Role of phosphatidylinositol 3-kinase in neuronal survival and axonal outgrowth of adult mouse dorsal root ganglia explants

2003 ◽  
Vol 74 (5) ◽  
pp. 726-735 ◽  
Author(s):  
Anders Edström ◽  
Per A.R. Ekström
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Adult Mouse ◽  
Neuronal Survival ◽  
Axonal Outgrowth ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Role of phosphatidylinositol 3-kinase in oxidative stress-induced disruption of tight junctions. Vol. 278 (2003) 49239-49245

2004 ◽  
Vol 279 (7) ◽  
pp. 6204
Author(s):  
Parimal Sheth ◽  
Shyamali Basuroy ◽  
Chunying Li ◽  
Anjaparavanda P. Naren ◽  
Radhakrishna K. Rao
Keyword(s):  
Oxidative Stress ◽  
Tight Junctions ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Novel Role of Phosphatidylinositol 3-Kinase in CD28-mediated Costimulation

2000 ◽  
Vol 276 (12) ◽  
pp. 9003-9008 ◽  
Author(s):  
Yohsuke Harada ◽  
Eri Tanabe ◽  
Ryosuke Watanabe ◽  
Bonnie D. Weiss ◽  
Akira Matsumoto ◽  
...  
Keyword(s):  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

On the role of glial gaba uptake: Studies with dorsal root ganglia

1980 ◽  
Vol 5 ◽  
pp. 77-81 ◽  
Author(s):  
P.M. Headley ◽  
M. Desarmenien ◽  
G. Linck ◽  
F. Santangelo ◽  
P. Feltz
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Gaba Uptake ◽  
Uptake Studies

scholarly journals cAMP-stimulated Na+ transport in H441 distal lung epithelial cells: role of PKA, phosphatidylinositol 3-kinase, and sgk1

2004 ◽  
Vol 287 (4) ◽  
pp. L843-L851 ◽  
Author(s):  
Christie P. Thomas ◽  
Jason R. Campbell ◽  
Patrick J. Wright ◽  
Russell F. Husted
Keyword(s):  
Apical Cell ◽  
P38 Map Kinase ◽  
Lung Epithelial Cells ◽  
Epithelial Cell Line ◽  
Phosphatidylinositol 3 Kinase ◽  
Transport Pathway ◽  
Early Effect ◽  
Sustained Effect ◽  
Phosphatidylinositol 3

H441 cells, a bronchiolar epithelial cell line, develop a cAMP-regulated benzamil-sensitive Na+ transport pathway on permeable supports (Itani OA, Auerbach SD, Husted RF, Volk KA, Ageloff S, Knepper MA, Stokes JB, Thomas CP. Am J Physiol Lung Cell Mol Physiol 282: L631–L641, 2002). To understand the molecular basis for the stimulation of Na+ transport, we delineated the role of specific intracellular pathways and examined the effect of cAMP on αβγ-epithelial Na+ channel (ENaC) and sgk1 expression. Na+ transport increases within 5 min of cAMP stimulation and is sustained for >24 h. The sustained effect of cAMP on Na+ transport is abolished by LY-294002, an inhibitor of phosphatidylinositol 3-kinase, by H89, an inhibitor of PKA, or by SB-202190, an inhibitor of p38 MAP kinase. The sustained effect of cAMP was associated with increases in α-ENaC mRNA and protein but without a detectable increase in βγ-ENaC and sgk1. The early effect of cAMP on Na+ transport is brefeldin sensitive and is mediated via PKA. These results are consistent with a model where the early effect of cAMP is to increase trafficking of Na+ channels to the apical cell surface whereas the sustained effect requires the synthesis of α-ENaC.

scholarly journals PI(4,5)P2 controls slit diaphragm formation and endocytosis in Drosophila nephrocytes

2021 ◽  
Author(s):  
Max Gass ◽  
Sarah Borkowsky ◽  
Marie-Luise Lotz ◽  
Rita Schroeter ◽  
Pavel Nedvetsky ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Model System ◽  
Dominant Negative ◽  
Slit Diaphragm ◽  
Phosphatidylinositol 3 Kinase ◽  
Ectopic Activation ◽  
Phosphatidylinositol 4 ◽  
Asymmetrically Distributed ◽  
Phosphatidylinositol 3

Drosophila nephrocytes are an emerging model system for mammalian podocytes and podocyte-associated diseases. Like podocytes, nephrocytes exhibit characteristics of epithelial cells, but the role of phospholipids in polarization of these cells is yet unclear. In epithelia phosphatidylinositol(4,5)bisphosphate (PI(4,5)P2) and phosphatidylinositol(3,4,5)-trisphosphate (PI(3,4,5)P3) are asymmetrically distributed in the plasma membrane and determine apical-basal polarity. Here we demonstrate that both phospholipids are present in the plasma membrane of nephrocytes, but only PI(4,5)P2 accumulates at slit diaphragms. Knockdown of Skittles, a phosphatidylinositol(4)phosphate 5-kinase, which produces PI(4,5)P2, abolished slit diaphragm formation and led to strongly reduced endocytosis. Notably, reduction in PI(3,4,5)P3 by overexpression of PTEN or expression of a dominant-negative phosphatidylinositol-3-Kinase did not affect nephrocyte function, whereas enhanced formation of PI(3,4,5)P3 by constitutively active phosphatidylinositol-3-Kinase resulted in strong slit diaphragm and endocytosis defects by ectopic activation of the Akt/mTOR pathway. Thus, PI(4,5)P2 but not PI(3,4,5)P3 is essential for slit diaphragm formation and nephrocyte function. However, PI(3,4,5)P3 has to be tightly controlled to ensure nephrocyte development.

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