scholarly journals AAV8(Y733F)-mediated gene therapy in a Spata7 knockout mouse model of Leber congenital amaurosis and retinitis pigmentosa

Gene Therapy ◽  
2015 ◽  
Vol 22 (8) ◽  
pp. 619-627 ◽  
Author(s):  
H Zhong ◽  
A Eblimit ◽  
Y Moayedi ◽  
S L Boye ◽  
V A Chiodo ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Mouse Model ◽  
Retinitis Pigmentosa ◽  
Knockout Mouse ◽  
Knockout Mouse Model ◽  
Leber Congenital Amaurosis

In vivo potency testing of subretinal rAAV5.hCNGB1 gene therapy in the Cngb1 knockout mouse model of retinitis pigmentosa

2021 ◽  
Author(s):  
Johanna E Wagner ◽  
Lena Zobel ◽  
Maximilian Joachim Gerhardt ◽  
Catherine R O'Riordan ◽  
Amy Frederick ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Mouse Model ◽  
Retinitis Pigmentosa ◽  
Knockout Mouse ◽  
Knockout Mouse Model

scholarly journals AAV-Mediated Gene Therapy in the Guanylate Cyclase (RetGC1/RetGC2) Double Knockout Mouse Model of Leber Congenital Amaurosis

2013 ◽  
Vol 24 (2) ◽  
pp. 189-202 ◽  
Author(s):  
Sanford L. Boye ◽  
Igor V. Peshenko ◽  
Wei Chieh Huang ◽  
Seok Hong Min ◽  
Issam McDoom ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Mouse Model ◽  
Guanylate Cyclase ◽  
Knockout Mouse ◽  
Double Knockout ◽  
Knockout Mouse Model ◽  
Leber Congenital Amaurosis ◽  
Double Knockout Mouse

scholarly journals DNase1 Does Not Appear to Play a Major Role in the Fragmentation of Plasma DNA in a Knockout Mouse Model

2018 ◽  
Vol 64 (2) ◽  
pp. 406-408 ◽  
Author(s):  
Timothy H T Cheng ◽  
Kathy O Lui ◽  
Xianlu Laura Peng ◽  
Suk Hang Cheng ◽  
Peiyong Jiang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Knockout Mouse ◽  
Plasma Dna ◽  
Knockout Mouse Model

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.

Sign in / Sign up

Export Citation Format

Share Document