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-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-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-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-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 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].

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.

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

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-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].

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].

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].