Quantitative Aspects of Receptor Aggregation

1994 ◽  
pp. 175-183 ◽  
Author(s):  
Henry Metzger ◽  
Byron Goldstein ◽  
Ute Kent ◽  
Su-Yau Mao ◽  
Clara Pribluda ◽  
...  
Keyword(s):  
Receptor Aggregation

scholarly journals Neuregulin Inhibits Acetylcholine Receptor Aggregation in Myotubes

2004 ◽  
Vol 279 (30) ◽  
pp. 31622-31628 ◽  
Author(s):  
Jonathan C. Trinidad ◽  
Jonathan B. Cohen
Keyword(s):  
Acetylcholine Receptor ◽  
Receptor Aggregation

scholarly journals Erratum: ETS Related Gene mediated Androgen Receptor Aggregation and Endoplasmic Reticulum Stress in Prostate Cancer Development

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Taduru L. Sreenath ◽  
Shiela S. Macalindong ◽  
Natallia Mikhalkevich ◽  
Shashwat Sharad ◽  
Ahmed Mohamed ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endoplasmic Reticulum ◽  
Androgen Receptor ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Development ◽  
Related Gene ◽  
Receptor Aggregation ◽  
Prostate Cancer Development

scholarly journals Major Histocompatibility Complex Class II Inhibits Fas Antigen-Mediated Gastric Mucosal Cell Apoptosis through Actin-Dependent Inhibition of Receptor Aggregation

2005 ◽  
Vol 73 (10) ◽  
pp. 6311-6321 ◽  
Author(s):  
Calin Stoicov ◽  
Xun Cai ◽  
Hanchen Li ◽  
Kristine Klucevsek ◽  
Jane Carlson ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Mucosal Cell ◽  
Complex Class ◽  
Gastric Mucosal Cells ◽  
Fas Antigen ◽  
Histocompatibility Complex ◽  
Receptor Aggregation ◽  
Mucosal Cells

ABSTRACT Escape from normal apoptotic controls is thought to be essential for the development of cancer. During Helicobacter pylori infection, the leading cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible for early atrophy and tissue loss. As disease progresses, metaplastic and dysplastic glands arise which express Fas Ag but are resistant to apoptosis and are believed to be the precursor cells for adenocarcinoma. In this report, we show that one mechanism of acquired Fas resistance is inhibition of receptor aggregation via a major histocompatibility complex class II (MHCII)-mediated, actin-dependent mechanism. For these studies we used the well-described C57BL/6 mouse model of Helicobacter pylori and Helicobacter felis infection. Under normal conditions, Fas Ag is expressed at low levels, and MHCII expression on gastric mucosal cells is negligible. With infection and inflammation, both receptors are upregulated, and 6.1% of gastric mucosal cells express MHCII in combination with Fas Ag. Using the rat gastric mucosal cell line RGM-1 transfected with murine Fas Ag and MHCIIαβ chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signaling through its effects on the actin cytoskeleton. Depolymerization of actin with cytochalasin D allows receptors to aggregate and restores Fas sensitivity. These findings offer one mechanism by which gastric mucosal cells acquire Fas resistance.

scholarly journals Receptor aggregation induced by antilutropin receptor antibody and biological response in rat testis Leydig cells.

1983 ◽  
Vol 80 (13) ◽  
pp. 3986-3990 ◽  
Author(s):  
E. J. Podesta ◽  
A. R. Solano ◽  
R. Attar ◽  
M. L. Sanchez ◽  
L. Molina y Vedia
Keyword(s):  
Leydig Cells ◽  
Biological Response ◽  
Receptor Antibody ◽  
Rat Testis ◽  
Receptor Aggregation

scholarly journals Laminin induces acetylcholine receptor aggregation on cultured myotubes and enhances the receptor aggregation activity of a neuronal factor

1983 ◽  
Vol 3 (5) ◽  
pp. 1058-1068 ◽  
Author(s):  
Z Vogel ◽  
CN Christian ◽  
M Vigny ◽  
HC Bauer ◽  
P Sonderegger ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Receptor Aggregation ◽  
Cultured Myotubes ◽  
Aggregation Activity

Adhesion of Lipid Membranes Mediated by Electrostatic and Specific Interactions

1997 ◽  
Vol 489 ◽  
Author(s):  
Christian W. Maier ◽  
Almuth Behrisch ◽  
Annette Kloboucek ◽  
Rudolf Merkel
Keyword(s):  
Lipid Membranes ◽  
Cell Adhesion Molecule ◽  
Lipid Vesicles ◽  
Membrane Properties ◽  
Specific Cell ◽  
Receptor Aggregation ◽  
Host Membrane ◽  
Aspiration Technique ◽  
Membrane Adhesion ◽  
Positively Charged

AbstractWe used the micropipet aspiration technique for a study of biomembrane adhesion. Adhesion was caused by contact site A, a highly specific cell adhesion molecule, reconstituted in lipid vesicles of DOPC with 5 %(mol/mol) DOPE-PEG2000. We found adhesion and subsequent receptor aggregation in the contact zone. Additionally, electrostatic modulation of membrane adhesion was studied. Whereas addition of the negatively charged lipid SOPS to the lecithin (SOPC) host membrane suppressed adhesion due to electrostatic repulsion, a positively charged lipid (DOTAP) was surprisingly ineffective. This might be due to either phase separation of the mixture or DOTAP changing other membrane properties as bending stiffness and the Hamaker constant.

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