https://pubs.rsc.org/en/content/articlepdf/2019/NP/C8NP00092A

Marine natural products.

Phenolics are broadly distributed in the plant kingdom and are the most abundant secondary metabolites of plants. Plant polyphenols have drawn increasing attention due to their potent antioxidant properties and their marked effects in the prevention of various oxidative stress associated diseases such as cancer. In the last few years, the identification and development of phenolic compounds or extracts from different plants has become a major area of health- and medical-related research. This review provides an updated and comprehensive overview on phenolic extraction, purification, analysis and quantification as well as their antioxidant properties. Furthermore, the anticancer effects of phenolics in-vitro and in-vivo animal models are viewed, including recent human intervention studies. Finally, possible mechanisms of action involving antioxidant and pro-oxidant activity as well as interference with cellular functions are discussed.

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Plant phenolics: extraction, analysis and their antioxidant and anticancer properties.

The Transcriptional Coactivators p300 and CBP Are Histone Acetyltransferases

■ Abstract Apoptosis is a genetically programmed, morphologically distinct form of cell death that can be triggered by a variety of physiological and pathological stimuli. Studies performed over the past 10 years have demonstrated that proteases play critical roles in initiation and execution of this process. The caspases, a family of cysteine-dependent aspartate-directed proteases, are prominent among the death proteases. Caspases are synthesized as relatively inactive zymogens that become activated by scaffold-mediated transactivation or by cleavage via upstream proteases in an intracellular cascade. Regulation of caspase activation and activity occurs at several different levels: ( a) Zymogen gene transcription is regulated; ( b) antiapoptotic members of the Bcl-2 family and other cellular polypeptides block proximity-induced activation of certain procaspases; and ( c) certain cellular inhibitor of apoptosis proteins (cIAPs) can bind to and inhibit active caspases. Once activated, caspases cleave a variety of intracellular polypeptides, including major structural elements of the cytoplasm and nucleus, components of the DNA repair machinery, and a number of protein kinases. Collectively, these scissions disrupt survival pathways and disassemble important architectural components of the cell, contributing to the stereotypic morphological and biochemical changes that characterize apoptotic cell death.

Mammalian caspases: structure ,a ctivation ,s ubstrates, and functions during apoptosis

Activation of p53 Sequence-Specific DNA Binding by Acetylation of the p53 C-Terminal Domain

Anthocyanins are the chemical components that give the intense color to many fruits and vegetables, such as blueberries, red cabbages and purple sweet potatoes. Epidemiological investigations have indicated that the moderate consumption of anthocyanin products such as red wine or bilberry extract is associated with a lower risk of cardiovascular disease and improvement of visual functions. Recently, there is increasing interesting in the pharmaceutical function of anthocyanins. This review summarizes current knowledge on the various molecular evidences of cancer chemoprevention by anthocyanins. These mechanisms can be subdivided into the following aspects: 1) the antioxidation; 2) the molecular mechanisms involved in anticarcinogenesis; 3) the molecular mechanisms involved in the apoptosis induction of tumor cells. Finally, the bioavailability and structure-activity relationship of anthocyanins are also summarized.

Potential mechanisms of cancer chemoprevention by anthocyanins.

Action of Nrf2 and Keap1 in ARE-mediated NQO1 expression by quercetin.

CBP (CREB-binding protein) is a transcriptional coactivator of CREB (cAMP response element-binding) protein, which is directly phosphorylated by PKA (cAMP-dependent protein kinase A). CBP interacts with the activated phosphorylated form of CREB but not with the nonphosphorylated form. We report here that CBP is also a coactivator of the c-myb proto-oncogene product (c-Myb), which is a sequence-specific transcriptional activator. CBP directly binds to the region containing the transcriptional activation domain of c-Myb in a phosphorylation-independent manner in vitro. The domain of CBP that touches c-Myb is also required for binding to CREB. A c-Myb/CBP complex in vivo was demonstrated by a yeast two-hybrid assay. CBP stimulates the c-Myb-dependent transcriptional activation. Conversely, the expression of antisense RNA of CBP represses c-Myb-induced transcriptional activation. In addition, adenovirus EIA, which binds to CBP, inhibits c-Myb-induced transcriptional activation. Our data thus identify CBP as a coactivator of c-Myb. These results suggest that CBP functions as a coactivator for more transcriptional activators than were thought previously.

/pdf/cbp-as-a-transcriptional-coactivator-of-c-myb-2ib46i71ow.pdf

CBP as a transcriptional coactivator of c-Myb.

The transcription factor CBP, originally identified as a coactivator for CREB1,2, enhances transcription mediated by many other transcription factors3–7. Mutations in the human CBP gene are associated with Rubinstein–Taybi syndrome, a haploinsufficiency disorder characterized by abnormal pattern formation8, but the mechanism by which decreased CBP levels affect pattern formation is unclear. The hedgehog (hh) signalling pathway is an important determinant of pattern formation, cubitus interruptus (ci), a component in hh signalling, encodes a transcription factor homologous to the Gli family of proteins9 and is required for induction of the hh-dependent expression of patched (ptc), decapentaplegic (dpp) and wingless (wg)10. Haploinsufficiency for the ci-related transcription factor Gli3 causes phenotypic changes in mice (known as 'extra-toes)11 and humans (Greig's cephalopolysyndactyly syndrome)12 that have similarities to Rubinstein-Taybi syndrome. Here we show that Drosophila CBP (dCBP) functions as a coactivator of Ci, suggesting that the dCBP-Ci interaction may shed light on the contribution of CBP to pattern formation in mammals.

De-Xing Hou

Papers

Potential mechanisms of cancer chemoprevention by anthocyanins.

Action of Nrf2 and Keap1 in ARE-mediated NQO1 expression by quercetin.

CBP as a transcriptional coactivator of c-Myb.

Drosophila CBP is a co-activator of cubitus interruptus in hedgehog signalling

Anthocyanidins inhibit cyclooxygenase-2 expression in LPS-evoked macrophages: Structure–activity relationship and molecular mechanisms involved