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PubMed1995

Trimeric G protein alpha subunits of the Gs and Gi families localized at the Golgi membrane.

The occurrence of individual G proteins within Golgi membranes from liver and from adrenal medulla were analyzed by Western blotting. Two splice variants of G alpha s and also G alpha i-3 were found in both tissues. Additionally, G alpha i-2, its 43-kDa splice variant and G alpha o were strongly labeled in Golgi of adrenal medulla. Golgi preparations of liver contained comparable quantities of G alpha i-2 and a second variant of 46 kDa, but no G alpha o was detected. Immunoelectron microscopic studies of the above Golgi preparations showed that both G alpha i-2 and G alpha i-3 are localized at multivesicular structures identified as Golgi complexes. The occurrence of two stimulatory G proteins (G alpha s-S and G alpha s-L) and three or four alpha subunits of the Gi/Go type as components of the Golgi membrane support the notion that formation of different vesicle types might be regulated by individual stimulatory and inhibitory G proteins.

Adrenal Medulla↗
PubMed1993

Interactions between forskolin, GS, and divalent cations on ciliary process adenylyl cyclase and intraocular pressure in the rabbit eye.

The major adenylyl cyclase activity (AC) of rabbit ocular ciliary processes was investigated by dose-response analysis with respect to interactions of its regulators [the stimulatory G-protein (alpha S) and forskolin] under both saturating and suboptimal divalent cation (M2+) conditions. alpha S was generated directly with fluoroaluminate or via receptors for vasoactive intestinal peptide or isoproterenol. Forskolin and alpha S when liganded simultaneously to AC at suboptimal M2+, potentiated maximal enzyme activity (approximately twice the sum of the separate activities), while the responses were additive (no potentiation) under saturating M2+ conditions. The results demonstrate that the three ligands (forskolin, M2+ and alpha S) mutually interact in a cooperative manner as follows: (1) The apparent k(act) of forskolin for AC was decreased by 1.7-1.9 log units when alpha S was liganded to AC. (2) Conversely, with forskolin liganded to AC the apparent k(act) of alpha S for AC also decreased by a factor of at least 3-4. (3) The nature of the divalent cation M2+ had no effect on the k(act) of alpha S for AC alone and for the AC:FSK complex, and also did not affect the apparent k(act) of forskolin for AC alone, or for the AC: alpha S complex. The nature of M2+ (Mg2+ or Mn2+) affected only the maximal catalytic rate (Emax). (4) Potentiation of adenylyl cyclase by alpha S + FSK was demonstrable in vivo by the increased ocular pressure response of the rabbit eye when a low topical dose of isoproterenol (125 ng per eye) and a subthreshold dose of forskolin (100 micrograms per eye) were given in combination.

Adenylyl Cyclases↗
PubMed2007

Progressive retinal dystrophy in two sisters with glutathione synthetase (GS) deficiency.

We report the ophthalmological findings of two sisters with severe glutathione synthetase deficiency, an autosomal recessive inborn error of metabolism resulting in very low intracellular levels of the free-radical scavenger glutathione. The patients were investigated because of declining visual acuity. The most prominent finding was progressive retinal dystrophy with hyperpigmentations and maculopathy. Generally disturbed functioning of both the outer and inner layers of the retina resulted in attenuated or nearly abolished electroretinograms. These findings agree with a rod/cone type of retinal dystrophy, and we suggest that this is due to glutathione deficiency. Treatment with antioxidants such as vitamins E and C seems to prevent the progression of CNS damage. We speculate that it might also prevent retinal dystrophy in patients with glutathione synthetase deficiency. We suggest that patients with retinal dystrophy and additional neurological signs should be investigated for a defect in glutathione metabolism. Also, we recommend that patients with low levels of glutathione should be examined for retinal dystrophy. Our results suggest that a decreased capacity for scavenging reactive oxygen species and/or increased oxidative stress may cause retinal dystrophy. If this is the case, the redox state in the retina should be a potentially useful therapeutic target to prevent reduced visual function and blindness.

Antioxidants↗