GBP3 Activators

BSO is a specific inhibitor of gamma-glutamylcysteine synthetase, which results in the depletion of intracellular glutathione (GSH). The reduction in GSH can lead to increased reactive oxygen species (ROS), which can enhance the activation of GBP3, as it is known to respond to oxidative stress signals.

DFO is an iron chelator that can lead to the induction of hypoxia-inducible factor 1-alpha (HIF-1α). HIF-1α is known to induce the transcription of many genes, including those involved in the response to inflammation and infection. The activation of HIF-1α can enhance the functional activity of GBP3 as it is involved in cellular responses to inflammation and infection.

Tunicamycin blocks the formation of protein N-glycosylation, leading to endoplasmic reticulum stress. This can induce the unfolded protein response (UPR). GBP3 is responsive to the UPR and can be functionally activated by this stress signal.

Thapsigargin induces endoplasmic reticulum stress by inhibiting the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA), leading to a decrease in ER calcium levels and the induction of the UPR. The UPR can enhance the functional activity of GBP3.

2-DG inhibits glycolysis by blocking glucose metabolism at the level of hexokinase, which can lead to cellular stress. This cellular stress can enhance the activation of GBP3, given its role in responding to cellular stress signals.

Dexamethasone is a glucocorticoid that can activate the glucocorticoid receptor (GR). Activation of GR can lead to the upregulation of genes involved in cell survival and inflammation, and thus can enhance the functional activity of GBP3, given its roles in these processes.

Bafilomycin A1 inhibits vacuolar-type H+-ATPase (V-ATPase), leading to the accumulation of autophagosomes. The induction of autophagy can enhance the functional activity of GBP3 as it is known to be involved in autophagy.

Rapamycin is an inducer of autophagy by inhibiting mTOR, a kinase that regulates cell growth and metabolism. The induction of autophagy can enhance the functional activity of GBP3, given its role in this process.

Tamoxifen is an estrogen receptor modulator. It can alter the activity of nuclear receptors and transcription factors, potentially affecting the transcription of genes involved in cell survival and inflammation. This can enhance the functional activity of GBP3, given its roles in these processes.

MG-132 is a proteasome inhibitor that can lead to the accumulation of ubiquitinated proteins, inducing cellular stress. This cellular stress can enhance the activation of GBP3, given its role in responding to cellular stress signals.