Date published: 2025-9-18

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mKIAA1530 Activators

mKIAA1530 Activators are a diverse group of chemical compounds that indirectly enhance the functional activity of mKIAA1530 through various cellular pathways, particularly focusing on DNA repair mechanisms and responses to UV damage. Curcumin and Sulforaphane, by modulating DNA repair pathways, indirectly augment mKIAA1530's involvement in transcription-coupled nucleotide-excision repair (TC-NER). These compounds, through their respective roles in enhancing DNA repair mechanisms, indirectly facilitate the function of mKIAA1530, especially in response to UV-induced DNA damage. Resveratrol, through its influence on sirtuin pathways, particularly SIRT1, and Ellagic Acid, by modulating DNA repair processes, support mKIAA1530's activity in the nucleoplasm and on chromosomes. Similarly, Caffeine, by inhibiting ATM and ATR kinases, and KU-55933, as an ATM kinase inhibitor, indirectly impact TC-NER pathways where mKIAA1530 is pivotal. These compounds, by influencing key kinases involved in DNA damage response, indirectly enhance mKIAA1530's role in DNA repair.

Additionally, compounds like Olaparib, a PARP inhibitor, and Nordihydroguaiaretic Acid, which affects oxidative stress response pathways, further influence the DNA repair mechanisms in which mKIAA1530 is involved. Olaparib, by inhibiting PARP, an enzyme crucial in DNA repair, indirectly supports mKIAA1530's function in TC-NER. Quercetin and Epigallocatechin Gallate, by influencing the cellular response to oxidative stress, play a role in enhancing mKIAA1530's function in UV-induced DNA damage repair. Genistein's modulation of tyrosine kinase-dependent signaling pathways also indirectly supports mKIAA1530's involvement in DNA repair, providing an additional layer of regulation. Lastly, Urolithin A, by influencing mitophagy and the oxidative stress response, supports DNA repair mechanisms, including those involving mKIAA1530, particularly in response to UV and oxidative damage, thus contributing to the overall enhancement of mKIAA1530's activity. These compounds, through their targeted effects on different aspects of cellular signaling and stress response, collectively enhance the functional role of mKIAA1530 in crucial biological processes such as transcription-coupled nucleotide-excision repair, DNA damage response, and maintenance of genomic integrity. Their actions, although varied in mechanism, converge on the common goal of facilitating mKIAA1530's role in maintaining cellular health in the face of DNA damage, particularly damage caused by UV exposure. The synergy between these activators and mKIAA1530's functions exemplifies the intricate network of cellular responses to environmental stressors and the essential role of mKIAA1530 in navigating these responses to preserve genomic stability.

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