Date published: 2025-12-23

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MRP-L41 Activators

Resveratrol is a polyphenol that activates SIRT1, a sirtuin that plays a crucial role in promoting mitochondrial biogenesis. This activation potentially leads to an increased demand for mitochondrial ribosomal proteins like MRP-L41, as new mitochondria require a full complement of proteins for function. Similarly, pioglitazone, a PPAR-gamma agonist, and nicotinamide mononucleotide (NMN), a NAD+ precursor, also support the process of mitochondrial biogenesis, potentially ramping up the production of mitochondrial components, including MRP-L41. Contrastingly, certain compounds disrupt mitochondrial function, eliciting a stress response that can indirectly affect MRP-L41 levels. Oligomycin A, for example, inhibits ATP synthase, resulting in mitochondrial stress that might upregulate MRP-L41 as part of a broader cellular attempt to compensate for impaired energy production. FCCP, another mitochondrial disruptor, decouples oxidative phosphorylation, which could lead to a similar compensatory increase in mitochondrial proteins. Substances like sodium azide, rotenone, and antimycin A target different enzymes within the electron transport chain, potentially triggering a response that upregulates protective proteins, including MRP-L41, to preserve mitochondrial integrity and function.

Rapamycin, an inhibitor of the mTOR pathway, induces autophagy – a cellular degradation process that can lead to the turnover of mitochondrial components. This process may necessitate the synthesis of new mitochondrial proteins, including MRP-L41, to replace those that are degraded. 1,1-Dimethylbiguanide, Hydrochloride, widely known for its role in diabetes management, activates AMPK, leading to increased mitochondrial biogenesis and possibly a higher expression level of MRP-L41 as cells seek to meet energy demands. Chloramphenicol, traditionally used as an antibiotic, can affect the mitochondrial ribosome due to its similarity to bacterial ribosomes. This off-target effect may influence the stability and expression of mitochondrial ribosomal proteins, including MRP-L41.

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