Spatial organization of PI3K-PI(3,4,5)P-AKT signaling by focal adhesions.

The class I phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway is a key regulator of cell survival, growth, and proliferation and is among the most frequently mutated pathways in cancer. However, where and how PI3K-AKT signaling is spatially activated and organized in mammalian cells remains poorly understood. Here, we identify focal adhesions (FAs) as subcellular signaling hubs organizing the activation of PI3K-PI(3,4,5)P-AKT signaling in human cancer cells containing p110α mutations under basal conditions.

Formoterol Acting via β2-Adrenoreceptor Restores Mitochondrial Dysfunction Caused by Parkinson's Disease-Related UQCRC1 Mutation and Improves Mitochondrial Homeostasis Including Dynamic and Transport.

Formoterol, a β2-adrenergic receptor (β2AR) agonist, shows promise in various diseases, but its effectiveness in Parkinson's disease (PD) is debated, with unclear regulation of mitochondrial homeostasis. This study employed a cell model featuring mitochondrial ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) variants associated with familial parkinsonism, demonstrating mitochondrial dysfunction and dynamic imbalance, exploring the therapeutic effects and underlying mechanisms of formoterol. Results revealed that 24-h formoterol treatment enhanced cell proliferation, viability, and neuroprotection against oxidative stress.

The protein phosphatase qGL3/OsPPKL1 self-regulates its degradation to orchestrate brassinosteroid signaling in rice.

Brassinosteroids (BRs) are a class of phytohormones that regulate plant growth and development. In previous studies, we cloned and identified PROTEIN PHOSPHATASE WITH KELCH-LIKE1 (OsPPKL1) as the causal gene for the quantitative trait locus GRAIN LENGTH3 (qGL3) in rice (Oryza sativa). We also showed that qGL3/OsPPKL1 is mainly located in the cytoplasm and nucleus and negatively regulates BR signaling and grain length.

The protocol of tagging endogenous proteins with fluorescent tags using CRISPR-Cas9 genome editing.

The currently widely used CRISPR-Cas9 genome editing technology enables the editing of target genes (knock-out or knock-in) with high accuracy and efficiency. Guided by the small guide RNA, the Cas9 nuclease induces a DNA double-strand break at the targeted genomic locus. The DNA double-strand break can be repaired by the homology-directed repair pathway in the presence of a repair template.

Surface-tension-confined assembly of a metal-organic framework in femtoliter droplet arrays.

Metal-organic frameworks (MOFs), produced by metal ions coordinated to organic linkers, have attracted increasing attention in recent years. For the utilization in MOFs in numerous applications, achieving positioned MOF growth on surfaces is essential to fabricate multiple-functional devices. We develop a novel miniaturized method to realize surface-tension-confined assembly of HKUST-1 in femtoliter droplet arrays.

Mildly alkaline preparation and methylene blue adsorption capacity of hierarchical flower-like sodium titanate.

The hydrothermal preparation of flower-like layered sodium titanate architectures in a weakly alkaline medium is reported. NaCl was used as a morphology-directing agent, and a growth mechanism was proposed. The hierarchical structure is assembled from one-dimensional nanoribbons and exhibits an excellent removal capacity toward methylene blue (MB).

Trichostatin A modulates thiazolidinedione-mediated suppression of tumor necrosis factor α-induced lipolysis in 3T3-L1 adipocytes.

In obesity, high levels of tumor necrosis factor α (TNFα) stimulate lipolysis in adipocytes, leading to hyperlipidemia and insulin resistance. Thiazolidinediones (TZDs), the insulin-sensitizing drugs, antagonize TNFα-induced lipolysis in adipocytes, thereby increasing insulin sensitivity in diabetes patients. The cellular target of TZDs is peroxisome proliferator-activated receptor γ (PPARγ), a nuclear receptor that controls many adipocyte functions.