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As an important cellular signal transduction messenger, Ca has the capability to regulate cell function and control many biochemical processes, including metabolism, gene expression, and cell survival and death. Here, we introduce an accessible method for the photoactivation of Ca channels mediated by squaraine (SQ) to rapidly induce cellular Ca release and activate signal transduction. With a short preparation time, the maximum Ca concentration increase could reach approximately 450% in 30 s, resulting from marked Ca release channel opening in the endoplasmic reticulum (ER). This release was enhanced by another target location of SQ, that is, the outer mitochondrial-associated membrane where Ca channels accumulate, and by the consequent large amounts of reactive oxygen species resulting from the respiratory chain activity stimulated by Ca load. We used this method to investigate cellular signal transduction in different cancer cells and revealed rapid intracellular Ca flow, unidirectional intercellular signaling processes, and neuronal signaling activity, which demonstrated the potential and convenience of the method for routine Ca research.
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http://dx.doi.org/10.1021/acs.analchem.0c01243 | DOI Listing |
JCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Medicine, Institute for Transformative Molecular Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
The β-adrenergic receptor (βAR), a prototype G protein-coupled receptor, controls cardiopulmonary function underpinning O delivery. Abundance of the βAR is canonically regulated by G protein-coupled receptor kinases and β-arrestins, but neither controls constitutive receptor levels, which are dependent on ambient O. Basal βAR expression is instead regulated by the prolyl hydroxylase/pVHL-E3 ubiquitin ligase system, explaining O responsivity.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
Background: Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide. The tumor microenvironment (TME), particularly the interactions between endothelial cells and cancer-associated fibroblasts (CAFs), plays a pivotal role in promoting tumor growth, angiogenesis, oxidative stress, and therapy resistance. The HUVEC-fibroblast co-culture model closely mimics stromal-endothelial interactions observed in CRC, enabling mechanistic insights not achievable in monocultures.
View Article and Find Full Text PDFCurr Genet
September 2025
Fermentation and Microbial Biotechnology Division, CSIR-Indian Institute of Integrative Medicine, Canal Road, Jammu-Tawi, 180001, India.
Trichoderma species exhibit remarkable versatility in adaptability and in occupying habitats with lifestyles ranging from mycoparasitism and saprotrophy to endophytism. In this study, we present the first high-quality whole-genome assembly and annotation of T. lixii using Illumina HiSeq technology to explore the mechanisms of endophytic lifestyle and plant colonization.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Chitkara College of Pharmacy, Chitkara University, Rajpura, 140401, Punjab, India.
Neuroinflammation, a vital protective response for tissue homeostasis, becomes a detrimental force when chronic and dysregulated, driving neurological disorders like Alzheimer's, Parkinson's, and Huntington's diseases. Potassium (K) channels maintain membrane potential and cellular excitability in neurons and glia within the intricate CNS signaling network. Neuronal injury or inflammation can disrupt K channel activity, leading to hyperexcitability and chronic pain.
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