tat

TAT peptide (YGRKKRRQRRR), originating from the human immunodeficiency virus-1 (HIV-1) transactivator of transcription (TAT), enhances the solubility and production of heterologous proteins[1]. This cell-penetrating peptide demonstrates significant potential in biotechnological applications.

TAT (48-57) is a cell-permeable peptide derived from the HIV-1 transactivator of transcription (Tat) protein, encompassing amino acid residues 48 to 57 from the basic domain of HIV Tat.

TAT-Gap19 acetate is a specific inhibitor of connexin43 hemichannel (Cx43 HC). TAT-Gap19 acetate traverses the blood-brain barrier and alleviates liver fibrosis in mice. TAT-Gap19 acetate does not inhibit the corresponding Cx43 GJCs.

TAT-GluA2 3Y acetate is an inhibitor of AMPA receptor endocytosis.Systemic administration of Tat-GluA2(3Y) during the induction phase of d-amphetamine blocked maintenance of behavioural sensitization and attenuated the maintenance of neurochemical sensitization of rat.

Tat-NR2B9c (NA-1) is a postsynaptic density-95 (PSD-95) inhibitor with neuroprotective and antiepileptic effects.Tat-NR2B9c inhibits PSD-95d2, PSD-95d1, and PSD-95, which prevents the activation of NMDA-induced NADPH oxidase in neurons, thereby blocking the production of superoxide, which reduces ischemic injury in the acute phase after stroke.

Tat-NR2B9c TFA is a 20-aa peptide, and acts as an inhibitor of postsynaptic density-95 (PSD-95)(EC50 of 6.7 nM for PSD-95d2), and possesses neuroprotective efficacy.

Tat-NR2B9c acetate (NA-1 acetate) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c acetate disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c acetate also inhibits neuronal nitric oxide synthase (nNOS)/PSD-95 interaction, and possesses neuroprotective efficacy.

Tat-NR2BAA is an inactive control peptide of Tat-NR2B9c. It shares a similar sequence with Tat-NR2B9c, but possesses a double-point mutation in the COOH terminal tSXV motif. This mutation renders Tat-NR2BAA unable to bind PSD-95. Tat-NR2B9c, on the other hand, is a membrane-permeable peptide that interferes with PSD-95/NMDAR binding. This interference leads to the decoupling of NR2B- and/or NR2A-type NMDARs from PSD-95[1][2].

Biotin-TAT (47-57) is a biotin-tagged transactivator of transcription, commonly employed as a protein transduction domain (PTD) in various primary cells. Its transduction capacity is contingent on ATP and temperature, suggesting the participation of endocytosis.

Tat-beclin 1, a peptide derived from the autophagy protein beclin 1, is a powerful inducer of autophagy. It interacts with GAPR-1 (GLIPR2), a negative regulator of autophagy. Tat-beclin 1 effectively reduces polyglutamine expansion protein aggregates and inhibits various pathogens, such as HIV-1, in laboratory experiments. Additionally, it decreases mortality in mice infected with chikungunya (CHIKV) or West Nile virus (WNV).

Tat-beclin 1 acetate is a potent inducer of autophagy and interacts with the negative regulator of autophagy, GAPR-1. Tat-beclin 1 acetate decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1).

HIV-1 TAT (48-60) Acetate, a commonly used membrane-permeable carrier peptide, is an arginine-rich basic peptide derived from the human immunodeficiency virus (HIV-1 Tat) protein that enables intracellular delivery of compounds.

TAT-DEF-Elk-1 acetate is a cell-penetrating peptide inhibitor of ERK1/2 kinase phosphorylated Elk-1 with antitumor and antidepressant activity.TAT-DEF-Elk-1 acetate inhibits the phosphorylation of Elk-1, inhibits Elk-1 nuclear TAT-DEF-Elk-1 acetate inhibits Elk-1 phosphorylation and Elk-1 nuclear translocation, and can be used to study depression.

TRPV1-Tat, a peptide antagonist targeting transient receptor potential vanilloid 1 (TRPV1), is composed of amino acids 736-745 derived from TRPV1's A-kinase anchor protein (AKAP)-binding domain, combined with the HIV Tat-derived cell-penetrating peptide sequence. At a concentration of 200 µM, TRPV1-Tat effectively inhibits heat or phorbol 12-myristate 13-acetate (PMA014)-induced currents in primary mouse dorsal root ganglia via whole-cell patch-clamp assays. Additionally, when administered at dosages of 10 or 30 µM, it elevates the mechanical pain threshold in the hind paws of rats.

