nuclear translocation

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).

RS09 2TFA (1449566-36-2 free base) is a TLR4 agonist. Promotes NF-κB nuclear translocation and induces inflammatory cytokine secretion in RAW264.7 macrophages in vitro. It acts as an adjuvant in vivo and enhances X-15 specific antibody serum concentrations.

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

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.

Gastric inhibitory peptide (GIP) (22-51), a pro-atherogenic peptide comprised of 30 amino acids from the residues 22-51 of its precursor protein proGIP, is present in human plasma. It activates the degradation of IκB-α and the nuclear translocation of NF-κB in both macrophage-differentiated THP-1 cells and human aortic endothelial cells at a concentration of 1 µM. Additionally, in ApoE-/- mice, GIP (22-51) escalates the area of atherosclerotic lesions and plaque development in vivo.

SN52 is a powerful, competitive, and cell-permeable inhibitor of NF-κB2. It is a variant of the SN50 peptide. SN52 effectively prevents the nuclear translocation of p52-RelB heterodimers, exhibiting a robust radiosensitization effect on prostate cancer cells. This compound holds significant potential for cancer research purposes.

TLR4 agonist. Promotes NF-κB nuclear translocation and induces inflammatory cytokine secretion in RAW264.7 macrophages in vitro. Acts as an adjuvant in vivo; enhances X-15 specific antibody serum concentrations, when administered with X-15-KLH in mice.

SN50M (NF-κB Control) is a synthetic peptide containing a hydrophobic region and a mutant nuclear localization sequence that enters cells but does not inhibit NF-κB nuclear translocation or induce apoptosis.

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 nuclear translocation without affecting ERK or MSK1 activation. This compound is a valuable tool for investigating Elk-1's role in neuronal plasticity development [1].