Date published: 2025-9-11

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Bcl-G Activators

Bcl-G, also known as BCL2L14, is a protein-coding gene that belongs to the BCL2 protein family. These proteins play a significant role in the regulation of apoptosis, commonly referred to as programmed cell death. Bcl-G, like other members of its family, can form hetero- or homodimers and function as anti- or pro-apoptotic regulators. This positions Bcl-G at the heart of a wide array of cellular activities that are integral to the maintenance of cellular health. Overexpression of Bcl-G has been demonstrated to induce apoptosis in cells, highlighting its ability as a key player in maintaining cellular equilibrium. Interestingly, Bcl-G's expression has been found to be biased in certain tissues, such as the testis and duodenum, among others, indicating its tissue-specific roles.

There are several chemical substances that could induce the expression of Bcl-G. For instance, retinoic acid, a metabolite of Vitamin A, may stimulate the production of Bcl-G by activating retinoic acid receptors, which could upregulate the transcription of the Bcl-G gene. Similarly, curcumin, a polyphenol found in turmeric, could increase Bcl-G expression by altering the transcriptional activity of genes involved in apoptosis. Other substances like resveratrol, a polyphenol found in grapes and berries, and sulforaphane, a compound in cruciferous vegetables, could also elevate Bcl-G levels by triggering cellular pathways associated with apoptosis. Certain compounds like dexamethasone, a synthetic glucocorticoid, and doxorubicin might increase Bcl-G expression due to their roles in cellular stress response and cytotoxic effects, respectively. Additionally, epigenetic modifiers such as 5-Azacytidine, a nucleoside analogue, and sodium butyrate, a short-chain fatty acid, could enhance Bcl-G expression by modulating DNA methylation and histone acetylation, respectively. These are just a few examples of how different chemicals can interact with the cellular machinery to influence the expression of Bcl-G.

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