>>Signaling Pathways>> Immunology/Inflammation>> NO Synthase>>Tat-NR2B9c

Tat-NR2B9c (Synonyms: Tat-NR2Bct; NA-1)

Catalog No.GC30774

Tat-NR2B9c는 postsynaptic density protein 95 (PSD-95)가 N-메틸-D-아스파르트산(NMDA) 수용체와 신경 세포 산화 질소 합성 효소에 결합하는 것을 방지하여 일산화질소(NO) 생성을 방지하기 위해 설계되었습니다.

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Tat-NR2B9c Chemical Structure

Cas No.: 500992-11-0

Size 가격 재고 수량
1mg
US$65.00
재고 있음
5mg
US$166.00
재고 있음
10mg
US$258.00
재고 있음
25mg
US$506.00
재고 있음

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Sample solution is provided at 25 µL, 10mM.

Product has been cited by 1 publications

Description Protocol Chemical Properties Product Documents Related Products

Tat-NR2B9c is designed to prevent nitric oxide (NO) production by preventing postsynaptic density protein 95 (PSD-95) binding to N-methyl-D-aspartate (NMDA) receptors and neuronal nitric oxide synthase. Tat-NR2B9c dissociates NMDA glutamate receptors from downstream excitotoxic signaling pathways without affecting normal glutamate receptor function. Neuroprotective effects of Tat-NR2B9c have been demonstrated in a diverse range of stroke models in several species including rodents, primates, and humans. Moreover, Tat-NR2B9c peptide has shown clinical efficacy as a neuroprotective agent in acute stroke.[1][2]

In vitro study indicated that Tat-NR2B9c have no measurable effect on the rate or magnitude of NMDA-induced calcium influx. However, Tat-NR2B9c prevented NMDA-induced DNA breaks, and the neuronal death could be significantly reduced by Tat-NR2B9c. Tat-NR2B9c also prevented NMDA-induced superoxide p47phox formation by blocking phosphorylation, and neuroprotective effect of Tat-NR2B9c may be partly or wholly attributable to its suppression of NOX2 activation. In addition, Tat-NR2B9c, which targets the PDZ domain of PSD-95, disrupts the functional coupling between NR2B and NOX2.[2]

In vivo experiments demonstrated that Tat-NR2B9c would be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders. Results indicated that Tat-NR2B9c reduced brain damage caused by hypoxic-ischemic injury when administered either before or after ischemia and improved post-HI neurobehavioral outcomes when delivered before or after ischemia. Moreover, Tat-NR2B9c might exert neuroprotective effects through the promotion of pro-survival signaling and inhibition of pro-apoptotic signaling.[1]

References:
[1]. Xu B, et al. Neuroprotective Effects of a PSD-95 Inhibitor in Neonatal Hypoxic-Ischemic Brain Injury. Mol Neurobiol. 2016 Nov;53(9):5962-5970.
[2]. Chen Y, et al. Tat-NR2B9c prevents excitotoxic neuronal superoxide production. J Cereb Blood Flow Metab. 2015 May;35(5):739-42.

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