tat peptide

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

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-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 at the peptide's least conserved region confers cellular permeability. This compound promotes axon growth and enhances neurite formation 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-NSF222 Fusion Peptide is a bifunctional polypeptide comprising a TAT domain for cellular uptake via macropinocytosis and an NSF domain that inhibits N-ethylmaleimide-sensitive factor (NSF), serving as an exocytosis inhibitor [1].

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-HA2 Fusion Peptide, a peptide-based delivery agent, synergizes the pH-sensitive HA2 fusion peptide from Influenza with the cell-penetrating peptide TAT from HIV. This compound facilitates the cellular uptake of macromolecules through the TAT component and triggers their release into cells by exploiting the acidifying endosomal lumen to induce membrane leakage via the HA2 component [1].

TAT-GluR23A Fusion Peptide is a bioactive peptide comprising the GluR23A sequence—residues 869 to 877 of GluR23Y with alanine replacing tyrosine—and an 11 amino acid cell-permeable HIV Trans-Activator of Transcription (TAT) protein transduction domain (PTD). It serves as an inactive control counterpart to the glutamate receptor endocytosis inhibitor GluR23Y, devoid of crucial phosphorylation sites.

TAT-NSF700 Fusion Peptide, a potent inhibitor of N-ethyl-maleimide-sensitive factor (NSF), possesses the ability to penetrate cell membranes and directly interact with intracellular organelles [1].

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-NSF700 Fusion Peptide acetate is a membrane-permeable inhibitor of N-ethyl-maleimide-sensitive factor (NSF), a fusion peptide with potential anti-inflammatory activity.TAT-NSF700 Fusion Peptide acetate interacts with intracellular organelles and can be used to investigate Myocardial ischemia and reperfusion injury.

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

F1, an anti-inflammatory peptide, incorporates the HIV-1 Tat protein transduction domain linked with a 15-amino acid sequence from residues 46-60 of the inhibitor of NF-κB kinase-interacting peptide (IKIP). It effectively blocks LPS-induced phosphorylation of IκB kinase α (IKKα) and IKKβ, along with the nuclear translocation of NF-κB (p65) in mouse peritoneal macrophages at 5 µM concentration. F1, administered at 5 mg/kg in vivo, significantly reduces IL-6, TNF-α, and IL-1β serum levels and enhances survival in a mouse sepsis model induced by LPS.

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 14 acetate, a 14-mer peptide, is an Nrf2 activator with anti-inflammatory properties. TAT 14 acetate increases Nrf2 protein levels due to targeting the Nrf2 binding site on Keap1, but has no effect on Nrf2 mRNA expression.

Cys-TAT(47-57) acetate is derived from the HIV-1 transactivating protein. Cys-TAT(47-57) acetate is an arginine rich peptide that can penetrate cells.

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-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, 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).

HIV-1 TAT (48-60), a cell-penetrating peptide originating from residues 48-60 of the human immunodeficiency virus (HIV)-1 Tat protein, facilitates the non-disruptive delivery of exogenous macromolecules into cells.

TAT 2-4 is a peptide derived from HIV-1 transactivator of transcription (Tat) protein. This small, basic peptide has demonstrated efficacy in delivering a wide range of cargoes, including small particles, proteins, peptides, and nucleic acids.

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

Cys(Npys)-TAT (47-57), a peptide fragment corresponding to the transduction domain of the TAT peptide, contains an activated cysteine residue C and can electrostatically interact with plasmid DNA. Notably, TAT is a small nuclear transcriptional activator protein encoded by HIV-1 [1].

HIV-1 TAT (48-60) is a cell-penetrating peptide derived from the human immunodeficient virus (HIV)-1 Tat protein residue 48-60. This is one of the cell-penetrating peptides generated from the human immunodeficient virus -1 Tat protein residue 48-60.

Peptide A5K acetate, an INF7-TAT derivative, facilitates CRISPR RNP delivery to T cells and effectively enhances Cas9 RNP transport to natural killer (NK) cells [1].

A11, a cell-penetrating peptide, integrates the HIV-1 Tat protein transduction domain with an 11-amino acid segment from the annexin A1 N-terminus (residues 20-30). This compound disrupts the interaction between annexin A1 and the Eph receptor tyrosine kinase A2 (EphA2), leading to enhanced EphA2 ubiquitination in HK1 nasopharyngeal carcinoma (NPC) cells. At a concentration of 10 µM, A11 curtails proliferation, migration, and invasion of HK1 and 5-8F NPC cells. Furthermore, A11 demonstrably diminishes tumor volume in mouse xenograft models of 5-8F and HK1 NPC in vivo.

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.

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

TAT (48-57) (TFA) is a cell-penetrating peptide obtained from residues 48-57 of the HIV-1 Tat (transactivator of transcription) protein.

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-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-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-BH4 (Bcl-xL), primarily localized at the mitochondria, inhibits apoptotic cell death. This compound comprises an N-terminal eosin-labeled cysteine and the protein transduction domain of the HIV TAT protein (amino acids 49 to 57), fused to the Bcl-xL BH4 peptide. It serves as a tool for research into diseases characterized by accelerated apoptosis [1].

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-GluN2BCTM is a membrane-permeable peptide that selectively targets active DAPK1 (Death-associated protein kinase 1) for lysosomal degradation, protecting neurons against oxidative stress and NMDAR-mediated excitotoxicity, making it valuable for neuroprotection research studies [1].

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.

Shepherdin is a synthetic peptide mirroring amino acids 79-87 of human survivin, acting as an inhibitor of the survivin-heat shock protein 90 (Hsp90) interaction. It specifically targets the N-terminal domain of Hsp90, blocking the survivin-Hsp90 interaction in human reticulocyte extracts at a 150 µM concentration. Conjugates of Shepherdin with cell-permeable peptides, such as penetratin or the HIV Tat sequence, exhibit anticancer properties both in vitro and in vivo.

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-NSF700scr comprises the complete TAT domain and a glycine linker, succeeded by the NSF amino acids arranged randomly. It serves as a control peptide, ineffective in inhibiting SNARE-mediated exocytosis [1] [2].

Tat-beclin 1 TFA, a peptide derived from a segment of the autophagy protein beclin 1, effectively induces autophagy and interacts with the autophagy negative regulator GAPR-1 (GLIPR2). It reduces the accumulation of polyglutamine expansion protein aggregates and limits the in vitro replication of various pathogens, including HIV-1. Additionally, Tat-beclin 1 TFA has been shown to decrease mortality rates in mice infected with chikungunya (CHIKV) or West Nile virus (WNV) [1].

TAT-CIRP, a trans-activating (Tat) cold-inducible RNA-binding protein-derived peptide, functions as an inhibitor of myeloid differentiation protein 2 (MD2). It has demonstrated significant neuroprotective effects against ischemic and hemorrhagic stroke in mouse models [1].

FITC-LC-TAT (47-57), a fluorescein isothiocyanate (FITC)-labeled trans-activator of transcription (TAT) peptide, is recognized as a cell-penetrating peptide (CPP) and enhances the yield and solubility of heterologous proteins [1].

GluR23Y, a biologically active peptide, was utilized in an ELISA-based cell-surface assay to assess insulin-stimulated endocytosis of native AMPA receptors in cultured hippocampal neurons. GluR23Y effectively inhibited the insulin-induced decrease in receptor presence. The inhibition of insulin effects was achieved by introducing GluR23Y into neurons through fusion with the membrane transduction domain of HIV-1 TAT.

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-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.

D-JBD19 [D-JNKI1-TAT (residues 153-163)] is a non-permeable peptide that offers neuroprotective effects.

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