Cellular mechanism of HCO 3 − and Cl− transport in insect salt gland

1985 ◽  
Vol 83 (1-2) ◽  
pp. 25-37 ◽  
Author(s):  
K. Strange ◽  
J. E. Phillips
Keyword(s):  
Salt Gland ◽  
Cellular Mechanism ◽  
Cl Transport

scholarly journals DJ-1 regulates the integrity and function of ER-mitochondria association through interaction with IP3R3-Grp75-VDAC1

2019 ◽  
Vol 116 (50) ◽  
pp. 25322-25328 ◽  
Author(s):  
Yi Liu ◽  
Xiaopin Ma ◽  
Hisashi Fujioka ◽  
Jun Liu ◽  
Shengdi Chen ◽  
...  
Keyword(s):  
Autosomal Recessive ◽  
Cellular Mechanism ◽  
Loss Of Function ◽  
Wild Type ◽  
Calcium Efflux ◽  
And Function ◽  
The Brain ◽  
Early Onset Parkinson’S Disease

Loss-of-function mutations in DJ-1 are associated with autosomal recessive early onset Parkinson’s disease (PD), yet the underlying pathogenic mechanism remains elusive. Here we demonstrate that DJ-1 localized to the mitochondria-associated membrane (MAM) both in vitro and in vivo. In fact, DJ-1 physically interacts with and is an essential component of the IP3R3-Grp75-VDAC1 complexes at MAM. Loss of DJ-1 disrupted the IP3R3-Grp75-VDAC1 complex and led to reduced endoplasmic reticulum (ER)-mitochondria association and disturbed function of MAM and mitochondria in vitro. These deficits could be rescued by wild-type DJ-1 but not by the familial PD-associated L166P mutant which had demonstrated reduced interaction with IP3R3-Grp75. Furthermore, DJ-1 ablation disturbed calcium efflux-induced IP3R3 degradation after carbachol treatment and caused IP3R3 accumulation at the MAM in vitro. Importantly, similar deficits in IP3R3-Grp75-VDAC1 complexes and MAM were found in the brain of DJ-1 knockout mice in vivo. The DJ-1 level was reduced in the substantia nigra of sporadic PD patients, which was associated with reduced IP3R3-DJ-1 interaction and ER-mitochondria association. Together, these findings offer insights into the cellular mechanism in the involvement of DJ-1 in the regulation of the integrity and calcium cross-talk between ER and mitochondria and suggests that impaired ER-mitochondria association could contribute to the pathogenesis of PD.

Cellular mechanism of thrombin on endothelin-1 biosynthesis and release in bovine endothelial cell

1992 ◽  
Vol 44 (12) ◽  
pp. 2409-2411 ◽  
Author(s):  
Toshiaki Emori ◽  
Yukio Hirata ◽  
Taihei Imai ◽  
Kazuki Ohta ◽  
Kazuo Kanno ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cellular Mechanism ◽  
Endothelin 1 ◽  
Bovine Endothelial Cell

Electrogenic, K + -dependent chloride transport in locust hindgut

1982 ◽  
Vol 299 (1097) ◽  
pp. 585-595 ◽  
Keyword(s):  
Chloride Transport ◽  
Passive Movement ◽  
Water Reabsorption ◽  
Experimental Conditions ◽  
Cl Transport ◽  
Neuropeptide Hormone ◽  
Flux Measurements ◽  
Ion Sensitive Microelectrodes ◽  
Voltage Clamping ◽  
Electrochemical Potentials

Potassium chloride is the major salt recycled in most insect excretory systems. Ion and water reabsorption occur in the rectum by active transport of Cl- and largely passive movement of K+. Both these processes are stimulated several fold by a neuropeptide hormone acting via cyclic AMP (cAMP). This Cl- transport process was investigated by using intracellular ion-sensitive microelectrodes, radiotracer flux measurements, voltage clamping, ion substitutions and inhibitors. The mucosal entry step for Cl- is energy-requiring and highly selective, and is stimulated directly by cAMP and luminal K +. Under some experimental conditions, measured electrochemical potentials for cations across the mucosal membrane are too small to drive Cl- entry by NaCl or KC1 cotransport mechanisms; moreover, net 36C1- flux is independent of the apical Na+ potential. Similarly no evidence for a HCO 3 -Cl- exchange was obtained. We conclude that Cl- transport in locust gut is different from mechanisms currently proposed for vertebrate tissues.

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