GABARAPL2 Activators
The chemical class of GABARAPL2 activators encompasses compounds that modulate the activation and function of GABARAPL2, a key player in autophagy regulation. These activators operate through diverse molecular mechanisms, shedding light on the intricate interplay between cellular signaling pathways and the modulation of GABARAPL2 activity. One notable subgroup within GABARAPL2 activators includes mTOR inhibitors like rapamycin, Torin 1, AZD8055, and SBI-0206965. These compounds directly activate GABARAPL2 by inhibiting mTOR, a central regulator of autophagy. Inhibition of mTOR induces autophagy, leading to increased GABARAPL2 expression and facilitating its involvement in autophagosome assembly. This subgroup underscores the pivotal role of mTOR-dependent regulation in GABARAPL2 activation and autophagic processes.
Another subgroup represented by Spautin-1, MK-2206, and PF-4708671 focuses on inhibiting specific kinases (USP10, AKT, and AMPK, respectively) to activate GABARAPL2. Spautin-1 inhibits USP10 and USP13, leading to increased GABARAPL2 stability and participation in autophagy. MK-2206 inhibits AKT, inducing autophagy and enhancing GABARAPL2 expression. PF-4708671 inhibits AMPK, promoting GABARAPL2 activation and autophagosome assembly. These compounds highlight the diverse kinase-dependent mechanisms that can modulate GABARAPL2 activity and autophagy. Additionally, GSK-3β inhibitors like SB 216763 and modulators of the AKT/mTOR pathway such as NSC 228155 contribute to GABARAPL2 activation by preventing its degradation and inducing autophagy. The connections between GSK-3β inhibition, AKT/mTOR modulation, and GABARAPL2 activation provide insights into the regulatory network governing GABARAPL2 stability and function in autophagy. The chemical class of GABARAPL2 activators, characterized by its diverse mechanisms of action, unveils the complexity of GABARAPL2 regulation and its integration into cellular signaling networks. Understanding these activators broadens our perspective on the molecular underpinnings of autophagy and opens new avenues for targeted interventions in autophagy-related pathologies.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Torin 1 | 1222998-36-8 | sc-396760 | 10 mg | $245.00 | 7 | |
Torin 1, an mTOR inhibitor, activates GABARAPL2 similarly to rapamycin. By inhibiting mTOR, Torin 1 induces autophagy, promoting GABARAPL2 expression and function in autophagosome assembly. This class of mTOR inhibitors emphasizes the significance of mTOR-dependent regulation in GABARAPL2 activation and autophagic processes. | ||||||
SBI-0206965 | 1884220-36-3 | sc-507431 | 10 mg | $124.00 | ||
SBI-0206965 activates GABARAPL2 by inhibiting ULK1. ULK1 inhibition induces autophagy, leading to increased GABARAPL2 expression and participation in autophagosome formation. The direct link between ULK1 inhibition and GABARAPL2 activation sheds light on the intricate regulatory network governing autophagy and GABARAPL2 function. | ||||||
AZD8055 | 1009298-09-2 | sc-364424 sc-364424A | 10 mg 50 mg | $163.00 $352.00 | 12 | |
AZD8055, an mTOR kinase inhibitor, activates GABARAPL2 by suppressing mTOR signaling. Inhibition of mTOR by AZD8055 induces autophagy, enhancing GABARAPL2 expression and involvement in autophagosome maturation. The relationship between mTOR kinase activity and GABARAPL2 activation underscores the pivotal role of mTOR in modulating autophagy and GABARAPL2 function. | ||||||
MK-2206 dihydrochloride | 1032350-13-2 | sc-364537 sc-364537A | 5 mg 10 mg | $182.00 $332.00 | 67 | |
MK-2206 activates GABARAPL2 by inhibiting AKT. AKT inhibition induces autophagy, leading to increased GABARAPL2 expression and involvement in autophagosome formation. The link between AKT inhibition and GABARAPL2 activation emphasizes the regulatory role of the AKT pathway in autophagy and GABARAPL2 function. | ||||||
SB-216763 | 280744-09-4 | sc-200646 sc-200646A | 1 mg 5 mg | $71.00 $202.00 | 18 | |
SB 216763, a GSK-3β inhibitor, activates GABARAPL2 by preventing its degradation. Inhibition of GSK-3β stabilizes GABARAPL2 and enhances its participation in autophagy. This pharmacological approach reveals a potential link between GSK-3β-mediated regulation and GABARAPL2 stability, providing insights into the modulation of autophagy through GSK-3β and GABARAPL2 interaction. | ||||||
NSC 185058 | 39122-38-8 | sc-507531 | 1 mg | $85.00 | ||
NSC 185058 activates GABARAPL2 by modulating the AMPK/mTOR pathway. By influencing AMPK and mTOR signaling, NSC 185058 induces autophagy, leading to increased GABARAPL2 expression and involvement in autophagosome assembly. The connection between AMPK/mTOR modulation and GABARAPL2 activation underscores the intricate regulatory network governing autophagy and GABARAPL2 function. | ||||||
Verteporfin | 129497-78-5 | sc-475698 sc-475698A | 10 mg 100 mg | $354.00 $2764.00 | 5 | |
Verteporfin activates GABARAPL2 by modulating the Hippo/YAP pathway. By influencing YAP activity, Verteporfin induces autophagy, leading to increased GABARAPL2 expression and participation in autophagosome maturation. The connection between Hippo/YAP signaling and GABARAPL2 activation highlights the crosstalk between cellular pathways in regulating autophagy and GABARAPL2 function. | ||||||