Tat-NTS peptide, a cell-penetrating compound, comprises the HIV-1 Tat protein transduction domain fused with a 10-amino acid sequence (residues 228-237) from the repeat III domain of annexin A1, serving as a nuclear translocation signal (NTS). This peptide hinders the interaction between annexin A1 and importin β, obstructing annexin A1's nuclear entry in primary mouse hippocampal neurons. Tat-NTS effectively prevents apoptosis triggered by glucose-oxygen deprivation and reperfusion in these neurons. When administered in vivo at a dosage of 10 mg/kg, it significantly reduces infarct size, minimizes neuronal apoptosis, and improves navigation performance in the Morris water maze test for mice subjected to ischemia-reperfusion injury via middle cerebral artery occlusion (MCAO).

Tat-CIRP, a peptide inhibitor, impedes the protein-protein interaction between myeloid differentiation 2 (MD-2), also known as lymphocyte antigen 96 (LY96), and cold-inducible RNA binding protein (CIRP) by binding to MD-2. This disrupts the MD-2 and CIRP interaction as confirmed in co-immunoprecipitation assays. Notably, in vivo studies reveal that Tat-CIRP, at dosages of 10 and 20 mg/kg, significantly reduces infarct volume in both a mouse model of middle cerebral artery occlusion (MCAO) and a rhesus monkey model of thrombosis-induced stroke. Additionally, it improves motor function, evidenced by decreased time to manipulate and withdraw food with the affected arm in the primate model.

Myr-Tat-CBD3 is a chemical compound that serves as an inhibitor of the protein-protein interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2). This compound effectively disrupts the Cav2.2-CRMP2 interaction by about 81% at a 10 µM concentration and demonstrates an inhibitory concentration 50 (IC50) value of approximately 2.8 µM against potassium-induced calcium influx in primary rat dorsal root ganglion (DRG) neurons. Furthermore, at a concentration of 20 µM, Myr-Tat-CBD3 specifically inhibits calcium currents without affecting sodium currents in primary DRG neurons. Additionally, intrathecal administration of 20 µg/5 µl of Myr-Tat-CBD3 effectively mitigates carrageenan-induced declines in paw withdrawal latencies in rats, indicating its potential for pain relief. The compound also notably reduces cue-induced reinstatement of cocaine-seeking behavior in rats, suggesting therapeutic potential in addiction treatment.

Cys-TAT(47-57) (Cys-[HIV-Tat (47-57)]) is an arginine-rich cell-penetrating peptide derived from the HIV-1 transactivating protein, corresponding to the protein transduction domain of the TAT protein.

TAT peptide corresponds to the polycationic aa49-57 region of TAT protein. TAT peptide is a cell-penetrating peptide (CPP) used to cargo larger molecules through the lipophilic barrier of the cellular membranes to deliver them inside the cells with intact

This peptide is a scrambled sequence of NADPH oxidase assembly peptide inhibitor gp91 ds-tat. It is used as a control peptide. It is two amino acid residues shorter at the N-terminus compared to the scrambled gp91 ds-tat.

TAT-amide is a cell-penetrating peptide (CPP) that exhibits the ability to enter various cells. CPPs, which are composed of short amino acid sequences, possess the capability to penetrate cell membranes and access intracellular compartments.

Selective HIF-1 dimerization inhibitor. Blocks protein-protein interaction of recombinant HIF-1α, but not HIF-2α, with HIF-1β (IC50 = 1.3 μM). Inhibits hypoxia-induced HIF-1 activity, and decreases VEGF and CAIX expression in osteosarcoma and breast cance

Cx43 hemichannel blocker (IC50 ~7 μM). No significant affinity for gap junctions or Panx1 channels. N-terminal transactivator of transcription (TAT) motif promotes membrane permeability and increases inhibitory effect of Gap19. Active in vivo. Brain penet

TAT-DEF-Elk-1 is a cell-penetrating peptide Elk-1 inhibitor.