scholarly journals FAK regulates actin polymerization during sperm capacitation via the ERK2/GEF-H1/RhoA signaling pathway

2020 ◽  
Vol 133 (8) ◽  
pp. jcs239186 ◽  
Author(s):  
Monica L. Salgado-Lucio ◽  
Danelia Ramírez-Ramírez ◽  
Coral Y. Jorge-Cruz ◽  
Ana L. Roa-Espitia ◽  
Enrique O. Hernández-González
2017 ◽  
Vol 18 (10) ◽  
pp. 783-791 ◽  
Author(s):  
Xiao Huaitong ◽  
Feng Yuanyong ◽  
Tao Yueqin ◽  
Zhao Peng ◽  
Shang Wei ◽  
...  

2021 ◽  
Vol 14 ◽  
Author(s):  
Xue Li ◽  
Yanan Pan ◽  
Jianxiong Gui ◽  
Zhixu Fang ◽  
Dishu Huang ◽  
...  

Leucine rich repeat and immunoglobulin-like domain-containing protein 1 (Lingo-1) has gained considerable interest as a potential therapy for demyelinating diseases since it inhibits axonal regeneration and myelin production. However, the results of clinical trials targeted at Lingo-1 have been unsatisfactory. Amphoterin-induced gene and open reading frame-3 (AMIGO3), which is an analog of Lingo-1, might be an alternative therapeutic target for brain damage. In the present study, we investigated the effects of AMIGO3 on neural circuits in immature mice after status convulsion (SC) induced by kainic acid. The expression of both AMIGO3 and Lingo-1 was significantly increased after SC, with levels maintained to 20 days after SC. Following SC, transmission electron microscopy revealed the impaired microstructure of myelin sheaths and Western blot analysis showed a decrease in myelin basic protein expression, and this damage was alleviated by downregulation of AMIGO3 expression. The ROCK/RhoA signaling pathway was inhibited at 20 days after SC by downregulating AMIGO3 expression. These results indicate that AMIGO3 plays important roles in seizure-induced damage of myelin sheaths as well as axon growth and synaptic plasticity via the ROCK/RhoA signaling pathway.


2012 ◽  
Vol 362 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Sarit Bar-Sheshet Itach ◽  
Maya Finklestein ◽  
Nir Etkovitz ◽  
Haim Breitbart

Biology Open ◽  
2016 ◽  
Vol 5 (9) ◽  
pp. 1189-1199 ◽  
Author(s):  
Ana L. Roa-Espitia ◽  
Eva R. Hernández-Rendón ◽  
Rafael Baltiérrez-Hoyos ◽  
Rafaela J. Muñoz-Gotera ◽  
Antonieta Cote-Vélez ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 230
Author(s):  
Dandan Tan ◽  
Haowen Zhang ◽  
Junyao Deng ◽  
Jingmin Liu ◽  
Jinkun Wen ◽  
...  

RhoA-GTPase (RhoA) is widely regarded as a key molecular switch to inhibit neurite outgrowth by rigidifying the actin cytoskeleton. However, during neurite outgrowth, whether and how microtubule dynamics are regulated by RhoA remains to be elucidated. Herein, CT04 and Y27632 were used to inactivate RhoA and its downstream effector Rho-associated coiled coil-forming kinase (ROCK), while the RhoAQ63L lentiviral vector was utilized to overexpress the constitutively activated RhoA in dorsal root ganglion (DRG) neurons or neuronal differentiated PC12 cells. The current data illustrate that the RhoA signaling pathway negatively modulates neurite outgrowth and elevates the expression of Glu-tubulin (a marker for a stabilized microtubule). Meanwhile, the microtubule-severing proteins spastin and p60-katanin were downregulated by the RhoA signaling pathway. When spastin and p60-katanin were knocked down, the effects of RhoA inhibition on neurite outgrowth were significantly reversed. Taken together, this study demonstrates that the RhoA pathway-mediated inhibition of neurite outgrowth is not only related to the modulation of microfilament dynamics but is also attributable to the regulation of the expression of spastin and p60-katanin and thus influences microtubule dynamics.


2012 ◽  
Vol 50 (1-2) ◽  
pp. 98-107 ◽  
Author(s):  
Feng Guo ◽  
Jiajun Tang ◽  
Zengding Zhou ◽  
Yi Dou ◽  
Derek Van Lonkhuyzen ◽  
...  

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