PARL Inhibitors
PARL inhibitors belong to a specific class of chemical compounds that target an enzyme known as Presenilin-Associated Rhomboid-Like Protein (PARL). PARL is a transmembrane protease that plays a crucial role in the mitochondria, the cell's powerhouse, where it is responsible for cleaving and processing various mitochondrial proteins. These inhibitors are designed to selectively bind to the active site of PARL, inhibiting its enzymatic activity. By doing so, they modulate the proteolytic processing of specific mitochondrial proteins, which can have significant implications for cellular processes and functions.
The inhibition of PARL activity may impact various mitochondrial functions, including the regulation of apoptosis (cell death), mitochondrial dynamics, and bioenergetics. Through their targeted action on PARL, these inhibitors have the potential to influence mitochondrial homeostasis, leading to alterations in cellular signaling pathways and cellular responses to stress. As a consequence, PARL inhibitors have drawn significant attention from researchers exploring new avenues for understanding mitochondrial biology and its impact on various cellular processes. Due to their precise mechanism of action and the central role of mitochondria in cellular physiology, PARL inhibitors offer promising avenues for research and investigation in multiple fields, including cell biology, biochemistry, and neurobiology. The ability to specifically modulate PARL activity using these inhibitors can provide invaluable insights into the complex interplay between mitochondrial function and cellular health, opening new avenues for understanding cellular processes that are governed by these organelles.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Mdivi-1 | 338967-87-6 | sc-215291 sc-215291B sc-215291A sc-215291C | 5 mg 10 mg 25 mg 50 mg | $66.00 $124.00 $246.00 $456.00 | 13 | |
Mdivi-1 is a selective inhibitor of mitochondrial division DRP1. By inhibiting DRP1, it prevents mitochondrial fission, potentially influencing PARL's role in mitochondrial quality control by stabilizing mitochondrial morphology. | ||||||
Cyclosporin A | 59865-13-3 | sc-3503 sc-3503-CW sc-3503A sc-3503B sc-3503C sc-3503D | 100 mg 100 mg 500 mg 10 g 25 g 100 g | $62.00 $90.00 $299.00 $475.00 $1015.00 $2099.00 | 69 | |
Cyclosporin A inhibits the mitochondrial permeability transition pore, indirectly affecting mitochondrial regulation processes where PARL might be involved, particularly in preventing apoptosis by maintaining mitochondrial integrity. | ||||||
Oligomycin A | 579-13-5 | sc-201551 sc-201551A sc-201551B sc-201551C sc-201551D | 5 mg 25 mg 100 mg 500 mg 1 g | $175.00 $600.00 $1179.00 $5100.00 $9180.00 | 26 | |
Oligomycin A is an inhibitor of the mitochondrial ATP synthase, affecting mitochondrial energy metabolism. This can indirectly impact PARL's function related to mitochondrial homeostasis by altering the mitochondrial energy status. | ||||||
Bongkrekic acid | 11076-19-0 | sc-205606 | 100 µg | $418.00 | 10 | |
Bongkrekic Acid inhibits the opening of the adenine nucleotide translocator pore in mitochondria, affecting mitochondrial permeability. This action can indirectly modulate the environment in which PARL operates, particularly in apoptosis regulation. | ||||||
Z-VAD-FMK | 187389-52-2 | sc-3067 | 500 µg | $74.00 | 256 | |
Z-VAD-FMK is a broad-spectrum caspase inhibitor, affecting apoptotic processes. While not directly inhibiting PARL, it modulates apoptosis, where PARL has a regulatory role, potentially altering PARL-related pathways. | ||||||
Omi/HtrA2 Protease Inhibitor, Ucf-101 | 313649-08-0 | sc-222101 | 10 mg | $200.00 | 1 | |
UCF-101 inhibits Omi/HtrA2 serine protease, involved in mitochondrial stress response. This inhibitor might indirectly affect PARL's function in mitochondrial quality control by stabilizing the mitochondrial environment. | ||||||
Metformin | 657-24-9 | sc-507370 | 10 mg | $77.00 | 2 | |
Metformin activates AMP-activated protein kinase (AMPK) and impacts mitochondrial respiration. This indirect action can influence PARL-related mitochondrial quality control mechanisms by altering cellular energy metabolism. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin inhibits mTOR, affecting cellular growth and metabolism. This inhibition can indirectly influence PARL function by modulating mitochondrial dynamics and autophagy processes. | ||||||
Akt Inhibitor X | 925681-41-0 | sc-203811A sc-203811 sc-203811B sc-203811C sc-203811D sc-203811E | 1 mg 5 mg 10 mg 25 mg 50 mg 100 mg | $199.00 $235.00 $444.00 $923.00 $1538.00 $2759.00 | 23 | |
10-NCP (Akt Inhibitor X) is a ROS scavenger, reducing oxidative stress in mitochondria. By modulating mitochondrial oxidative status, it may indirectly influence PARL′s role in mitochondrial maintenance and apoptosis. | ||||||
β-Nicotinamide mononucleotide | 1094-61-7 | sc-212376 sc-212376A sc-212376B sc-212376C sc-212376D | 25 mg 100 mg 1 g 2 g 5 g | $92.00 $269.00 $337.00 $510.00 $969.00 | 4 | |
NMN enhances NAD+ levels, supporting mitochondrial function. This can indirectly benefit PARL's role in mitochondrial dynamics by improving mitochondrial health and function. | ||||||