The extracellular matrix (ECM) is a dynamic and heterogeneous environment that controls many aspects of cell behavior. Not surprisingly, many different approaches have focused on creating model substrates that recapitulate the biomolecular, topographical, and mechanical properties of the ECM for in vitro studies of cell behavior. This chapter details a general, versatile method for the spatially controlled deposition of multiple biomolecules onto both planar and topographically complex support structures with micrometer resolution. This approach is based upon the well-understood photochemical UV crosslinking of benzophenone (BP) to solution-phase biomolecules. This is a molecularly general strategy that can be utilized to immobilize biomolecules onto any surface prefunctionalized with BP. Examples described herein include modification of planar and corrugated glass substrates as well as collagen-glycosaminoglycan biomaterials configured either as highly porous scaffolds or nonporous membranes with a variety of biomolecular targets, including proteins, glycoproteins, and carbohydrates.
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ACS Nano
January 2025
School of Materials Science and Engineering, Peking University, Beijing 100871, People's Republic of China.
Single-crystal Au(111), renowned for its chemically inert surface, long-range "herringbone" reconstruction, and high electrical conductivity, has long served as an exemplary template in diverse fields, , crystal epitaxy, electronics, and electrocatalysis. However, commercial Au(111) products are high-priced and limited to centimeter sizes, largely restricting their broad applications. Herein, a low-cost, high-reproducible method is developed to produce 4 in.
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January 2025
Atelier de Biologie Chimie Informatique Structurale, Centre de Biologie Structurale, Univ Montpellier, CNRS, INSERM, 29 rue de Navacelles, 34090 Montpellier, France.
Reduced nicotinamide adenine dinucleotide phosphate (NADPH) is a crucial reducing cofactor for reductive biosynthesis and protection from oxidative stress. To fulfill their heightened anabolic and reductive power demands, cancer cells must boost their NADPH production. Progrowth and mitogenic protein kinases promote the activity of cytosolic NAD kinase (NADK), which produces NADP, a limiting NADPH precursor.
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January 2025
Simpson Querrey Institute for Epigenetics, Department of Biochemistry and Molecular Genetics Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
The stability of RNA polymerase II (Pol II) is tightly regulated during transcriptional elongation for proper control of gene expression. Our recent studies revealed that promoter-proximal Pol II is destabilized via the ubiquitin E3 ligase cullin 3 (CUL3) upon loss of transcription elongation factor SPT5. Here, we investigate how CUL3 recognizes chromatin-bound Pol II as a substrate.
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January 2025
MOE Key Laboratory of Biosystems Homeostasis & Protection, and Zhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China; Center for Life Sciences, Shaoxing Institute, Zhejiang University, Shaoxing, Zhejiang 321000, China; Cancer Center, Zhejiang University, Hangzhou, Zhejiang 310058, China; The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang 310009, China. Electronic address:
Transforming growth factor β (TGF-β) is well known to play paradoxical roles in tumorigenesis as it has both growth-inhibitory and pro-metastatic effects. However, the underlying mechanisms of how TGF-β drives the opposing responses remain largely unknown. Here, we report that ERBB4, a member of the ERBB receptor tyrosine kinase family, specifically promotes TGF-β's metastatic response but not its anti-growth response.
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
January 2025
Human and Animal Physiology, Wageningen University, Wageningen, The Netherlands.
The Respiratory Exchange Ratio (RER), which is the ratio of total carbon dioxide produced over total oxygen consumed, serves as a qualitative measure to determine the substrate usage of a particular organism on the whole-body level. Quantification of RER by its direct conversion into %Glucose (%G) and %Lipid oxidation (%L) at a given timepoint can be done by utilizing nonprotein respiratory quotient tables. These tables, however, are limited to specific increments, and intermediate RER values are not covered by these tables.
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