2. Membrane Transporter/Ion Channel Neuronal Signaling
  3. TRP Channel iGluR Calcium Channel
  4. TAT-EE3

TAT-EE3 is a neuroprotective peptide which can uncouple TRPM2-NMDARs interaction. TAT-EE3 inhibits TRPM2-induced enhancement of NMDAR surface expression and current amplitude.TAT-EE3 protects neurons against ischemic injury in vitro and in vivo. TAT-EE3can be used for the study of ischemic stroke.

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TAT-EE3

TAT-EE3 Chemical Structure

CAS No. : 2899218-49-4

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TAT-EE3 Related Antibodies

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Description

TAT-EE3 is a neuroprotective peptide which can uncouple TRPM2-NMDARs interaction. TAT-EE3 inhibits TRPM2-induced enhancement of NMDAR surface expression and current amplitude.TAT-EE3 protects neurons against ischemic injury in vitro and in vivo. TAT-EE3can be used for the study of ischemic stroke[1].

In Vitro

TAT-EE3 (10 μM, overnight) disrupts the interaction between TRPM2 and GluN2a/GluN2b in HEK293T cells and neurons, inhibits TRPM2-induced enhancement of NMDAR surface expression and current amplitude[1].
TAT-EE3 (10 μM, overnight) reduces OGD-induced intracellular Ca2+ overload, neuronal death, and mitochondrial depolarization in wild-type neurons, but has no effect on gM2KO neurons[1].
TAT-EE3 (10 μM, 30-90 min) eliminates PMA-induced NMDAR current potentiation in wild-type neurons, without additional inhibition in gM2KO neurons[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TAT-EE3 Related Antibodies
In Vivo

AT-EE3 (0.33 mg/kg (100 nmol/kg), i.p., 15 min before middle cerebral artery occlusion (MCAO) or post-MCAO with reinjection every 12 h, 7 days) reduces infarct volume and improves neurological deficit score in wild-type mice, but shows no further protective effect in neuron-specific TRPM2 knockout (nM2KO) mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Focal cerebral ischemia models were constructed by performing right middle cerebral artery occlusion (MCAO) on 8-9 week-old male mice, with 120 minutes of occlusion followed by 24 hours of reperfusion, or 60 minutes of occlusion followed by 7 days of reperfusion[1]
Dosage: 0.33 mg/kg (100 nmol/kg)
Administration: i.p. repeated every 12 h after MCAO for 7 days
Result: Reduced infarct volume.
Inhibited MCAO-induced increase in NMDAR surface expression in wild-type mice, but did not exert further Protective effects in neuron-specific TRPM2 knockout (nM2KO) mice.
Improved long-term neurological deficit scores and rotarod test performance in mice.
Maintained the phosphorylation levels of ERK1/2 and CREB in the brain.
Molecular Weight

3339.61

Formula

C135H228N48O49S
CAS No.
Sequence

Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Glu-Glu-Asp-Thr-Asp-Ser-Ser-Glu-Glu-Met-Leu-Ala-Leu-Ala-Glu-Glu
Sequence Shortening

YGRKKRRQRRREEDTDSSEEMLALAEE
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Purity & Documentation
References
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TAT-EE3 Related Classifications

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

TAT-EE32899218-49-4TRP ChanneliGluRCalcium ChannelTransient receptor potential channelsIonotropic glutamate receptorsCa2+ channelsCa channelsneuroprotective peptideTRPM2NMDARsischemic strokeInhibitorinhibitorinhibit

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