scholarly journals Analytical investigation of non-Fickian receptor-mediated endocytosis

2019 ◽  
Author(s):  
Milad Rismanian ◽  
Behzad Damirchi
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Lipid Bilayer ◽  
Animal Cell ◽  
Analytical Investigation ◽  
Maximum Diameter ◽  
Host Cell Membrane ◽  
Critical Limit ◽  
Target Molecule ◽  
Receptor Mediated Endocytosis

AbstractThe most important process in which viruses and bioparticles can enter the animal cell is receptor mediated endocytosis. The main propellant of this phenomenon is the attraction between receptor molecules floating in the lipid bilayer membrane of the host cell and ligand molecules on the target. In this paper, the aforementioned phenomenon is investigated analytically assuming that the diffusion model of the receptor molecules in the lipid bilayer is non-Fickian. Penetration time of the target molecule in the host cell shows that there is a critical limit for the target molecule size. The molecules larger than this critical size will experience an oscillatory motion without passing the host cell membrane. For instance, it is found that the maximum diameter for a typical target molecule with dimensionless relaxation time of 5 for receptor diffusion into a cell membrane is 0.22 of the membrane length.

scholarly journals Statin Drug Therapy May Increase COVID-19 Infection

2020 ◽  
Vol 3 (1) ◽  
pp. 326-327 ◽  
Author(s):  
Sanjaya Kumar Shrestha
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Mevalonate Pathway ◽  
No Production ◽  
Host Cell Membrane ◽  
Enveloped Viruses ◽  
Receptor Mediated Endocytosis ◽  
Key Enzyme ◽  
Statin Drug

Enveloped viruses like Coronavirus acquire their envelope from the host cell membrane which is a bilayer of phospholipid interspersed with cholesterol molecules and proteins. Viruses enter their host cell by coming in contact with their specific receptors. Experiments have shown that when cell membranes are depleted of cholesterol in vitro by Methyl beta cyclodextrin (MβCD) these Coronaviruses are not able to enter the host cell membrane by the process of receptor mediated endocytosis. Statin inhibits HMG Co-A reductase, a key enzyme in the Mevalonate pathway resulting into either very low or no production of endogenous cholesterol by the human cells. This results into upregulation of LDL-R in the cell membrane which may lead to more cholesterol getting incorporated into the cell membrane through LDL-C from the plasma creating greater number of lipid rafts suitable for entry of enveloped viruses by receptor-mediated endocytosis.

scholarly journals Exaptation of Retroviral Syncytin for Development of Syncytialized Placenta, Its Limited Homology to the SARS-CoV-2 Spike Protein and Arguments against Disturbing Narrative in the Context of COVID-19 Vaccination

Biology ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 238
Author(s):  
Malgorzata Kloc ◽  
Ahmed Uosef ◽  
Jacek Z. Kubiak ◽  
Rafik M. Ghobrial
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Envelope Glycoprotein ◽  
Mammalian Species ◽  
Viral Envelope ◽  
Spike Protein ◽  
Mammalian Evolution ◽  
Trophoblast Cells ◽  
Host Cell Membrane ◽  
Uterine Endometrium

Human placenta formation relies on the interaction between fused trophoblast cells of the embryo with uterine endometrium. The fusion between trophoblast cells, first into cytotrophoblast and then into syncytiotrophoblast, is facilitated by the fusogenic protein syncytin. Syncytin derives from an envelope glycoprotein (ENV) of retroviral origin. In exogenous retroviruses, the envelope glycoproteins coded by env genes allow fusion of the viral envelope with the host cell membrane and entry of the virus into a host cell. During mammalian evolution, the env genes have been repeatedly, and independently, captured by various mammalian species to facilitate the formation of the placenta. Such a shift in the function of a gene, or a trait, for a different purpose during evolution is called an exaptation (co-option). We discuss the structure and origin of the placenta, the fusogenic and non-fusogenic functions of syncytin, and the mechanism of cell fusion. We also comment on an alleged danger of the COVID-19 vaccine based on the presupposed similarity between syncytin and the SARS-CoV-2 spike protein.

scholarly journals Intracellular host cell membrane remodelling induced by SARS‐CoV‐2 infection in vitro

2021 ◽  
Author(s):  
Lucio Ayres Caldas ◽  
Fabiana Avila Carneiro ◽  
Fabio Luis Monteiro ◽  
Ingrid Augusto ◽  
Luiza Mendonça Higa ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Host Cell Membrane

scholarly journals The Photorhabdus asymbiotica virulence cassettes deliver protein effectors directly into target eukaryotic cells

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Isabella Vlisidou ◽  
Alexia Hapeshi ◽  
Joseph RJ Healey ◽  
Katie Smart ◽  
Guowei Yang ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Small Molecule ◽  
Rho Gtpase ◽  
Eukaryotic Cells ◽  
Host Cell Membrane ◽  
Western Blots ◽  
Insect Pathogen ◽  
Protein Toxins ◽  
Delivery Mechanism

