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http://dx.doi.org/10.1371/journal.ppat.1012847 | DOI Listing |
PLoS Pathog
January 2025
Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States of America.
Proteins
January 2025
Institute of Transformative bio-Molecules, Nagoya University, Nagoya, Japan.
In plants, sugar will eventually be exported transporters (SWEETs) facilitate the translocation of mono- and disaccharides across membranes and play a critical role in modulating responses to gibberellin (GA3), a key growth hormone. However, the dynamic mechanisms underlying sucrose and GA3 binding and transport remain elusive. Here, we employed microsecond-scale molecular dynamics (MD) simulations to investigate the influence of sucrose and GA3 binding on SWEET13 transporter motions.
View Article and Find Full Text PDFHCA Healthc J Med
December 2024
University of North Texas Health Science Center at Fort Worth, Fort Worth, TX.
Introduction: Bortezomib is a reversible proteasome inhibitor that is a first-line chemotherapeutic agent for multiple myeloma. Bortezomib can be administered intravenously or subcutaneously with similar efficacy. Subcutaneous administration has fewer side effects.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
Research Institute, Suntory Global Innovation Center Ltd., Kyoto 618-8504, Japan.
Steviol glycosides (SGs) are noncaloric natural sweeteners found in the leaves of stevia (). These diterpene glycosides are biosynthesized by attaching varying numbers of monosaccharides, primarily glucose, to steviol aglycone. Rebaudioside (Reb) D and Reb M are highly glucosylated SGs that are valued for their superior sweetness and organoleptic properties, yet they are present in limited quantities in stevia leaves.
View Article and Find Full Text PDFJ Med Chem
January 2025
Department of Chemistry, The Hong Kong University of Science and Technology, Hong Kong SAR 999077, China.
CDK4/6 inhibitors are effective in treating HR/HER2 breast cancer but face limitations due to therapeutic resistance and hematological toxicity, particularly from strong CDK6 inhibition. To address these challenges, designing selective inhibitors targeting specific cyclin-dependent kinases (CDK) members could offer clinical advantages and broaden CDK inhibitor indications. However, the highly conserved binding pockets of CDKs complicate selective targeting.
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