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Displaying 7 of 7 results for "PDE7B"
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  1. Discovery of PDE7B as a novel effector of GBM growth by computational deconvolution of an in vitro physical coculture system BioProject

    ID: PRJNA222317

    Keywords: Transcriptome or Gene expression

    Access Type: download

  2. Discovery of PDE7B as a novel effector of GBM growth by computational deconvolution of an in vitro physical coculture system ArrayExpress

    ID: E-GEOD-51253

    Description: , we identified upregulation of the cAMP specific phosphodiesterase PDE7B in GBM cells in response to ECs. We further found that elevated PDE7B expression occurs in most GBM cases and has a negative effect on survival. PDE7B overexpression resulted in the expansion of a stem-like cell subpopulation, increased tumor aggressiveness, and increased growth in an intracranial GBM model. This deconvolution algorithm provides a new tool for cancer biology, and these results identify PDE7B as a therapeutic target in GBM. 3 replicates from U87 monocultures, 3 replicates from HBMEC monocultures, 3 replic...

  3. Discovery of PDE7B as a novel effector of GBM growth by computational deconvolution of an in vitro physical coculture system OmicsDI

    ID: E-GEOD-51253

    Date Released: 06-03-2014

    Description: , we identified upregulation of the cAMP specific phosphodiesterase PDE7B in GBM cells in response to ECs. We further found that elevated PDE7B expression occurs in most GBM cases and has a negative effect on survival. PDE7B overexpression resulted in the expansion of a stem-like cell subpopulation, increased tumor aggressiveness, and increased growth in an intracranial GBM model. This deconvolution algorithm provides a new tool for cancer biology, and these results identify PDE7B as a therapeutic target in GBM. 3 replicates from U87 monocultures, 3 replicates from HBMEC monocultures, 3 replic...

  4. A53T-ë±-synuclein overexpression mouse model signaling and striatal synaptic plasticity ArrayExpress

    ID: E-GEOD-20547

    Description: T-PCR validation of altered Homer1, Cb1, Atf2 and Pde7b transcript levels indicated a progressive reduction in the postsynaptic DA response. As functional consequences, long term depression was absent in corticostriatal slices from aged transgenic mice and an insidious decrease of spontaneous locomotor activity of these animals was found in open field tests. Taken together, the dysfunctional neurotransmission and decreased synaptic plasticity seen in the A53T-SNCA overexpressing mice reflects early functional changes within the basal ganglia resulting from synucleinopathy prior to frank neurodegeneration. Thus, preclinical stages of PD may be modeled in this mouse. Parkinson’s disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression, or the A53T mutation, of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. Here, we used two mouse lines overexpressing human A53T-SNCA around ages 6 and 18 months and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. High pressure liquid chromatography analysis of striatal neurotransmitter con...

  5. A53T-α-synuclein overexpression mouse model signaling and striatal synaptic plasticity BioProject

    ID: PRJNA125303

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: T-PCR validation of altered Homer1, Cb1, Atf2 and Pde7b transcript levels indicated a progressive reduction in the postsynaptic DA response. As functional consequences, long term depression was absent in corticostriatal slices from aged transgenic mice and an insidious decrease of spontaneous locomotor activity of these animals was found in open field tests. Taken together, the dysfunctional neurotransmission and decreased synaptic plasticity seen in the A53T-SNCA overexpressing mice reflects early functional changes within the basal ganglia resulting from synucleinopathy prior to frank neurodegeneration. Thus, preclinical stages of PD may be modeled in this mouse. Parkinson’s disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression, or the A53T mutation, of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. Here, we used two mouse lines overexpressing human A53T-SNCA around ages 6 and 18 months and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. High pressure liquid chromatography analysis of striatal neurotransmitter con...
  6. A53T-?-synuclein overexpression mouse model signaling and striatal synaptic plasticity GEMMA

    ID: 1904

    Keywords: functional genomics

    Description: T-PCR validation of altered Homer1, Cb1, Atf2 and Pde7b transcript levels indicated a progressive reduction in the postsynaptic DA response. As functional consequences, long term depression was absent in corticostriatal slices from aged transgenic mice and an insidious decrease of spontaneous locomotor activity of these animals was found in open field tests. Taken together, the dysfunctional neurotransmission and decreased synaptic plasticity seen in the A53T-SNCA overexpressing mice reflects early functional changes within the basal ganglia resulting from synucleinopathy prior to frank neurodegeneration. Thus, preclinical stages of PD may be modeled in this mouse. Parkinson’s disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression, or the A53T mutation, of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. Here, we used two mouse lines overexpressing human A53T-SNCA around ages 6 and 18 months and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. High pressure liquid chromatography analysis of striatal neurotransmitter con...

  7. A53T-ë±-synuclein overexpression mouse model signaling and striatal synaptic plasticity OmicsDI

    ID: E-GEOD-20547

    Date Released: 05-01-2014

    Description: T-PCR validation of altered Homer1, Cb1, Atf2 and Pde7b transcript levels indicated a progressive reduction in the postsynaptic DA response. As functional consequences, long term depression was absent in corticostriatal slices from aged transgenic mice and an insidious decrease of spontaneous locomotor activity of these animals was found in open field tests. Taken together, the dysfunctional neurotransmission and decreased synaptic plasticity seen in the A53T-SNCA overexpressing mice reflects early functional changes within the basal ganglia resulting from synucleinopathy prior to frank neurodegeneration. Thus, preclinical stages of PD may be modeled in this mouse. Parkinson’s disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression, or the A53T mutation, of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. Here, we used two mouse lines overexpressing human A53T-SNCA around ages 6 and 18 months and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. High pressure liquid chromatography analysis of striatal neurotransmitter con...


Displaying 7 of 7 results for "PDE7B"