tat peptide tfa

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

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

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 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-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-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 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-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].

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-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-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 cell-penetrating peptide obtained 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-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].