Acylglycerol kinase, abbreviated as AGK and also known by its alias MULK, is a mitochondrial membrane protein that plays a crucial role in lipid and glycerolipid metabolism. The AGK enzyme catalyzes the phosphorylation of acylglycerols to produce phosphatidic acid and lysophosphatidic acid, both of which are vital lipid signaling molecules with roles in various cellular processes. AGK's activity is integral to the maintenance of lipid homeostasis within the cell, and it is ubiquitously expressed across a wide range of tissues, with notable expression in the heart and brain. The gene encoding AGK is situated within the human genome and has been the subject of considerable study due to its involvement in metabolic pathways and its association with mitochondrial DNA depletion syndrome 10. As a protein-coding gene, AGK's expression can be influenced by several factors, including the cellular environment and the presence of specific chemical compounds.
Certain compounds have been identified as potential activators of AGK expression due to their ability to upregulate the transcriptional machinery linked to lipid metabolism. Eicosapentaenoic acid (EPA), a polyunsaturated fatty acid found abundantly in fish oil, is one such compound. As an omega-3 fatty acid, EPA incorporates into cellular membranes, altering membrane fluidity and dynamics, which can lead to the activation of transcription factors such as peroxisome proliferator-activated receptors (PPARs). Activation of PPARs has been shown to stimulate the expression of a variety of genes involved in fatty acid metabolism, including those encoding enzymes like AGK. The influence of EPA on gene expression extends beyond the direct interactions with PPARs; it also encompasses the modulation of cell signaling pathways that converge on the transcriptional regulation of metabolic genes. The heightened transcriptional activity fostered by EPA may therefore elevate the levels of AGK, fortifying the cellular lipid metabolic processes and ensuring an efficient turnover and synthesis of crucial lipid signaling molecules. The role of AGK in these pathways underscores the importance of understanding how its expression can be induced by naturally occurring dietary components, which in turn sheds light on the intricate network of nutritional biochemistry and gene expression.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
Retinoic acid may upregulate MULK expression by binding to retinoic acid receptors, which can initiate transcriptional activation of genes involved in lipid metabolism. | ||||||
Fenofibrate | 49562-28-9 | sc-204751 | 5 g | $40.00 | 9 | |
Fenofibrate activates PPARα, potentially leading to an increase in MULK expression as part of the cascade of lipid oxidation genes upregulated by this pathway. | ||||||
Rosiglitazone | 122320-73-4 | sc-202795 sc-202795A sc-202795C sc-202795D sc-202795B | 25 mg 100 mg 500 mg 1 g 5 g | $118.00 $320.00 $622.00 $928.00 $1234.00 | 38 | |
As a PPARγ agonist, Rosiglitazone could directly stimulate the transcription of MULK by promoting the transcriptional activity of genes within the lipid synthesis pathways. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $36.00 $68.00 $107.00 $214.00 $234.00 $862.00 $1968.00 | 47 | |
Curcumin may enhance MULK expression through its ability to activate transcription factors like Nrf2, which upregulate genes responsible for combating oxidative stress, and may include lipid-metabolizing enzymes. | ||||||
25-Hydroxycholesterol | 2140-46-7 | sc-214091B sc-214091 sc-214091A sc-214091C | 5 mg 10 mg 25 mg 100 mg | $52.00 $89.00 $166.00 $465.00 | 8 | |
25-Hydroxycholesterol can induce MULK expression by serving as a ligand for LXRs, which upon activation, can increase the transcription of genes that govern lipid homeostasis. | ||||||
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium may stimulate MULK expression by inhibiting glycogen synthase kinase-3, which in turn can lead to enhanced activity of transcription factors that promote gene expression related to lipid metabolism. | ||||||
Metformin-d6, Hydrochloride | 1185166-01-1 | sc-218701 sc-218701A sc-218701B | 1 mg 5 mg 10 mg | $286.00 $806.00 $1510.00 | 1 | |
Metformin activates AMPK, which may subsequently upregulate MULK expression as part of its role in restoring energy balance, often by accelerating lipid catabolism. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol can stimulate the expression of MULK by activating sirtuins and AMPK, leading to an enhanced transcription of genes involved in mitochondrial function and lipid metabolism. | ||||||
Pioglitazone | 111025-46-8 | sc-202289 sc-202289A | 1 mg 5 mg | $54.00 $123.00 | 13 | |
Pioglitazone, through PPARγ activation, could induce MULK expression, thereby promoting lipid storage in adipocytes but also potentially stimulating lipid utilization pathways. | ||||||
Eicosa-5Z,8Z,11Z,14Z,17Z-pentaenoic Acid (20:5, n-3) | 10417-94-4 | sc-200766 sc-200766A | 100 mg 1 g | $102.00 $423.00 | ||
EPA may upregulate MULK expression through its role in activating PPARs, which are nuclear receptors that can stimulate the transcription of genes involved in lipid metabolism. Additionally, EPA's incorporation into cell membranes can alter membrane fluidity and signaling pathways, leading to an upsurge in MULK transcription as part of the cellular response to maintain lipid homeostasis. |