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Genesis and regulation of C-terminal cyclic imides from protein damage.
Proc Natl Acad Sci U S A
January 2025
Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138.
C-Terminal cyclic imides are posttranslational modifications that can arise from spontaneous intramolecular cleavage of asparagine or glutamine residues resulting in a form of irreversible protein damage. These protein damage events are recognized and removed by the E3 ligase substrate adapter cereblon (CRBN), indicating that these aging-related modifications may require cellular quality control mechanisms to prevent deleterious effects. However, the factors that determine protein or peptide susceptibility to C-terminal cyclic imide formation or their effect on protein stability have not been explored in detail.
View Article and Find Full Text PDFNovel Leech Antimicrobial Peptides, Hirunipins: Real-Time 3D Monitoring of Antimicrobial and Antibiofilm Mechanisms Using Optical Diffraction Tomography.
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Department of Biological Sciences and Biotechnology, College of Natural Sciences, Chungbuk National University, Cheongju, Chungbuk, 28644, Republic of Korea.
Antimicrobial peptides (AMPs) are promising agents for treating antibiotic-resistant bacterial infections. Although discovering novel AMPs is crucial for combating multidrug-resistant bacteria and biofilm-related infections, their clinical potential relies on precise, real-time evaluation of efficacy, toxicity, and mechanisms. Optical diffraction tomography (ODT), a label-free imaging technology, enables real-time visualization of bacterial morphological changes, membrane damage, and biofilm formation over time.
View Article and Find Full Text PDFThe adiponectin-PPARγ axis in hepatic stellate cells regulates liver fibrosis.
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Touchstone Diabetes Center, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
Hepatic stellate cells (HSCs) are key drivers of local fibrosis. Adiponectin, conventionally thought of as an adipokine, is also expressed in quiescent HSCs. However, the impact of its local expression on the progression of liver fibrosis remains unclear.
View Article and Find Full Text PDFSenolytic agent ABT-263 mitigates low- and high-LET radiation-induced gastrointestinal cancer development in mice.
Aging (Albany NY)
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Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC 20057, USA.
Exposure to ionizing radiation (IR), both low-LET (e.g., X-rays, γ rays) and high-LET (e.
View Article and Find Full Text PDFp63: A Master Regulator at the Crossroads Between Development, Senescence, Aging, and Cancer.
Cells
January 2025
Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, MN 55455, USA.
The p63 protein is a master regulatory transcription factor that plays crucial roles in cell differentiation, adult tissue homeostasis, and chromatin remodeling, and its dysregulation is associated with genetic disorders, physiological and premature aging, and cancer. The effects of p63 are carried out by two main isoforms that regulate cell proliferation and senescence. p63 also controls the epigenome by regulating interactions with histone modulators, such as the histone acetyltransferase p300, deacetylase HDAC1/2, and DNA methyltransferases.
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