IRE1β Activators
IRE1β Activators encompass a range of compounds that indirectly stimulate the activity of IRE1β, a key enzyme in the unfolded protein response (UPR) pathway, particularly essential in intestinal epithelial cells. This protein's activation is closely tied to the management of ER stress, a condition arising from the accumulation of misfolded proteins within the endoplasmic reticulum. Compounds such as Tunicamycin, Thapsigargin, DTT, and Brefeldin A induce ER stress through various mechanisms, thereby activating IRE1β. Tunicamycin disrupts glycosylation, while Thapsigargin interferes with calcium homeostasis, and DTT affects protein folding by reducing disulfide bonds. Brefeldin A hampers ER-Golgi transport, leading to protein accumulation. These stressors activate IRE1β as part of the UPR, enabling it to play its crucial role in restoring ER function and cellular homeostasis.
Additionally, compounds like 2-Deoxy-D-glucose, Tauroursodeoxycholic Acid, Sodium Salt, and 4-Phenylbutyric acid modulate IRE1β activity by influencing metabolic processes and chemical chaperoning, respectively. 2-Deoxy-D-glucose, a glucose analog, induces stress by impairing glycolysis, while Tauroursodeoxycholic Acid, Sodium Salt and 4-Phenylbutyric acid, as chemical chaperones, help in protein folding, thus modulating ER stress and subsequently IRE1β activation. Suberoylanilide Hydroxamic Acid and MG-132 [Z-Leu- Leu-Leu-CHO] further contribute to IRE1β activation by altering gene expression and inhibiting protein degradation, leading to increased ER stress. AICAR and Chloroquine, through AMPK activation and autophagy inhibition, respectively, also trigger ER stress, thereby enhancing IRE1β's role in the UPR. Lastly, elevated DL-Homocysteine levels induce ER stress, contributing to IRE1β activation. Collectively, these IRE1β Activators, by modulating ER stress and the UPR, highlight the essential role of IRE1β in maintaining ER function and cellular homeostasis, particularly in response to various forms of cellular stress.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Tunicamycin | 11089-65-9 | sc-3506A sc-3506 | 5 mg 10 mg | $172.00 $305.00 | 66 | |
Tunicamycin, an inhibitor of N-linked glycosylation, indirectly enhances IRE1β activity. By disrupting glycosylation, it leads to the accumulation of misfolded proteins in the ER, thereby activating the unfolded protein response (UPR) in which IRE1β plays a crucial role, particularly in intestinal epithelial cells. | ||||||
Thapsigargin | 67526-95-8 | sc-24017 sc-24017A | 1 mg 5 mg | $136.00 $446.00 | 114 | |
Thapsigargin, a SERCA pump inhibitor, indirectly activates IRE1β. By depleting ER calcium stores, it induces ER stress and activates the UPR pathway. IRE1β, as a critical sensor in this pathway, becomes activated in response to such stress, particularly in handling misfolded protein accumulation. | ||||||
Brefeldin A | 20350-15-6 | sc-200861C sc-200861 sc-200861A sc-200861B | 1 mg 5 mg 25 mg 100 mg | $31.00 $53.00 $124.00 $374.00 | 25 | |
Brefeldin A, an ER-Golgi transport inhibitor, indirectly activates IRE1β. By disrupting protein trafficking between the ER and Golgi, it induces ER stress, leading to the activation of the UPR. IRE1β, as an ER stress sensor, becomes more active in response to such disturbances in protein processing. | ||||||
2-Deoxy-D-glucose | 154-17-6 | sc-202010 sc-202010A | 1 g 5 g | $70.00 $215.00 | 26 | |
2-Deoxy-D-glucose, a glucose analog and glycolysis inhibitor, indirectly enhances IRE1β activity. By impeding glycolysis and energy production, it induces ER stress, subsequently activating the UPR. IRE1β's role in the UPR is thus upregulated, particularly in maintaining cellular homeostasis under metabolic stress. | ||||||
Suberoylanilide Hydroxamic Acid | 149647-78-9 | sc-220139 sc-220139A | 100 mg 500 mg | $133.00 $275.00 | 37 | |
Suberoylanilide Hydroxamic Acid, a histone deacetylase inhibitor, indirectly activates IRE1β. By altering gene expression and protein acetylation, it can induce ER stress, leading to the activation of the UPR. IRE1β, involved in this response, becomes more active in managing the cellular stress response. | ||||||
MG-132 [Z-Leu- Leu-Leu-CHO] | 133407-82-6 | sc-201270 sc-201270A sc-201270B | 5 mg 25 mg 100 mg | $60.00 $265.00 $1000.00 | 163 | |
MG-132 [Z-Leu- Leu-Leu-CHO], a proteasome inhibitor, indirectly enhances IRE1β activity. By blocking protein degradation, it causes protein accumulation and ER stress, activating the UPR. IRE1β, as part of this pathway, responds to increased protein load, playing a significant role in alleviating stress-induced damage. | ||||||
AICAR | 2627-69-2 | sc-200659 sc-200659A sc-200659B | 50 mg 250 mg 1 g | $65.00 $280.00 $400.00 | 48 | |
AICAR, an AMPK activator, indirectly enhances IRE1β activity. By mimicking energy depletion and activating AMPK, it can induce ER stress, leading to the activation of the UPR. IRE1β, as an ER stress sensor, becomes more active in regulating cellular responses to metabolic stress. | ||||||
Chloroquine | 54-05-7 | sc-507304 | 250 mg | $69.00 | 2 | |
Chloroquine, an autophagy inhibitor, indirectly activates IRE1β. By inhibiting lysosomal function and autophagy, it can induce ER stress, subsequently activating the UPR. IRE1β, essential in the UPR, becomes more active in response to the increased demand for dealing with misfolded proteins. | ||||||
4-Phenylbutyric acid | 1821-12-1 | sc-232961 sc-232961A sc-232961B | 25 g 100 g 500 g | $53.00 $136.00 $418.00 | 10 | |
4-Phenylbutyric acid, a chemical chaperone, indirectly enhances IRE1β activity. It alleviates ER stress and modulates the UPR. This modulation potentially leads to a controlled activation of IRE1β, crucial in the UPR's role in managing ER stress and maintaining protein homeostasis. | ||||||
Homocysteine | 6027-13-0 | sc-507315 | 250 mg | $195.00 | ||
DL-Homocysteine, when elevated, indirectly activates IRE1β. High levels of homocysteine can induce ER stress, leading to the activation of the UPR. IRE1β, as a sensor and mediator of the UPR, plays a key role in responding to such metabolic disturbances, particularly in maintaining ER function. | ||||||