Tat-NR2B9c (NA-1) is an peptide that inhibits PSD-95, thus disrupting binding to N-methyl-D-aspartate receptors (NMDARs) and neuronal nitric oxide synthases (nNOS) and reducing excitoxicity induced by cerebral ischemia.
CAT No: 10-101-142
CAS No:500992-11-0
Synonyms/Alias:Tat-NR2B9c;500992-11-0;Nerinetide;Tat-NR2B9c TFA;NA-1;FN023;1834571-04-8;Nerinetida;Nerinetide [USAN];Tat NR2B9c;UNII-D45TI2TWMA;D45TI2TWMA;Tat-NR2Bct TFA;NA-1 TFA;GTPL12332;FN-023;WHO 10857;AKOS040740169;AS-82902;DA-58297;DA-58298;D84054;L-tyrosylglycyl-L-arginyl-L-lysyl-L-lysyl-L-arginyl-L-arginyl-L- glutaminyl-L-arginyl-L-arginyl-L-arginyl-L-lysyl-L-leucyl-L-seryl-L-seryl-L-isoleucyl-L-alpha-glutamyl-L-seryl-L-alpha-aspartyl-L-valine;L-Valine, L-tyrosylglycyl-L-arginyl-L-lysyl-L-lysyl-L-arginyl-L-arginyl-L- glutaminyl-L-arginyl-L-arginyl-L-arginyl-L-lysyl-L-leucyl-L-seryl-L-seryl-L-isoleucyl-L-alpha-glutamyl-L-seryl-L-alpha-aspartyl-;
TAT-NR2B9c is a synthetic peptide conjugate that combines the cell-penetrating properties of the TAT (trans-activator of transcription) peptide with the NR2B9c sequence, derived from the C-terminus of the NR2B subunit of the NMDA receptor. This fusion enables the molecule to traverse cellular membranes efficiently, facilitating intracellular delivery and modulation of protein-protein interactions within neural cells. Recognized for its specificity in targeting postsynaptic density protein-95 (PSD-95), TAT-NR2B9c has emerged as a valuable research tool in neurobiology, particularly in elucidating the molecular mechanisms underlying excitotoxicity and synaptic signaling. Its unique design allows for the selective disruption of NMDA receptor-PSD-95-nNOS (neuronal nitric oxide synthase) complexes without broadly affecting NMDA receptor function, providing researchers with a precise means to investigate downstream signaling pathways and neuroprotective strategies in various experimental models.
Neuroprotection research: TAT-NR2B9c is widely utilized in studies focused on neuroprotection, especially in the context of excitotoxic neuronal injury. By interfering with the interaction between NMDA receptors and PSD-95, the peptide effectively attenuates the excessive activation of nNOS and subsequent overproduction of neurotoxic nitric oxide. This targeted disruption helps delineate the molecular events that contribute to cell death in response to glutamate excitotoxicity, providing an experimental platform for exploring neuroprotective interventions. Researchers often employ the compound in in vitro and in vivo models to assess its capacity to modulate signaling cascades, thereby gaining insights into the potential mechanisms that underlie neuronal survival and resilience.
Synaptic signaling studies: In the realm of synaptic biology, TAT-NR2B9c serves as a critical probe for dissecting the functional architecture of postsynaptic signaling complexes. Its ability to selectively uncouple NMDA receptor-mediated signaling from PSD-95-dependent pathways enables scientists to investigate the distinct roles of these molecular assemblies in synaptic plasticity, learning, and memory. Utilizing this peptide, researchers can parse out the contributions of specific protein interactions to long-term potentiation and other forms of synaptic adaptation, advancing the understanding of how synaptic strength and connectivity are regulated at the molecular level.
Ischemia and stroke modeling: The application of TAT-NR2B9c extends to experimental models of cerebral ischemia and stroke, where it is employed to characterize the cellular and molecular responses to acute brain injury. By inhibiting the recruitment of nNOS to the NMDA receptor complex, the peptide mitigates downstream neurotoxic signaling events that are implicated in ischemic damage. This approach allows for the exploration of neuroprotective pathways and the identification of potential molecular targets for reducing neuronal loss following ischemic insults, thereby enriching the repertoire of experimental tools available for stroke research.
Pain pathway investigation: TAT-NR2B9c also finds utility in studies of pain signaling, particularly in the context of central sensitization and chronic pain states. By modulating NMDA receptor-PSD-95 interactions within spinal cord neurons, the peptide provides a means to probe the molecular underpinnings of nociceptive transmission and the development of pain hypersensitivity. Researchers leverage this tool to unravel the complex signaling networks that govern pain processing, enabling the identification of key regulatory nodes that may be amenable to therapeutic intervention in pain disorders.
Neurodegenerative disease research: In investigations centered on neurodegenerative disorders, TAT-NR2B9c is employed to examine the role of dysregulated NMDA receptor signaling in disease progression. Its targeted mechanism permits the dissection of specific protein interactions that contribute to synaptic dysfunction and neuronal loss in models of conditions such as Alzheimer's and Parkinson's disease. Through these studies, the peptide aids in clarifying the contribution of excitotoxic mechanisms to neurodegeneration, fostering a deeper understanding of disease pathogenesis and the identification of novel molecular targets for intervention. Collectively, the multifaceted applications of TAT-NR2B9c underscore its significance as a versatile and powerful tool for advancing research in neuroscience, synaptic biology, and neurodegenerative disease modeling.
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