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Submit Review(±)-threo-3-Methylglutamic acid is a potent blocker of glutamate transport; selective for EAAT2 and EAAT4 (IC50 values are 90, 109, 1600 and 1080 μM for EAAT2, EAAT4, EAAT1 and EAAT3 respectively).
M. Wt | 161.16 |
Formula | C6H11NO4 |
Storage | Store at RT |
Purity | ≥98% (HPLC) |
CAS Number | 63088-04-0 |
PubChem ID | 90479741 |
InChI Key | GZKDJYLZHGMSFM-KSTNSCRMSA-N |
Smiles | N[C@@]([C@@]([H])(C)CC(O)=O)([H])C(O)=O.[H][C@](CC(O)=O)(C)[C@@](N)([H])C(O)=O |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Eliasof et al (2001) Pharmacological characterization of threo-3-methylglutamic acid with excitatory amino acid transporters in native and recombinant systems. J.Neurochem. 77 550 PMID: 11299317
Mitrovic et al (1998) Identification of functional domains of the human glutamate transporters EAAT1 and EAAT2. J.Biol.Chem. 273 14698 PMID: 9614067
Vandenberg et al (1997) Contrasting modes of action of methylglutamate derivatives on the excitatory amino acid transporters, EAAT1 and EAAT2. Mol.Pharmacol. 51 809 PMID: 9145919
Keywords: (±)-threo-3-Methylglutamic acid, (±)-threo-3-Methylglutamic acid supplier, EAAT2, EAAT4, blockers, Excitatory, Amino, Acid, Transporters, GLT-1, Glutamate, Monoamine, Neurotransmitter, 0811, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for (±)-threo-3-Methylglutamic acid include:
Jarzylo and Man (2012) Parasynaptic NMDA receptor signaling couples neuronal glutamate transporter function to AMPA receptor synaptic distribution and stability. J Neurosci 32 2552 PMID: 22396428
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.