nogo receptor
Recently Published Documents


TOTAL DOCUMENTS

166
(FIVE YEARS 15)

H-INDEX

37
(FIVE YEARS 3)

Cell ◽  
2022 ◽  
Vol 185 (1) ◽  
pp. 218
Author(s):  
Jie Wang ◽  
Yi Miao ◽  
Rebecca Wicklein ◽  
Zijun Sun ◽  
Jinzhao Wang ◽  
...  

2021 ◽  
Author(s):  
Caitlin M Rodriguez ◽  
Sophia C Bechek ◽  
Graham L Jones ◽  
Lisa Nakayama ◽  
Tetsuya Akiyama ◽  
...  

Gene-based therapeutic strategies to lower ataxin-2 levels are emerging for neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and spinocerebellar ataxia type 2 (SCA2). To identify additional ways of reducing ataxin-2 levels, we performed a genome-wide screen in human cells for regulators of ataxin-2 and identified RTN4R, the gene encoding the RTN4/NoGo-Receptor, as a top hit. RTN4R knockdown, or treatment with a peptide inhibitor, was sufficient to lower ataxin-2 protein levels in mouse and human neurons in vitro and Rtn4r knockout mice have reduced ataxin-2 levels in vivo. Remarkably, we observed that ataxin-2 shares a role with the RTN4/NoGo-Receptor in limiting axonal regeneration. Reduction of either protein increases axonal regrowth following axotomy. These data define the RTN4/NoGo-Receptor as a novel therapeutic target for ALS and SCA2 and implicate the targeting of ataxin-2 as a potential treatment following nerve injury.


Aging Cell ◽  
2021 ◽  
Author(s):  
Jianing Wang ◽  
Xiaoying Qin ◽  
Hao Sun ◽  
Meijun He ◽  
Qunyu Lv ◽  
...  

Cell ◽  
2021 ◽  
Author(s):  
Jie Wang ◽  
Yi Miao ◽  
Rebecca Wicklein ◽  
Zijun Sun ◽  
Jinzhao Wang ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryohei Nishida ◽  
Yuki Kawaguchi ◽  
Junpei Matsubayashi ◽  
Rie Ishikawa ◽  
Satoshi Kida ◽  
...  

AbstractThe Nogo signal is involved in impairment of memory formation. We previously reported the lateral olfactory tract usher substance (LOTUS) as an endogenous antagonist of the Nogo receptor 1 that mediates the inhibition of axon growth and synapse formation. Moreover, we found that LOTUS plays an essential role in neural circuit formation and nerve regeneration. However, the effects of LOTUS on synapse formation and memory function have not been elucidated. Here, we clearly showed the involvement of LOTUS in synapse formation and memory function. The cultured hippocampal neurons derived from lotus gene knockout (LOTUS-KO) mice exhibited a decrease in synaptic density compared with those from wild-type mice. We also found decrease of dendritic spine formation in the adult hippocampus of LOTUS-KO mice. Finally, we demonstrated that LOTUS deficiency impairs memory formation in the social recognition test and the Morris water maze test, indicating that LOTUS is involved in functions of social and spatial learning and memory. These findings suggest that LOTUS affects synapse formation and memory function.


2020 ◽  
Vol 14 ◽  
Author(s):  
Steven Petratos ◽  
Paschalis Theotokis ◽  
Min Jung Kim ◽  
Michael F. Azari ◽  
Jae Young Lee
Keyword(s):  

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1618-1622
Author(s):  
Elizabeth J Bradbury ◽  
Raquel Oliveira

This scientific commentary refers to ‘Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury’, by Wang et al. (doi:10.1093/brain/awaa116).


Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1697-1713 ◽  
Author(s):  
Xingxing Wang ◽  
Tianna Zhou ◽  
George D Maynard ◽  
Pramod S Terse ◽  
William B Cafferty ◽  
...  

Abstract After CNS trauma such as spinal cord injury, the ability of surviving neural elements to sprout axons, reorganize neural networks and support recovery of function is severely restricted, contributing to chronic neurological deficits. Among limitations on neural recovery are myelin-associated inhibitors functioning as ligands for neuronal Nogo receptor 1 (NgR1). A soluble decoy (NgR1-Fc, AXER-204) blocks these ligands and provides a means to promote recovery of function in multiple preclinical rodent models of spinal cord injury. However, the safety and efficacy of this reagent in non-human primate spinal cord injury and its toxicological profile have not been described. Here, we provide evidence that chronic intrathecal and intravenous administration of NgR1-Fc to cynomolgus monkey and to rat are without evident toxicity at doses of 20 mg and greater every other day (≥2.0 mg/kg/day), and far greater than the projected human dose. Adult female African green monkeys underwent right C5/6 lateral hemisection with evidence of persistent disuse of the right forelimb during feeding and right hindlimb during locomotion. At 1 month post-injury, the animals were randomized to treatment with vehicle (n = 6) or 0.10–0.17 mg/kg/day of NgR1-Fc (n = 8) delivered via intrathecal lumbar catheter and osmotic minipump for 4 months. One animal was removed from the study because of surgical complications of the catheter, but no treatment-related adverse events were noted in either group. Animal behaviour was evaluated at 6–7 months post-injury, i.e. 1–2 months after treatment cessation. The use of the impaired forelimb during spontaneous feeding and the impaired hindlimb during locomotion were both significantly greater in the treatment group. Tissue collected at 7–12 months post-injury showed no significant differences in lesion size, fibrotic scar, gliosis or neuroinflammation between groups. Serotoninergic raphespinal fibres below the lesion showed no deficit, with equal density on the lesioned and intact side below the level of the injury in both groups. Corticospinal axons traced from biotin-dextran-amine injections in the left motor cortex were equally labelled across groups and reduced caudal to the injury. The NgR1-Fc group tissue exhibited a significant 2–3-fold increased corticospinal axon density in the cervical cord below the level of the injury relative to the vehicle group. The data show that NgR1-Fc does not have preclinical toxicological issues in healthy animals or safety concerns in spinal cord injury animals. Thus, it presents as a potential therapeutic for spinal cord injury with evidence for behavioural improvement and growth of injured pathways in non-human primate spinal cord injury.


2020 ◽  
Vol 155 (3) ◽  
pp. 285-299
Author(s):  
Yuji Kurihara ◽  
Toshiyuki Takai ◽  
Kohtaro Takei

2020 ◽  
Vol 323 ◽  
pp. 113068 ◽  
Author(s):  
Ryu Ueno ◽  
Hajime Takase ◽  
Jun Suenaga ◽  
Masao Kishimoto ◽  
Yuji Kurihara ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document