TAT TFA

TAT TFA, derived from the transactivator of transcription (TAT) of human immunodeficiency virus (HIV-1), is a cell-penetrating peptide known for its ability to enhance the yields and solubility of heterologous proteins [1].

TAT TFA (YGRKKRRQRRR) is derived from human immunodeficiency virus (hiv-1) transcription reverse activator TAT, is a cell penetrating peptide.

TAT-P4-(DATC5)2 TFA, a high-affinity peptide inhibitor targeting the PDZ domain of protein interacting with C kinase-1 (PICK1), exhibits a K i of 1.7 nM and demonstrates potential in mitigating addiction behaviors in rats [1].

TAT-Gap19 TFA, a Cx mimetic peptide and specific connexin43 hemichannel (Cx43 HC) inhibitor, does not inhibit the corresponding Cx43 gap junction channels (GJCs). It crosses the blood-brain barrier and has been shown to alleviate liver fibrosis in mice [1] [2] [3].

TAT-DEF-Elk-1 TFA (TDE TFA) is a cell-penetrating peptide that inhibits Elk-1 by mimicking its DEF domain and disrupting its function. It effectively blocks Elk-1 phosphorylation and its subsequent nuclear translocation, without affecting the activation of ERK or MSK1. This compound serves as a valuable tool for investigating Elk-1's involvement in the development of neuronal plasticity [1].

Tat-peptide 190-208 TFA is a Tat-labeled, cell-permeable fusion peptide derived from residues 190-208 of rat G3BP1. The HIV-derived Tat sequence, positioned at the peptide's least conserved region, confers cellular permeability. This compound promotes axon growth and enhances the formation of neurites per neuron, suggesting an axon intrinsic mechanism of action. Additionally, it has potential applications in providing ischemic protection during endovascular repair of intracranial aneurysms [1].

Tat-peptide 168-189, a cell-permeable, Tat-labeled fusion peptide derived from residues 168-189 of rat G3BP1, features the HIV Tat sequence at its least conserved terminus to enhance cellular uptake. It serves as the negative control for Tat-peptide 168-189 TFA, which promotes axon growth and neurite proliferation [1].

TAT-DEF-Elk-1 TFA is a cell-penetrating peptide Elk-1 inhibitor, mimics and specifically interferes with the DEF domain of Elk-1. TAT-DEF-Elk-1 blocks Elk-1 phosphorylation and prevents Elk-1 nuclear translocation without interfering with ERK nor MSK1 act

Tat-beclin 1 TFA, a peptide originating from a segment of the autophagy protein beclin 1, effectively initiates autophagy and engages with the autophagy negative regulator, GAPR-1 (GLIPR2). It notably reduces the buildup of polyglutamine expansion protein aggregates and curtails the in vitro replication of various pathogens, including HIV-1. Moreover, Tat-beclin 1 TFA has demonstrated a reduction in mortality rates in mice infected with either chikungunya (CHIKV) or West Nile virus (WNV) [1].

TAT-BH4 (Bcl-xL) TFA, primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an eosin-labeled cysteine at the N-terminal and the protein transduction domain from the HIV TAT protein (amino acids 49 to 57), fused to the Bcl-xL BH4 peptide. It is utilized in research concerning diseases associated with accelerated apoptosis [1].

TAT-cyclo-CLLFVY TFA is a cyclic peptide inhibitor specifically targeting HIF-1 heterodimerization to mitigate hypoxia signaling within cancer cells. It effectively disrupts the protein-protein interaction between HIF-1α and HIF-1β, demonstrating an inhibitory concentration (IC 50) of 1.3 μM [1].

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 peptide (TFA), a cell-penetrating peptide (GRKKRRQRRRPQ) originating from HIV-1's trans-activating transcriptional activator (Tat), facilitates intracellular delivery [1] [2].

TAT-NEP1-40 TFA, a blood-brain barrier-permeable peptide, safeguards PC12 cells against oxygen and glucose deprivation (OGD) and fosters neurite outgrowth. Additionally, it enhances neurological outcomes post-ischemia by curtailing apoptosis in ischemic cerebral tissues. This compound has utility in investigating central nervous system (CNS) injuries, encompassing axonal regeneration and functional recuperation following a stroke [1].

TAT-amide TFA is a cell penetrating peptide. The cell - penetrating peptides (CPPs) is a kind of access to the short amino acid sequence of different cells.

TAT-14 TFA is a 14-mer peptide functioning as an Nrf2 activator possessing anti-inflammatory properties. It does not alter Nrf2 mRNA expression but elevates Nrf2 protein levels by targeting the Nrf2 binding site on Keap1 [1].

TAT (48-57) (TFA) is a peptide capable of penetrating cells, sourced from residues 48-57 of the HIV-1 Tat (transactivator of transcription) protein.

Tat-NR2BAA TFA serves as the inactive control peptide for Tat-NR2B9c, featuring a comparable sequence with a crucial distinction: a double-point mutation in its COOH-terminal tSXV motif. This alteration renders Tat-NR2BAA TFA unable to bind to PSD-95, in contrast to Tat-NR2B9c. The latter is a membrane-permeant peptide that impedes PSD-95/NMDAR interaction, specifically detaching NR2B- and/or NR2A-type NMDARs from PSD-95 [1].

