scholarly journals Mathematical Simulation of Membrane Protein Clustering for Efficient Signal Transduction

2012 ◽  
Vol 40 (11) ◽  
pp. 2307-2318 ◽  
Author(s):  
Krishnan Radhakrishnan ◽  
Ádám Halász ◽  
Meghan M. McCabe ◽  
Jeremy S. Edwards ◽  
Bridget S. Wilson
Keyword(s):  
Signal Transduction ◽  
Membrane Protein ◽  
Mathematical Simulation ◽  
Protein Clustering ◽  
Membrane Protein Clustering

scholarly journals Stability Analysis of a Bulk–Surface Reaction Model for Membrane Protein Clustering

2020 ◽  
Vol 82 (2) ◽  
Author(s):  
Lucas M. Stolerman ◽  
Michael Getz ◽  
Stefan G. Llewellyn Smith ◽  
Michael Holst ◽  
Padmini Rangamani
Keyword(s):  
Stability Analysis ◽  
Membrane Protein ◽  
Surface Reaction ◽  
Reaction Model ◽  
Protein Clustering ◽  
Bulk Surface ◽  
Membrane Protein Clustering ◽  
Surface Reaction Model

scholarly journals Lipid Composition Modulates Membrane Protein Clustering

2016 ◽  
Vol 110 (3) ◽  
pp. 81a
Author(s):  
Anna L. Duncan ◽  
Heidi Koldsø ◽  
Tyler Reddy ◽  
Jean Helie ◽  
Mark S.P. Sansom
Keyword(s):  
Membrane Protein ◽  
Lipid Composition ◽  
Protein Clustering ◽  
Membrane Protein Clustering

scholarly journals The packing density of a supramolecular membrane protein cluster is controlled by cytoplasmic interactions

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Elisa Merklinger ◽  
Jan-Gero Schloetel ◽  
Pascal Weber ◽  
Helena Batoulis ◽  
Sarah Holz ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Membrane Protein ◽  
Protein Interactions ◽  
Cluster Size ◽  
Protein Domain ◽  
Self Organization ◽  
Cytoplasmic Protein ◽  
Transmembrane Segment ◽  
Protein Clustering ◽  
Membrane Protein Clustering

Molecule clustering is an important mechanism underlying cellular self-organization. In the cell membrane, a variety of fundamentally different mechanisms drive membrane protein clustering into nanometre-sized assemblies. To date, it is unknown whether this clustering process can be dissected into steps differentially regulated by independent mechanisms. Using clustered syntaxin molecules as an example, we study the influence of a cytoplasmic protein domain on the clustering behaviour. Analysing protein mobility, cluster size and accessibility to myc-epitopes we show that forces acting on the transmembrane segment produce loose clusters, while cytoplasmic protein interactions mediate a tightly packed state. We conclude that the data identify a hierarchy in membrane protein clustering likely being a paradigm for many cellular self-organization processes.

Modulated red blood cell survival by membrane protein clustering

1995 ◽  
Vol 144 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Laura Chiarantini ◽  
Luigia Rossi ◽  
Alessandra Fraternale ◽  
Mauro Magnani
Keyword(s):  
Membrane Protein ◽  
Blood Cell ◽  
Cell Survival ◽  
Red Blood Cell ◽  
Protein Clustering ◽  
Membrane Protein Clustering

scholarly journals Independent membrane protein clustering

2007 ◽  
Vol 178 (7) ◽  
pp. 1096-1096
Author(s):  
Nicole LeBrasseur
Keyword(s):  
Membrane Protein ◽  
Protein Clustering ◽  
Membrane Protein Clustering

scholarly journals Leukocyte response integrin and integrin-associated protein act as a signal transduction unit in generation of a phagocyte respiratory burst.

1993 ◽  
Vol 178 (4) ◽  
pp. 1165-1174 ◽  
Author(s):  
M Zhou ◽  
E J Brown
Keyword(s):  
Signal Transduction ◽  
Membrane Protein ◽  
Respiratory Burst ◽  
Kinase Inhibitors ◽  
Solid Phase ◽  
Enhanced Sensitivity ◽  
Basement Membrane Protein ◽  
Coated Surfaces ◽  
Leukocyte Response ◽  
Distinct Membrane

The leukocyte response integrin (LRI) is a phagocyte integrin which recognizes the basement membrane protein entactin and the synthetic peptide Lys-Gly-Ala-Gly-Asp-Val (KGAGDV). The function of LRI is intimately associated with that of a distinct membrane protein, integrin-associated protein (IAP), as antibodies which recognizes IAP can inhibit all known functions of LRI. When adherent to surface, the LRI ligands entactin and KGAGDV activate the respiratory burst in polymorphonuclear leukocytes (PMN) and monocytes, as do monoclonal antibodies (mAb) directed at either LRI or IAP. When added in solution, peptides and antibodies specific for LRI, and some, but not all, anti-IAP antibodies, can inhibit the respiratory burst activated by any of these surface-adherent ligands. Only monoclonal anti-IAP antibodies which can inhibit LRI function when added in solution are competent to activate the respiratory burst when adherent to a surface. KGAGDV peptide and anti-LRI added in solution can inhibit anti-IAP-stimulated respiratory burst. The LRI-IAP-initiated respiratory burst is independent of CD18, as judged by: (a) blockade of inhibition by anti-CD18 mAb with the protein kinase A inhibitor HA1004; (b) enhanced sensitivity of CD18-dependent respiratory burst compared with LRI/IAP-dependent respiratory burst to the tyrosine kinase inhibitors genestein and herbimicin; and (c) generation of a respiratory burst in response to KGAGDV, anti-LRI, and anti-IAP coated surfaces in PMN from a patient with LAD. Despite its apparent CD18 independence, LRI/IAP-initiated respiratory burst requires a solid phase ligand and is sensitive to cytochalasin B. These data suggest a model in which LRI and IAP act together as a single signal transduction unit to activate the phagocyte respiratory burst, in a manner that requires CD18-independent cell adhesion.

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