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

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-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-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 is a Tat-tagged cell-penetrating fusion peptide that corresponds to residues 190-208 of rat G3BP1. The Tat sequence from HIV, positioned at the least conserved end of the sequence, facilitates cell permeability. Tat-peptide 190-208 enhances axonal growth and increases the number of axons per neuron, potentially demonstrating intrinsic axonal mechanisms. It may also be employed for ischemic protection during endovascular repair of intracranial aneurysms.

Tat-peptide 168-189 is a cell-permeable Tat-tagged fusion peptide corresponding to residues 168-189 of rat G3BP1. The Tat sequence from HIV is incorporated at the least conserved end of this sequence to enhance cellular permeability. Serving as a negative control for Tat-peptide 190-208, Tat-peptide 168-189 contrasts with Tat-peptide 190-208, which promotes axon growth and increases the number of neurites per neuron.

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-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-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].

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-PAK18 inhibitory peptide is a cell-permeable PAK inhibitor peptide. It is capable of reducing F-actin clusters and interfering with Shank3 knockdown effects.

Tat-NTS peptide is a cell-penetrating peptide with neuroprotective properties. It specifically inhibits the nuclear translocation of ANXA1, reducing neuronal apoptosis (apoptosis) in ischemic areas. Additionally, Tat-NTS peptide can decrease the volume of cerebral ischemic infarction, making it useful for research on ischemic stroke.

TAT-D1 peptide is a selective D1-D2 heteromer antagonist. It disrupts D1-D2 receptor heterodimers by interacting with specific domains of the D2 receptor through its unique amino acid sequence, especially the two glutamic acid residues at the C-terminus of the D1 receptor. TAT-D1 peptide is used for studying the role of D1-D2 receptor heterodimers in regulating depression and anxiety-like behaviors.

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-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].

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-Gap19(I130A) is a control peptide for TAT-Gap19, a Cx43 hemichannel blocker. TAT-Gap19(I130A) consists of TAT-GAP19 with a I130A amino acid residue change at a key residue for GAP19 activity. In C6 glioma cells expression Cx43, TAT-GAP19(1130A) does not inhibit [Ca2+]i-triggered ATP release at 200 μM. TAT-Gap19(I130A) is cell permeable.

TAT-Gap19(I130A) acetate is an inactive control peptide for the Cx43 inhibitor TAT-Gap19. It contains the I130A mutation and is used to verify biological specificity.

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

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