The study "The integrated stress response promotes immune evasion through lipocalin 2" published by scholars such as Bossowski J, Papagiannakopoulos T, and Koide S in the top international journal Nature conducted a systematic and in-depth investigation on this urgent scientific problem. Focusing on clinically common solid tumors with high immunotherapy resistance rates, such as lung cancer, pancreatic cancer, and melanoma, and combining in vitro and in vivo experiments, clinical sample analysis, and big data mining, this study for the first time revealed the molecular mechanism by which Lipocalin 2 (LCN2), as a key effector molecule downstream of the integrated stress response, mediates tumor immune evasion, and further confirmed the therapeutic potential of targeting LCN2.

In the world of cells, there exists a mysterious "messenger" that, despite its minuscule size, plays a crucial role in cellular communication. These are exosomes— the "secret weapon" of intercellular signaling.

DNA mismatch repair (MMR) is a highly conserved genome maintenance mechanism that identifies and corrects base mismatches generated during DNA replication, playing a vital role in maintaining genomic stability. This paper systematically introduces the core components and molecular processes of the eukaryotic MMR pathway, clarifies the correlation between MMR deficiency (dMMR) and microsatellite instability (MSI), and expounds the important relationship between dMMR/MSI status and Lynch syndrome as well as tumor immunotherapy response. In addition, a variety of specific antibodies targeting key MMR proteins (MSH2, MLH1, MSH6, PMS2, Exo1) are listed, which provide reliable experimental tools for the detection of MMR protein expression and functional research.

cMicroglia, as the resident immune cells in the central nervous system, exhibit distinct activation states under pathological conditions such as neurological diseases and aging, which are closely associated with neurodegeneration, inflammatory response and other processes. This paper systematically elaborates the classification of microglial activation states identified by RNA-seq technology, and summarizes the core molecular markers of microglia, including CD68, Galectin-3, Cathepsin B, HIF-1α and Axl, as well as their biological functions in phagocytosis, inflammatory regulation and neuronal injury. Meanwhile, a variety of commercial antibodies suitable for experimental detection of the above markers are collated, covering their application scenarios such as Western blot (WB), immunohistochemistry (IHC) and immunofluorescence (IF). This study provides a reference for the selection of specific detection tools and related basic research on microglial activation in neurological disease models.

Alzheimer's disease (AD) is the leading global cause of dementia, pathologically featured by extracellular amyloid plaques and intracellular neurofibrillary tangles that cause neuronal damage and death. Genome-wide association studies have identified multiple susceptibility genes for late-onset AD, including APOE, BIN1, SORL1, TREM2, EphA1, ABCA7, MEF2C, PTK2B. This paper reviews the functions of these key risk genes and their mechanisms in AD pathogenesis, such as Aβ production and aggregation, tau pathology, microglial immune regulation, synaptic plasticity, lipid metabolism, and cerebrovascular function. Meanwhile, a panel of antibodies targeting AD‑related proteins is provided for experimental detection. Clarifying the roles of these genes helps reveal the molecular basis of AD and supports biomarker and therapeutic development.

It is the first to identify a novel form of programmed necrosis characterized by sodium overload — NECSO(Necrosis by Sodium Overload). The research defines transient receptor potential cation channel TRPM4 as the core regulator of this process, elucidates its molecular mechanism, species specificity and disease association, and identifies the first inhibitor of NECSO, providing a novel target and strategy for cell death regulation and the treatment of related diseases.

Our DNA is the treasure trove of genetic information, but it's actually quite "fragile." It can be damaged by ultraviolet rays, radiation, chemical substances, and even metabolic by-products within the cell. If DNA damage is not repaired in time, it can lead to abnormal cell function and even cancer.

Glycolysis is the metabolic process by which glucose is converted to pyruvate in a sequence of enzymatic steps. Phosphofructokinase (PFK) catalyzes the phosphorylation of fructose-6-phosphate in glycolysis.

Glycolysis Glycolysis is the metabolic process by which glucose is converted to pyruvate in a sequence of enzymatic steps. Hexokinase catalyzes the conversion of glucose to glucose-6-phosphate, the first step in glycolysis. Hexokinases I, II, and III are associated with the outer mitochondrial membrane and are critical for maintaining an elevated rate of aerobic glycolysis in cancer cells (Warburg effect).