Using Transgenic Mouse Models to Dissect the Pathogenesis of Virus-Induced Autoimmune Disorders of the Islets of Langerhans and the Central Nervous System

1996 ◽  
Vol 152 (1) ◽  
pp. 111-143 ◽  
Author(s):  
Matthias G. Herrath ◽  
Claire F. Evans ◽  
Marc S. Horwitz ◽  
Michael B. A. Oldstone
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transgenic Mouse ◽  
Islets Of Langerhans ◽  
Mouse Models ◽  
Autoimmune Disorders ◽  
Transgenic Mouse Models ◽  
The Central Nervous System

scholarly journals Age-Dependent Lethality in Novel Transgenic Mouse Models of Central Nervous System Arteriovenous Malformations

Stroke ◽  
2012 ◽  
Vol 43 (5) ◽  
pp. 1432-1435 ◽  
Author(s):  
Ian Milton ◽  
Dan Ouyang ◽  
Caitlin J. Allen ◽  
Nathan E. Yanasak ◽  
James R. Gossage ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Arteriovenous Malformations ◽  
Transgenic Mouse Models ◽  
Age Dependent

scholarly journals The Function of Selenium in Central Nervous System: Lessons from MsrB1 Knockout Mouse Models

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1372
Author(s):  
Tengrui Shi ◽  
Jianxi Song ◽  
Guanying You ◽  
Yujie Yang ◽  
Qiong Liu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Mouse Models ◽  
Knockout Mouse ◽  
Methionine Sulfoxide ◽  
Methionine Sulfoxide Reductase ◽  
Knockout Mouse Model ◽  
The Central Nervous System

MsrB1 used to be named selenoprotein R, for it was first identified as a selenocysteine containing protein by searching for the selenocysteine insert sequence (SECIS) in the human genome. Later, it was found that MsrB1 is homologous to PilB in Neisseria gonorrhoeae, which is a methionine sulfoxide reductase (Msr), specifically reducing L-methionine sulfoxide (L-Met-O) in proteins. In humans and mice, four members constitute the Msr family, which are MsrA, MsrB1, MsrB2, and MsrB3. MsrA can reduce free or protein-containing L-Met-O (S), whereas MsrBs can only function on the L-Met-O (R) epimer in proteins. Though there are isomerases existent that could transfer L-Met-O (S) to L-Met-O (R) and vice-versa, the loss of Msr individually results in different phenotypes in mice models. These observations indicate that the function of one Msr cannot be totally complemented by another. Among the mammalian Msrs, MsrB1 is the only selenocysteine-containing protein, and we recently found that loss of MsrB1 perturbs the synaptic plasticity in mice, along with the astrogliosis in their brains. In this review, we summarized the effects resulting from Msr deficiency and the bioactivity of selenium in the central nervous system, especially those that we learned from the MsrB1 knockout mouse model. We hope it will be helpful in better understanding how the trace element selenium participates in the reduction of L-Met-O and becomes involved in neurobiology.

Clinical characteristics of autoimmune disorders in the central nervous system associated with myasthenia gravis

2019 ◽  
Vol 266 (11) ◽  
pp. 2743-2751 ◽  
Author(s):  
Kimitoshi Kimura ◽  
Yoichiro Okada ◽  
Chihiro Fujii ◽  
Kenichi Komatsu ◽  
Ryosuke Takahashi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Myasthenia Gravis ◽  
Clinical Characteristics ◽  
Autoimmune Disorders ◽  
The Central Nervous System
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