CED-3 is a pivotal protein in the programmed cell death pathway, a fundamental biological process essential for the development and maintenance of cellular homeostasis in multicellular organisms. It is a cysteine protease, evolutionarily conserved across species, and is known for its paramount role in the apoptosis cascade in the nematode Caenorhabditis elegans (C. elegans). Analogous to caspases in mammalian systems, CED-3 is synthesized as an inactive precursor that is proteolytically processed into an active form that then executes the cell death program. The activation of CED-3 is a highly regulated event, typically triggered by developmental cues or environmental stresses that necessitate the removal of cells that are either superfluous or potentially harmful to the organism. The expression of CED-3 is tightly controlled at both the transcriptional and post-transcriptional levels, ensuring that the cell death machinery is deployed at the correct time and place within the organism.
In the context of CED-3 expression inducers, a range of chemicals has been identified that can potentially lead to the upregulation of this crucial protein. These chemicals often exert their effects by engendering cellular stress or by modulating specific signaling pathways that converge on the control of apoptotic gene expression. For instance, compounds found in cruciferous vegetables, have been shown to activate cellular defense mechanisms against oxidative stress, which could result in the upregulation of CED-3. Similarly, polyphenolic compounds like resveratrol and curcumin, found in red grapes and turmeric respectively, are renowned for their antioxidant properties and could potentially augment the expression of CED-3 by precipitating a cellular stress response. Other natural compounds, such as the green tea component EGCG and the flavonoid quercetin, may also stimulate the expression of genes associated with the cellular apoptosis machinery by engaging with various cellular signaling cascades. It is important to note that while these chemicals have been linked with pathways that are capable of affecting apoptosis, the direct induction of CED-3 by these chemicals remains a subject for empirical investigation. The study of these interactions is an ongoing field of research, contributing to a deeper understanding of the intricate regulatory networks that govern cell death and survival.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol could initiate the activation of sirtuin pathways, which may, in turn, promote the upregulation of CED-3 expression as part of the apoptotic response to caloric restriction and stress. | ||||||
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 catalyze the transcriptional activation of genes associated with the apoptotic machinery, potentially resulting in an increase in CED-3 expression as part of the cellular demise program. | ||||||
(−)-Epigallocatechin Gallate | 989-51-5 | sc-200802 sc-200802A sc-200802B sc-200802C sc-200802D sc-200802E | 10 mg 50 mg 100 mg 500 mg 1 g 10 g | $42.00 $72.00 $124.00 $238.00 $520.00 $1234.00 | 11 | |
EGCG may enhance the transcription of detoxification-related genes, which could lead to the upregulation of CED-3, coinciding with the activation of the cell death program under conditions of oxidative stress. | ||||||
Quercetin | 117-39-5 | sc-206089 sc-206089A sc-206089E sc-206089C sc-206089D sc-206089B | 100 mg 500 mg 100 g 250 g 1 kg 25 g | $11.00 $17.00 $108.00 $245.00 $918.00 $49.00 | 33 | |
Quercetin could initiate a cascade that leads to the upregulation of CED-3 as a defensive response to environmental stresses that threaten cellular integrity, thereby prompting apoptosis. | ||||||
Indole-3-carbinol | 700-06-1 | sc-202662 sc-202662A sc-202662B sc-202662C sc-202662D | 1 g 5 g 100 g 250 g 1 kg | $38.00 $60.00 $143.00 $306.00 $1012.00 | 5 | |
Indole-3-carbinol may precipitate a series of reactions leading to cell cycle arrest and the subsequent transcriptional activation of CED-3, aligning with the organism's need to eliminate damaged cells. | ||||||
Cholecalciferol | 67-97-0 | sc-205630 sc-205630A sc-205630B | 1 g 5 g 10 g | $70.00 $160.00 $290.00 | 2 | |
Cholecalciferol (Vitamin D3) could promote the transcriptional activation of genes involved in the apoptosis pathway, which may include the upregulation of CED-3 as a response to cellular damage or dysfunction. | ||||||
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 initiate differentiation processes that involve the upregulation of CED-3, as part of the cellular turnover and renewal system, particularly in the context of development. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Camptothecin may induce a DNA damage response that necessitates the upregulation of CED-3, as the cell gears up for apoptosis in the face of irreparable genomic insult. | ||||||
Fluorouracil | 51-21-8 | sc-29060 sc-29060A | 1 g 5 g | $36.00 $149.00 | 11 | |
Fluorouracil may lead to the upregulation of CED-3 by initiating a response to misincorporated nucleotides during DNA replication, which often results in apoptosis. | ||||||
Taxol | 33069-62-4 | sc-201439D sc-201439 sc-201439A sc-201439E sc-201439B sc-201439C | 1 mg 5 mg 25 mg 100 mg 250 mg 1 g | $40.00 $73.00 $217.00 $242.00 $724.00 $1196.00 | 39 | |
Taxol (Paclitaxel) may induce the upregulation of CED-3 by destabilizing microtubule dynamics, which triggers apoptosis as a means to cull cells with compromised cytoskeletal integrity. |