TAT (48-57) (TFA) is a cellular permeability peptide derived from hiv-1 transcriptional activator (TAT) protein residue 48-57.

Tat-AKAP79 (326-336) is a peptide that links the HIV-1 Tat protein transduction domain with an 11-amino acid sequence from A-kinase anchor protein 79 (AKAP79). This compound effectively inhibits the activation-induced sensitization by protein kinase A (PKA) or PKC of the transient receptor potential vanilloid 1 (TRPV1) at a concentration of 200 µM in isolated rat dorsal root ganglion (DRG) neurons. Additionally, it mitigates nocifensive behavior in mice elicited by formalin or phorbol 12-myristate 13-acetate (PMA014), enhances latency for paw withdrawal from radiant heat, and raises the mechanical threshold force required for paw withdrawal in a carrageenan-induced mouse model of inflammatory pain.

Tat-QFNP12 is a peptide that combines a transcriptional transactivator (Tat) transmembrane domain with an inhibitor targeting the interaction between N-Myc downstream regulated gene 2 (NDRG2) and protein phosphatase Mg2+/Mn2+ dependent 1A (PPM1A). This compound effectively mitigates blood-brain barrier endothelial tight junction disruption caused by elevated levels of matrix metalloproteinase-9 (MMP-9), alleviates cerebral edema, and promotes spontaneous activity along with symmetric limb movement in a mouse model of subarachnoid hemorrhage induced by endovascular puncture. These benefits are observed at a dosage of 20 mg/kg.

Tat-Gap 19, a peptide inhibitor of connexin43 (Cx43) hemichannels, is derived from the HIV-1 Tat protein transduction domain fused with a nine-amino acid sequence from Cx43 residues 128-136. This compound, at a concentration of 10 µM, effectively suppresses glutamate-induced ATP release in primary rat hepatocytes, indicating inhibition of Cx43 hemichannel activity. Furthermore, Tat-Gap 19 demonstrates therapeutic potential by significantly reducing infarct volume in a mouse cerebral ischemia-reperfusion injury model following middle cerebral artery occlusion (MCAO) at a dosage of 25 mg/kg. Moreover, its intraperitoneal administration at 1 mg/kg per day ameliorates fibrosis and decreases the area of hepatic stellate cells, the precursors to myofibroblasts, expressing α-smooth muscle actin (α-SMA), in a model of thioacetamide-induced liver damage. Additionally, it enhances superoxide dismutase (SOD) activity in hepatic cells from the treated mice, indicating its antioxidative benefits.

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-βsyn-degron, an α-synuclein knockdown peptide, integrates three domains: the HIV-1 Tat plasma membrane transduction domain, an α-synuclein binding domain (βsyn) representing amino acids 36-45 of β-synuclein, and a proteasomal targeting domain (degron). It effectively binds to recombinant α-synuclein, demonstrating a significant reduction in α-synuclein levels in primary rat cortical neuron cultures.

Tat-CBD3 is a chemical compound inhibiting the interaction between the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2), as well as the interaction between CRMP2 and the NMDA receptor NR2B subunit. At a concentration of 10 µM, Tat-CBD3 reduces the Cav2.2-CRMP2 interaction by 43% in cell-free assays and impedes the NMDA receptor NR2B subunit-CRMP2 interaction in immunoprecipitation assays. It lowers voltage-induced calcium currents by about 60% in primary rat dorsal root ganglion (DRG) neurons and decreases glutamate-induced cytosolic calcium level rises in primary rat hippocampal neurons. When administered at 20 mg/kg, Tat-CBD3 lessens infarct volume in a rat model of cerebral ischemia following middle cerebral artery occlusion (MCAO). Additionally, intrathecal delivery of Tat-CBD3 at a dose of 20 µg/5 µl mitigates carrageenan-induced thermal hypersensitivity in rats.

Tat-M2NX, a peptide antagonist of transient receptor potential melastatin 2 (TRPM2), blocks hydrogen peroxide-induced calcium influx in HEK293 cells expressing human TRPM2 at concentrations between 25 to 100 µM. In male mice models of stroke caused by middle cerebral artery occlusion (MCAO), Tat-M2NX (20 mg/kg) demonstrates efficacy in reducing brain infarct volume when applied before or 3 hours-post occlusion, yet it shows no such effect in female mice.

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.

Tat-CBD3A6K, a peptide derivative of the N-type voltage-gated calcium channel Cav2.2 and collapsin response mediator protein 2 (CRMP2) interaction inhibitor Tat-CBD3, has demonstrated efficacy in a rat model of antiretroviral neuropathic pain caused by stavudine (d4T). Administered at 10 mg/kg, it preserves paw withdrawal threshold, indicating pain relief, and reduces the number of action potentials in dorsal root ganglia (DRG) neurons from affected rats. Additionally, a 30 µM/animal dural dose of Tat-CBD3A6K lessens meningeal blood flow escalation triggered by capsaicin, showcasing its potential in managing neuropathic pain and inflammation.

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.