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A histochemical approach to activity-based copper sensing reveals cuproplasia-dependent vulnerabilities in cancer.
Proc Natl Acad Sci U S A
January 2025
Department of Chemistry, University of California, Berkeley, CA 94720.
Copper is an essential nutrient for sustaining vital cellular processes spanning respiration, metabolism, and proliferation. However, loss of copper homeostasis, particularly misregulation of loosely bound copper ions which are defined as the labile copper pool, occurs in major diseases such as cancer, where tumor growth and metastasis have a heightened requirement for this metal. To help decipher the role of copper in the etiology of cancer, we report a histochemical activity-based sensing approach that enables systematic, high-throughput profiling of labile copper status across many cell lines in parallel.
View Article and Find Full Text PDFTarget Discovery Driven by Chemical Biology and Computational Biology.
Chem Rec
January 2025
Institute of Radiation Medicine, Peking Union Medical College & Chinese Academy of Medical Sciences, Tianjin, 300192, China.
Target identification is crucial for drug screening and development because it can reveal the mechanism of drug action and ensure the reliability and accuracy of the results. Chemical biology, an interdisciplinary field combining chemistry and biology, can assist in this process by studying the interactions between active molecular compounds and proteins and their physiological effects. It can also help predict potential drug targets or candidates, develop new biomarker assays and diagnostic reagents, and evaluate the selectivity and range of active compounds to reduce the risk of off-target effects.
View Article and Find Full Text PDFFlow Cytometry Analysis of Perturbations in the Bacterial Cell Envelope Enabled by Monitoring Generalized Polarization of the Solvatochromic Peptide UNR-1.
Anal Chem
January 2025
Laboratoire d'Innovation Thérapeutique, UMR7200 CNRS, Université de Strasbourg, Institut du Médicament de Strasbourg, 74 route du Rhin, Strasbourg F-67000, France.
The worldwide spread of antibiotic resistance is considered to be one of the major health threats to society. While developing new antibiotics is crucial, there is also a strong need for next-generation analytical methods for studying the physiological state of live bacteria in heterogeneous populations and their response to environmental stress. Here we report a single-cell high-throughput method to monitor changes in the bacterial cell envelope in response to stress based on ratiometric flow cytometry.
View Article and Find Full Text PDFGap junction intercellular communications regulates activation of SARM1 and protects against axonal degeneration.
Cell Death Dis
January 2025
State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China.
Sterile alpha and Toll/interleukin-1 receptor motif containing 1 (SARM1), a nicotinamide adenine dinucleotide (NAD)-utilizing enzyme, mediates axon degeneration (AxD) in various neurodegenerative diseases. It is activated by nicotinamide mononucleotide (NMN) to produce a calcium messenger, cyclic ADP-ribose (cADPR). This activity is blocked by elevated NAD level.
View Article and Find Full Text PDFNeuronal mechanisms of nociceptive-evoked gamma-band oscillations in rodents.
Neuron
January 2025
State Key Laboratory of Cognitive Science and Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China; Department of Psychology, University of Chinese Academy of Sciences, Beijing, China. Electronic address:
Gamma-band oscillations (GBOs) in the primary somatosensory cortex (S1) play key roles in nociceptive processing. Yet, one crucial question remains unaddressed: what neuronal mechanisms underlie nociceptive-evoked GBOs? Here, we addressed this question using a range of somatosensory stimuli (nociceptive and non-nociceptive), neural recording techniques (electroencephalography in humans and silicon probes and calcium imaging in rodents), and optogenetics (alone or simultaneously with electrophysiology in mice). We found that (1) GBOs encoded pain intensity independent of stimulus intensity in humans, (2) GBOs in S1 encoded pain intensity and were triggered by spiking of S1 interneurons, (3) parvalbumin (PV)-positive interneurons preferentially tracked pain intensity, and critically, (4) PV S1 interneurons causally modulated GBOs and pain-related behaviors for both thermal and mechanical pain.
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