Progesterone receptor‐Src kinase signaling pathway mediates neuroprogesterone induction of the luteinizing hormone surge in female rats

2021 ◽  
Author(s):  
Timbora Chuon ◽  
Micah Feri ◽  
Claire Carlson ◽  
Sharity Ondrejik ◽  
Paul Micevych ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Progesterone Receptor ◽  
Signaling Pathway ◽  
Src Kinase ◽  
Female Rats ◽  
Kinase Signaling ◽  
Luteinizing Hormone Surge ◽  
Kinase Signaling Pathway

scholarly journals Cortactin-Src Kinase Signaling Pathway Is Involved in N-syndecan-dependent Neurite Outgrowth

1998 ◽  
Vol 273 (17) ◽  
pp. 10702-10708 ◽  
Author(s):  
Tarja Kinnunen ◽  
Marko Kaksonen ◽  
Juhani Saarinen ◽  
Nisse Kalkkinen ◽  
H. Benjamin Peng ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Signaling Pathway ◽  
Src Kinase ◽  
Kinase Signaling ◽  
Kinase Signaling Pathway

scholarly journals Endothelial Cell-Surface Gp60 Activates Vesicle Formation and Trafficking via Gi-Coupled Src Kinase Signaling Pathway

2000 ◽  
Vol 150 (5) ◽  
pp. 1057-1070 ◽  
Author(s):  
Richard D. Minshall ◽  
Chinnaswamy Tiruppathi ◽  
Stephen M. Vogel ◽  
Walter D. Niles ◽  
Annette Gilchrist ◽  
...  
Keyword(s):  
Hydraulic Conductivity ◽  
Cell Surface ◽  
Signaling Pathway ◽  
Src Kinase ◽  
Dominant Negative ◽  
Vesicle Formation ◽  
Kinase Signaling ◽  
Caveolin 1 ◽  
Endocytic Vesicles ◽  
Kinase Signaling Pathway

We tested the hypothesis that the albumin-docking protein gp60, which is localized in caveolae, couples to the heterotrimeric GTP binding protein Gi, and thereby activates plasmalemmal vesicle formation and the directed migration of vesicles in endothelial cells (ECs). We used the water-soluble styryl pyridinium dye N-(3-triethylaminopropyl)-4-(p-dibutylaminostyryl) pyridinium dibromide (FM 1-43) to quantify vesicle trafficking by confocal and digital fluorescence microscopy. FM 1-43 and fluorescently labeled anti-gp60 antibody (Ab) were colocalized in endocytic vesicles within 5 min of gp60 activation. Vesicles migrated to the basolateral surface where they released FM 1-43, the fluid phase styryl probe. FM 1-43 fluorescence disappeared from the basolateral EC surface without the loss of anti-gp60 Ab fluorescence. Activation of cell-surface gp60 by cross-linking (using anti-gp60 Ab and secondary Ab) in EC grown on microporous filters increased transendothelial 125I-albumin permeability without altering liquid permeability (hydraulic conductivity), thus, indicating the dissociation of hydraulic conductivity from the albumin permeability pathway. The findings that the sterol-binding agent, filipin, prevented gp60-activated vesicle formation and that caveolin-1 and gp60 were colocalized in vesicles suggest the caveolar origin of endocytic vesicles. Pertussis toxin pretreatment and expression of the dominant negative construct encoding an 11–amino acid Gαi carboxyl-terminal peptide inhibited endothelial 125I-albumin endocytosis and vesicle formation induced by gp60 activation. Expression of dominant negative Src (dn-Src) and overexpression of wild-type caveolin-1 also prevented gp60-activated endocytosis. Caveolin-1 overexpression resulted in the sequestration of Gαi with the caveolin-1, whereas dn-Src inhibited Gαi binding to caveolin-1. Thus, vesicle formation induced by gp60 and migration of vesicles to the basolateral membrane requires the interaction of gp60 with caveolin-1, followed by the activation of the downstream Gi-coupled Src kinase signaling pathway.

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