User:Mrmille2/sandbox
Preclinical Research[edit]
There is inconclusive evidence for the clinical efficacy of sulforaphane, however the isothiocyanate has been extensively researched within in vivo and in vitro parameters. Sulforaphane has been reported to have anticancer, antioxidant, anti-inflammatory properties in laboratory conditions. [1]
HDAC Inhibition[edit]
During various in vitro and in vivo parameters, sulforaphane has shown to inhibit histone deacetylase (HDAC) enzyme activity: an enzyme responsible for the deacetylation of histones, and subsequent expression of respective DNA.[1][2]
DNMT Inhibition[edit]
DNA methyltransferase (DNMT) activity catalyzes the methylation of DNA, and has been found to be inhibited by sulforaphane during preclinical analyses. Specifically, sulforaphane has shown to inhibit DNMT1 and DNMT3a.[2][3] Research has further suggested it may be a result of HDAC inhibition. [3]
Keap1/Nrf2[edit]
Sulforaphane has also been shown to enhance the expression of the antioxidant response element (ARE) in a Nrf2-dependent manner in numerous in vitro and in vivo conditions.[1][4] [5]Moreover, as a transcription factor, the nuclear translocation of Nrf2 is mediated by the enzyme Keap1.[6] Sulforaphane has been repeatedly found to modify four cysteine residues of Keap1, primarily cysteine residue C151, and subsequently induce the release of Nrf2 into the nucleus to participate in transcription of the ARE. [4]
 | This is a user sandbox of Mrmille2. You can use it for testing or practicing edits. This is not the sandbox where you should draft your assigned article for a dashboard.wikiedu.org course. To find the right sandbox for your assignment, visit your Dashboard course page and follow the Sandbox Draft link for your assigned article in the My Articles section. |
- ^ a b c "Isothiocyanates". Linus Pauling Institute. 2014-04-29. Retrieved 2018-12-03.
- ^ a b Tortorella, Stephanie M.; Royce, Simon G.; Licciardi, Paul V.; Karagiannis, Tom C. (2015-06-01). "Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition". Antioxidants & Redox Signaling. 22 (16): 1382–1424. doi:10.1089/ars.2014.6097. ISSN 1523-0864. PMC 4432495. PMID 25364882.
{{cite journal}}: CS1 maint: PMC format (link) - ^ a b Kaufman-Szymczyk, Agnieszka; Majewski, Grzegorz; Lubecka-Pietruszewska, Katarzyna; Fabianowska-Majewska, Krystyna (2015-12-12). "The Role of Sulforaphane in Epigenetic Mechanisms, Including Interdependence between Histone Modification and DNA Methylation". International Journal of Molecular Sciences. 16 (12): 29732–29743. doi:10.3390/ijms161226195. ISSN 1422-0067. PMC 4691138. PMID 26703571.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ a b Kensler, Thomas W; Egner, Patricia A; Agyeman, Abena S.; Visvanathan, Kala; Groopman, John D; Chen, Jian-Guo; Chen, Tao-Yang; Fahey, Jed W; Talalay, Paul (2013). "Keap1-Nrf2 Signaling: A Target for Cancer Prevention by Sulforaphane". Topics in current chemistry. 329: 163–177. doi:10.1007/128_2012_339. ISSN 0340-1022. PMC 3553557. PMID 22752583.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Houghton, Christine A.; Fassett, Robert G.; Coombes, Jeff S. (2016). "Sulforaphane and Other Nutrigenomic Nrf2 Activators: Can the Clinician's Expectation Be Matched by the Reality?". Oxidative Medicine and Cellular Longevity. 2016. doi:10.1155/2016/7857186. ISSN 1942-0900. PMC 4736808. PMID 26881038.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link) - ^ Harder, Bryan; Jiang, Tao; Wu, Tongde; Tao, Shasha; de la Vega, Montserrat Rojo; Tian, Wang; Chapman, Eli; Zhang, Donna D. (2015-08-01). "Molecular mechanisms of Nrf2 regulation and how these influence chemical modulation for disease intervention". Biochemical Society Transactions. 43 (4): 680–686. doi:10.1042/BST20150020. ISSN 0300-5127. PMC 4613518. PMID 26551712.
{{cite journal}}: no-break space character in|first5=at position 11 (help); no-break space character in|first8=at position 6 (help)CS1 maint: PMC format (link)