Date published: 2025-9-12

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ULK1 Activators

Common ULK1 Activators include, but are not limited to Rapamycin CAS 53123-88-9, Torin 1 CAS 1222998-36-8, Spermidine CAS 124-20-9, Curcumin CAS 458-37-7 and Lithium CAS 7439-93-2.

ULK1, also known as Unc-51 like autophagy activating kinase 1, is a serine/threonine kinase that plays a crucial role in autophagy, a cellular process responsible for the degradation and recycling of cellular components. Autophagy is essential for maintaining cellular homeostasis, responding to stress, and removing damaged organelles and proteins. ULK1 is a key initiator of autophagy, as it phosphorylates downstream targets involved in autophagosome formation. ULK1 is regulated by nutrient availability, energy status, and various signaling pathways, making it a central player in the coordination of cellular responses to changing environmental conditions. ULK1 Activators, a theoretical class of chemical compounds, could potentially modulate the activity of ULK1, impacting its role in autophagy initiation and cellular homeostasis.

The potential mechanism of action of ULK1 Activators might involve the direct interaction with ULK1 itself or with regulatory proteins that modulate its activity. These activators could potentially enhance the phosphorylation of ULK1 and its downstream targets, leading to increased autophagy initiation. By promoting the activation of ULK1, these compounds might enhance the cellular capacity to degrade and recycle damaged organelles and proteins, contributing to overall cellular health and survival. ULK1 Activators might also influence the crosstalk between autophagy and other cellular pathways, such as mTOR signaling, which regulates nutrient sensing and growth. Additionally, these activators could impact the formation and dynamics of autophagosomes, the vesicles responsible for delivering cargo to lysosomes for degradation. As autophagy is implicated in various physiological and pathological processes, ULK1 Activators hold potential for further elucidating the intricate regulation of autophagy and its broader implications for cellular function. However, more research is needed to understand the precise mechanisms by which these activators could modulate ULK1 activity and autophagy initiation.

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