• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

Bioinformatics analyses show dysregulation of calcium-related genes in Angelman syndrome mouse model.
Abstract BACKGROUND: Angelman syndrome (AS) is a genetic neurodevelopmental disorder caused by the loss of function of the UBE3A protein in the brain. In a previous study, we showed that activity-dependent calcium dynamics in hippocampal CA1 pyramidal neurons of AS mice is compromised, and its normalization rescues the hippocampal-dependent deficits. Therefore, we expected that the expression profiles of calcium-related genes would be altered in AS mice hippocampi. METHODS: We analyzed mRNA sequencing data from AS model mice and WT controls in light of the newly published CaGeDB database of calcium-related ge...
Source: Neurobiology of Disease - November 16, 2020 Category: Neurology Authors: Panov J, Kaphzan H Tags: Neurobiol Dis Source Type: research

Hu Antigen R Is a Positive Regulator of ALS-Associated RNA Binding Proteins TDP-43 and FUS (P5.008)
Conclusions: 1. ALS-associated RNA abnormalities may stem from disruption of a network of RBPs. 2. HuR positively regulates TDP-43 and FUS through posttranscriptional mechanism. 3. Loss of HuR-mediated RNA processing in astrocytes may participate in ALS pathogenesis. Study supported by: Study supported by NIH/NINDS Grant NS057664, NS064133Disclosure: Dr. Lu has nothing to disclose. Dr. Zheng has nothing to disclose. Dr. Si has nothing to disclose. Dr. King has nothing to disclose.
Source: Neurology - April 3, 2016 Category: Neurology Authors: Lu, L., Zheng, L., Si, Y., King, P. Tags: Neuromuscular and Clinical Neurophysiology Poster Discussion Session Source Type: research

The Role of Staufen1 in Aberrant RNA Metabolism in SCA2 (P6.396)
Conclusions: Our results unravel a novel function for Staufen1 in aberrant RNA processing events and indicate its role in SCA2 pathogenesis. Our results further support a role for aberrant RNA metabolism in neurodegeneration thereby revealing its potential as a therapeutic target. Study Supported by: This work was supported by Grants RO1NS33123 and RC4NS073009 from the National Institutes of Neurological Disorders and Stroke to SMP.Disclosure: Dr. Paul has nothing to disclose. Dr. Dansithong has nothing to disclose. Dr. Figueroa has nothing to disclose. Dr. Scoles has nothing to disclose. Dr. Pulst has received personal co...
Source: Neurology - April 3, 2016 Category: Neurology Authors: Paul, S., Dansithong, W., Figueroa, K., Scoles, D., Pulst, S. Tags: Movement Disorders: Spinocerebellar Ataxias Source Type: research

HuR is Essential for TDP-43 Expression through Posttranscriptional Mechanisms: Implications for Motor Neuron Toxicity and ALS (1II-2.002)
Conclusions: 1. HuR is essential for proper expression of TDP-43. 2. HuR directly binds to TDP-43 mRNA and regulates its expression through the 3’ UTR. 3. Loss of HuR in astrocytes leads to the production of soluble factors that are toxic to cortical and motor neurons. These findings are consistent with our previous observations that impaired HuR function may contribute to ALS pathogenesis.Study supported by: Study supported by NIH/NINDS Grant NS057664.Disclosure: Dr. Lu has nothing to disclose. Dr. Zheng has nothing to disclose. Dr. Si has nothing to disclose. Dr. Oh has nothing to disclose. Dr. King has nothing to disclose.
Source: Neurology - April 9, 2014 Category: Neurology Authors: Lu, L., Zheng, L., Si, Y., Oh, S., King, P. Tags: Proteinopathy in Neurodegenerative Disease Data Blitz Presentations Source Type: research

HuR is Essential for TDP-43 Expression through Posttranscriptional Mechanisms: Implications for Motor Neuron Toxicity and ALS (S56.003)
Conclusions: 1. HuR is essential for proper expression of TDP-43. 2. HuR directly binds to TDP-43 mRNA and regulates its expression through the 3’ UTR. 3. Loss of HuR in astrocytes leads to the production of soluble factors that are toxic to cortical and motor neurons. These findings are consistent with our previous observations that impaired HuR function may contribute to ALS pathogenesis.Study supported by: Study supported by NIH/NINDS Grant NS057664.Disclosure: Dr. Lu has nothing to disclose. Dr. Zheng has nothing to disclose. Dr. Si has nothing to disclose. Dr. Oh has nothing to disclose. Dr. King has nothing to disclose.
Source: Neurology - April 9, 2014 Category: Neurology Authors: Lu, L., Zheng, L., Si, Y., Oh, S., King, P. Tags: Anterior Horn Disease Source Type: research