Response of carp central nervous system to hyperammonemic conditions: an immunocytochemical study of glutamine synthetase (GS), glial fibrillary acidic protein (GFAP) and 70 kDa heat-shock protein (HSP70)

1999 ◽  
Vol 45 (2-3) ◽  
pp. 195-207 ◽  
Author(s):  
C Hernández ◽  
M Martı́n ◽  
G Bodega ◽  
I Suárez ◽  
J Pérez ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heat Shock ◽  
Glutamine Synthetase ◽  
Glial Fibrillary Acidic Protein ◽  
Heat Shock Protein ◽  
Acidic Protein ◽  
Immunocytochemical Study ◽  
Heat Shock Protein Hsp70

scholarly journals Refining the concept of GFAP toxicity in Alexander disease

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Albee Messing
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Intermediate Filament ◽  
Alexander Disease ◽  
Acidic Protein ◽  
Sequence Variants ◽  
Main Body ◽  
Gain Of Function ◽  
The Central Nervous System

Abstract Background Alexander disease is caused by dominantly acting mutations in glial fibrillary acidic protein (GFAP), the major intermediate filament of astrocytes in the central nervous system. Main body In addition to the sequence variants that represent the origin of disease, GFAP accumulation also takes place, together leading to a gain-of-function that has sometimes been referred to as “GFAP toxicity.” Whether the nature of GFAP toxicity in patients, who have mixtures of both mutant and normal protein, is the same as that produced by simple GFAP excess, is not yet clear. Conclusion The implications of these questions for the design of effective treatments are discussed.

Hyperthermic induction of the 27-kDa heat shock protein (Hsp27) in neuroglia and neurons of the rat central nervous system

2000 ◽  
Vol 428 (3) ◽  
pp. 495-510 ◽  
Author(s):  
Anne Marie R. Krueger-Naug ◽  
David A. Hopkins ◽  
John N. Armstrong ◽  
Jean-Christophe L. Plumier ◽  
R. William Currie
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heat Shock ◽  
Heat Shock Protein

scholarly journals Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin

1999 ◽  
Vol 145 (3) ◽  
pp. 503-514 ◽  
Author(s):  
Milos Pekny ◽  
Clas B. Johansson ◽  
Camilla Eliasson ◽  
Josefina Stakeberg ◽  
Åsa Wallén ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Glial Fibrillary Acidic Protein ◽  
Intermediate Filament ◽  
Glial Scar ◽  
Scar Formation ◽  
Brain Lesions ◽  
Acidic Protein ◽  
The Central Nervous System

In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP−/−vim−/−) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP−/−, vimentin−/−, or GFAP−/−vim−/− mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP−/− or vimentin−/− mice, but was impaired in GFAP−/−vim−/− mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.

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