The 'omics' era, with its identification of genetic and protein components, has combined with systems biology, which provided insights into network structures, to set the stage for synthetic biology, an emerging interdisciplinary life science that uses engineering principles. By capitalizing on an iterative design cycle that involves molecular and computational biology tools to assemble functional designer devices from a comprehensive catalogue of standardized biological components with predictable functions, synthetic biology has significantly advanced our understanding of complex control dynamics that program living systems. Such insights, collected over the past decade, are priming a variety of synthetic biology-inspired biomedical applications that have the potential to revolutionize drug discovery and production technologies, as well as treatment strategies for infectious diseases and metabolic disorders.
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http://dx.doi.org/10.1016/j.cbpa.2012.06.008 | DOI Listing |
Org Biomol Chem
January 2025
Henan Key Laboratory of Chemical Biology and Organic Chemistry, Key Laboratory of Applied Chemistry of Henan Universities, Green Catalysis Center, and College of Chemistry, Zhengzhou University, Zhengzhou 450052, China.
We present a visible-light-promoted radical cascade cyclization reaction sulfonylmethylation, cyano insertion, and radical cyclization of unactivated alkenes bearing cyano groups. This strategy enables the rapid synthesis of sulfonylmethylated phenanthridines under mild conditions with broad substrate compatibility, operational simplicity, and mild reaction conditions. The developed approach provides a novel pathway for assembling complex polycyclic nitrogen-containing frameworks, addressing a critical synthetic challenge and expanding the toolbox of photochemical transformations in organic synthesis.
View Article and Find Full Text PDFNucleic Acids Res
January 2025
Biomolecular Sciences Institute, Florida International University, Miami, FL 33199, United States.
The mammalian high mobility group protein AT-hook 2 (HMGA2) is a small DNA-binding protein that specifically targets AT-rich DNA sequences. Structurally, HMGA2 is an intrinsically disordered protein (IDP), comprising three positively charged 'AT-hooks' and a negatively charged C-terminus. HMGA2 can form homodimers through electrostatic interactions between its 'AT-hooks' and C-terminus.
View Article and Find Full Text PDFCell Biol Int
January 2025
Microscopy and Microanalysis Center, Institute of Biosciences, Letters and Exact Sciences (IBILCE), São Paulo State University (Unesp), São José do Rio Preto, SP, Brazil.
Mammary glands development is influenced by endocrine signaling, which remodels epithelial and stromal compartments. Reactive stroma phenotype is observed when stromal disturbances occur, leading to changes in extracellular matrix composition and occurrence of reactive cell types. One of the triggers of these alterations is endocrine-disrupting chemical exposure, such as bisphenol A (BPA).
View Article and Find Full Text PDFBio Protoc
January 2025
Biochemistry Department, Western University, London, Canada.
Chloroplast genomes present an alternative strategy for large-scale engineering of photosynthetic eukaryotes. Prior to our work, the chloroplast genomes of (204 kb) and (140 kb) had been cloned using bacterial and yeast artificial chromosome (BAC/YAC) libraries, respectively. These methods lack design flexibility as they are reliant upon the random capture of genomic fragments during BAC/YAC library creation; additionally, both demonstrated a low efficiency (≤ 10%) for correct assembly of the genome in yeast.
View Article and Find Full Text PDFLife Metab
August 2024
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai 200438, China.
Bromodomain and extra-terminal domain (BET) proteins, which function partly through MYC proto-oncogene (MYC), are critical epigenetic readers and emerging therapeutic targets in cancer. Whether and how BET inhibition simultaneously induces metabolic remodeling in cancer cells remains unclear. Here we find that even transient BET inhibition by JQ-1 and other pan-BET inhibitors (pan-BETis) blunts liver cancer cell proliferation and tumor growth.
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