Photorhabdus is a highly effective insect pathogen and symbiont of insecticidal nematodes. To exert its potent insecticidal effects, it elaborates a myriad of toxins and small molecule effectors. Among these, the Photorhabdus Virulence Cassettes (PVCs) represent an elegant self-contained delivery mechanism for diverse protein toxins. Importantly, these self-contained nanosyringes overcome host cell membrane barriers, and act independently, at a distance from the bacteria itself. In this study, we demonstrate that Pnf, a PVC needle complex associated toxin, is a Rho-GTPase, which acts via deamidation and transglutamination to disrupt the cytoskeleton. TEM and Western blots have shown a physical association between Pnf and its cognate PVC delivery mechanism. We demonstrate that for Pnf to exert its effect, translocation across the cell membrane is absolutely essential.

scholarly journals Membrane and luminal proteins reach the apicoplast by different trafficking pathways in the malaria parasite Plasmodium falciparum

2017 ◽  
Author(s):  
Rahul Chaudhari ◽  
Vishakha Dey ◽  
Aishwarya Narayan ◽  
Shobhona Sharma ◽  
Swati Patankar
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Membrane ◽  
Membrane Protein ◽  
Host Cell ◽  
G Protein ◽  
Secretory Pathway ◽  
Protein Targeting ◽  
Acyl Carrier Protein ◽  
Secretory Proteins ◽  
Host Cell Membrane

The secretory pathway in Plasmodium falciparum has evolved to transport proteins to the host cell membrane and to an endosymbiotic organelle, the apicoplast. The latter can occur via the ER or the ER-Golgi route. Here, we study these three routes using proteins Erythrocyte Membrane Protein-1 (PfEMP1), Acyl Carrier Protein (ACP) and glutathione peroxidase-like thioredoxin peroxidase (PfTPxGl) and inhibitors of vesicular transport. As expected, the G protein dependent vesicular fusion inhibitor AlF4- and microtubule destabilizing drug vinblastine block the trafficking of PfEMP-1, a protein secreted to the host cell membrane. However, while both PfTPxGl and ACP are targeted to the apicoplast, only ACP trafficking remains unaffected by these treatments. This implies that G-protein dependent vesicles do not play a role in classical apicoplast protein targeting. Unlike the soluble protein ACP, we show that PfTPxGl is localized to the outermost membrane of the apicoplast. Thus, the parasite apicoplast acquires proteins via two different pathways: first, the vesicular trafficking pathway appears to handle not only secretory proteins, but an apicoplast membrane protein, PfTPxGl. Second, trafficking of apicoplast luminal proteins appear to be independent of G-protein coupled vesicles.

scholarly journals Membrane and luminal proteins reach the apicoplast by different trafficking pathways in the malaria parasite Plasmodium falciparum

2017 ◽  
Author(s):  
Rahul Chaudhari ◽  
Vishakha Dey ◽  
Aishwarya Narayan ◽  
Shobhona Sharma ◽  
Swati Patankar
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Membrane ◽  
Membrane Protein ◽  
Host Cell ◽  
G Protein ◽  
Secretory Pathway ◽  
Protein Targeting ◽  
Acyl Carrier Protein ◽  
Secretory Proteins ◽  
Host Cell Membrane

The secretory pathway in Plasmodium falciparum has evolved to transport proteins to the host cell membrane and to an endosymbiotic organelle, the apicoplast. The latter can occur via the ER or the ER-Golgi route. Here, we study these three routes using proteins Erythrocyte Membrane Protein-1 (PfEMP1), Acyl Carrier Protein (ACP) and glutathione peroxidase-like thioredoxin peroxidase (PfTPxGl) and inhibitors of vesicular transport. As expected, the G protein dependent vesicular fusion inhibitor AlF4- and microtubule destabilizing drug vinblastine block the trafficking of PfEMP-1, a protein secreted to the host cell membrane. However, while both PfTPxGl and ACP are targeted to the apicoplast, only ACP trafficking remains unaffected by these treatments. This implies that G-protein dependent vesicles do not play a role in classical apicoplast protein targeting. Unlike the soluble protein ACP, we show that PfTPxGl is localized to the outermost membrane of the apicoplast. Thus, the parasite apicoplast acquires proteins via two different pathways: first, the vesicular trafficking pathway appears to handle not only secretory proteins, but an apicoplast membrane protein, PfTPxGl. Second, trafficking of apicoplast luminal proteins appear to be independent of G-protein coupled vesicles.

scholarly journals Interaction between Filovirus Proteins and Host Cell Membrane

MEMBRANE ◽  
2005 ◽  
Vol 30 (2) ◽  
pp. 68-72
Author(s):  
Ayato Takada ◽  
Takeshi Noda ◽  
Yoshihiro Kawaoka
Keyword(s):  
Cell Membrane ◽  
Host Cell ◽  
Host Cell Membrane
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