafficking in human cells in health and disease.

One or more keywords matched the following items that are connected to Lupashin, Vladimir

Item Type	Name
Academic Article	Cog1p plays a central role in the organization of the yeast conserved oligomeric Golgi complex.
Academic Article	COG8 deficiency causes new congenital disorder of glycosylation type IIh.
Academic Article	Role of the conserved oligomeric Golgi (COG) complex in protein glycosylation.
Academic Article	Identification of a novel secreted glycoprotein of the yeast Saccharomyces cerevisiae stimulated by heat shock.
Academic Article	COG complex-mediated recycling of Golgi glycosyltransferases is essential for normal protein glycosylation.
Academic Article	Characterization of a novel yeast SNARE protein implicated in Golgi retrograde traffic.
Academic Article	Structural basis for a human glycosylation disorder caused by mutation of the COG4 gene.
Academic Article	Conserved oligomeric Golgi complex specifically regulates the maintenance of Golgi glycosylation machinery.
Academic Article	The Golgi puppet master: COG complex at center stage of membrane trafficking interactions.
Concept	Glycosylation
Concept	Congenital Disorders of Glycosylation
Academic Article	Mini-Review: Role of the Conserved Oligomeric Golgi (COG) complex in protein glycosylation
Academic Article	The COG Complex-mediated Docking of intra-Golgi Vesicles is Essential for Normal Protein Glycosylation
Academic Article	The COG complex interacts with the t-SNARE Syntaxin5 to direct trafficking of recyling intra-Golgi vesicles that is essential for normal protein glycosylation
Academic Article	The COG Complex-mediated Recyling of Golgi Enzymes is Essential for Normal Protein Glycosylation
Academic Article	Macromolecules in functioning cell
Academic Article	The role of glycosylation in protein secretion
Academic Article	Glycosylation of secreted proteins in yeast
Academic Article	COG lobe B sub-complex engages v-SNARE GS15 and functions via regulated interaction with lobe A sub-complex.
Academic Article	Creating Knockouts of Conserved Oligomeric Golgi Complex Subunits Using CRISPR-Mediated Gene Editing Paired with a Selection Strategy Based on Glycosylation Defects Associated with Impaired COG Complex Function.
Academic Article	Manganese-induced turnover of TMEM165.
Academic Article	Galactose Supplementation in Patients With TMEM165-CDG Rescues the Glycosylation Defects.
Academic Article	Conserved Oligomeric Golgi and Neuronal Vesicular Trafficking.
Academic Article	Membrane detachment is not essential for COG complex function.
Academic Article	More than just sugars: Conserved oligomeric Golgi complex deficiency causes glycosylation-independent cellular defects.
Academic Article	Detailed Analysis of the Interaction of Yeast COG Complex.
Grant	Characterization of mammalian COG complex-interacting Golgi trafficking machinery
Academic Article	Dissection of TMEM165 function in Golgi glycosylation and its Mn2+ sensitivity.
Academic Article	Fetal bovine serum impacts the observed N-glycosylation defects in TMEM165 KO HEK cells.
Academic Article	Conserved Oligomeric Golgi (COG) Complex Proteins Facilitate Orthopoxvirus Entry, Fusion and Spread.
Academic Article	Golgi inCOGnito: From vesicle tethering to human disease.
Academic Article	Proteoglycan synthesis in conserved oligomeric Golgi subunit deficient HEK293T cells is affected differently, depending on the lacking subunit.
Academic Article	The Golgi-associated retrograde protein (GARP) complex plays an essential role in the maintenance of the Golgi glycosylation machinery.
Academic Article	Getting Sugar Coating Right! The Role of the Golgi Trafficking Machinery in Glycosylation.
Academic Article	Rapid COG Depletion in Mammalian Cell by Auxin-Inducible Degradation System.
Academic Article	Acute COG complex inactivation unveiled its immediate impact on Golgi and illuminated the nature of intra-Golgi recycling vesicles.
Academic Article	A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation.
Academic Article	Biallelic missense variants in COG3 cause a congenital disorder of glycosylation with impairment of retrograde vesicular trafficking.

Search Criteria

Glycosylation