Difference between revisions of "Part:BBa K3030000"
 
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===Introdution===
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__NOTOC__
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<partinfo>BBa_K3030000 short</partinfo>
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EAAT2 is a member of a family of the solute carrier family of proteins. The membrane-bound protein is the principal transporter that clears the excitatory neurotransmitter glutamate from the extracellular space at synapses in the central nervous system. Glutamate clearance is necessary for proper synaptic activation and to prevent neuronal damage from excessive activation of glutamate receptors. EAAT2 is responsible for over 90% of glutamate reuptake within the brain.
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<br>
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===Usage and Biology===
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<span class='h3bb'>Sequence and Features</span>
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<partinfo>BBa_K3030000 SequenceAndFeatures</partinfo>
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===Functional Parameters===
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<partinfo>BBa_K3030000 parameters</partinfo>
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<p class=”text”><h3>Reference</h3></p>
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<br>
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Das, S. K. et al. (2012) ‘Role of excitatory amino acid transporter-2 (EAAT2) and glutamate in neurodegeneration: opportunities for developing novel therapeutics’, <i>Journal of Cellular Physiology</i>, 226(10), pp. 2484–2493. doi: 10.1002/jcp.22609.

Latest revision as of 22:20, 21 October 2019


The EAAT2-coding sequence

EAAT2 is a member of a family of the solute carrier family of proteins. The membrane-bound protein is the principal transporter that clears the excitatory neurotransmitter glutamate from the extracellular space at synapses in the central nervous system. Glutamate clearance is necessary for proper synaptic activation and to prevent neuronal damage from excessive activation of glutamate receptors. EAAT2 is responsible for over 90% of glutamate reuptake within the brain.
Sequence and Features


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]


Reference


Das, S. K. et al. (2012) ‘Role of excitatory amino acid transporter-2 (EAAT2) and glutamate in neurodegeneration: opportunities for developing novel therapeutics’, Journal of Cellular Physiology, 226(10), pp. 2484–2493. doi: 10.1002/jcp.22609.