scholarly journals PFTK1 kinase regulates axogenesis during development via RhoA activation.

2022 ◽  
Author(s):  
Alvin Joselin ◽  
Yasmilde Rodríguez González ◽  
Fatemeh Kamkar ◽  
Paymaan Jafar-nejad ◽  
Suzi Wang ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Ventral Nerve Cord ◽  
Axonal Outgrowth ◽  
Cyclin Dependent Kinase ◽  
Cns Development ◽  
Functional Interaction ◽  
Rhoa Activation ◽  
Cultured Cortical Neurons ◽  
Neuronal Functions

Cyclin Dependent Kinase family members include members of the non-cell cycle CDK, such as PFTK1/Eip63E. Eip63E expresses primarily in postnatal and adult nervous system in Drosophila melanogaster but its role in CNS development remains unknown. We sought to understand its role in the CNS by studying the fly ventral nerve cord during development. Eip63E regulates axogenesis in neurons and its deficiency leads to neuronal defects. We describe a functional interaction between Eip63E and Rho1. Studies in cultured cortical neurons from PFTK1 knockout mice, confirmed that PFTK1 plays a role in axonal outgrowth and its deficiency resulted in faster growing axons. We demonstrate that GDP bound RhoA is a substrate of PFTK1 and this phosphorylation resulted in higher activity of RhoA. In conclusion, our work represents the first steps in the characterization of the neuronal functions of PFTK1 and points to RhoA activation in the regulation of PFTK1 mediated axogenesis.

Characterization of the transportation of berberine inCoptidis rhizoma extract through rat primary cultured cortical neurons

2007 ◽  
Vol 22 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yunyun Chen ◽  
Xueli Wang ◽  
Hong Sun ◽  
Dongming Xing ◽  
Jun Hu ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Cultured Cortical Neurons

scholarly journals Characterization of Neuroprotection from Excitotoxicity by Moderate and Profound Hypothermia in Cultured Cortical Neurons Unmasks a Temperature-Insensitive Component of Glutamate Neurotoxicity

1998 ◽  
Vol 18 (8) ◽  
pp. 848-867 ◽  
Author(s):  
Michael Tymianski ◽  
Rita Sattler ◽  
Joseph M. Zabramski ◽  
Robert F. Spetzler
Keyword(s):  
Nmda Receptors ◽  
Cortical Neurons ◽  
Underlying Mechanism ◽  
The Other ◽  
Glutamate Toxicity ◽  
Protective Effects ◽  
Profound Hypothermia ◽  
Glutamate Neurotoxicity ◽  
Cultured Cortical Neurons

Although profound hypothermia has been used for decades to protect the human brain from hypoxic or ischemic insults, little is known about the underlying mechanism. We therefore report the first characterization of the effects of moderate (30°C) and profound hypothermia (12° to 20°C) on excitotoxicity in cultured cortical neurons exposed to excitatory amino acids (EAA; glutamate, N-methyl-D-aspartate [NMDA], AMPA, or kainate) at different temperatures (12° to 37°C). Cooling neurons to 30°C and 20°C was neuroprotective, but cooling to 12°C was toxic. The extent of protection depended on the temperature, the EAA receptor agonist employed, and the duration of the EAA challenge. Neurons challenged briefly (5 minutes) with all EAA were protected, as were neurons challenged for 60 minutes with NMDA, AMPA, or kainate. The protective effects of hypothermia (20° and 30°C) persisted after rewarming to 37°C, but rewarming from 12°C was deleterious. Surprisingly, however, prolonged (60 minutes) exposures to glutamate unmasked a temperature-insensitive component of glutamate neurotoxicity that was not seen with the other, synthetic EAA; this component was still mediated via NMDA receptors, not by ionotropic or metabotropic non-NMDA receptors. The temperature-insensitivity of glutamate toxicity was not explained by effects of hypothermia on EAA-evoked [Ca2+]i increases measured using high- and low-affinity Ca2+ indicators, nor by effects on mitochondrial production of reactive oxygen species. This first characterization of excitotoxicity at profoundly hypothermic temperatures reveals a previously unnoticed feature of glutamate neurotoxicity unseen with the other EAA, and also suggests that hypothermia protects the brain at the level of neurons by blocking, rather than slowing, excitotoxicity.

scholarly journals The Bacterial Enzyme Cas13 Interferes with Neurite Outgrowth from Cultured Cortical Neurons

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 262
Author(s):  
Qin-Wei Wu ◽  
Josef P. Kapfhammer
Keyword(s):  
Rna Editing ◽  
Cortical Neurons ◽  
High Efficiency ◽  
Primary Cultures ◽  
Cultured Neurons ◽  
Therapeutic Tool ◽  
Bacterial Enzyme ◽  
Rna Targeting ◽  
Cultured Cortical Neurons ◽  
New Generation

The CRISPR-Cas13 system based on a bacterial enzyme has been explored as a powerful new method for RNA manipulation. Due to the high efficiency and specificity of RNA editing/interference achieved by this system, it is currently being developed as a new therapeutic tool for the treatment of neurological and other diseases. However, the safety of this new generation of RNA therapies is still unclear. In this study, we constructed a vector expressing CRISPR-Cas13 under a constitutive neuron-specific promoter. CRISPR-Cas13 from Leptotrichia wadei was expressed in primary cultures of mouse cortical neurons. We found that the presence of CRISPR-Cas13 impedes the development of cultured neurons. These results show a neurotoxic action of Cas13 and call for more studies to test for and possibly mitigate the toxic effects of Cas13 enzymes in order to improve CRISPR-Cas13-based tools for RNA targeting.

scholarly journals Characterization of cortical neurons that transiently express TH during rat brain development

2006 ◽  
Vol 295 (1) ◽  
pp. 405
Author(s):  
Steve Asmus ◽  
Mark Ball ◽  
Angela Bohnen ◽  
Kevin Phelps ◽  
Cindy Hartley ◽  
...  
Keyword(s):  
Brain Development ◽  
Rat Brain ◽  
Cortical Neurons

scholarly journals Functional characterization of human PFTK1 as a cyclin-dependent kinase

2007 ◽  
Vol 104 (22) ◽  
pp. 9248-9253 ◽  
Author(s):  
F. Shu ◽  
S. Lv ◽  
Y. Qin ◽  
X. Ma ◽  
X. Wang ◽  
...  
Keyword(s):  
Functional Characterization ◽  
Cyclin Dependent Kinase
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