Mitochondrial dynamics, encompassing fission and fusion processes, plays a critical role in the regulation of mitochondrial morphology, metabolism, apoptosis, and autophagy. Protein import into mitochondria is primarily mediated by the translocase of the outer mitochondrial membrane (TOM) complex and the translocase of the inner membrane (TIM) complex, in which Tom20, a key component of the TOM complex, initiates the recognition of protein precursors. Mitochondrial dynamics are tightly governed by dynamin-related GTPases: DRP1 modulates mitochondrial fission, while mitofusin-1, mitofusin-2, and OPA1 control mitochondrial fusion. The activities of these core proteins are precisely regulated via post-translational modifications. OPA1 is regulated by alternative splicing and proteolytic processing, and its expression can be induced by metabolic stress. DRP1 activity is differentially modulated by phosphorylation at distinct sites, with Ser616 phosphorylation promoting fission and Ser637 phosphorylation inhibiting this process. Furthermore, mitochondrial fission factor (MFF) acts as a receptor for DRP1, and its phosphorylation by AMPK facilitates the recruitment of DRP1 to mitochondria. This review summarizes the molecular mechanisms underlying mitochondrial protein import and the regulatory network of mitochondrial dynamics.

Adult NSCs are primarily quiescent, a reversible cell state where they have exited the cell cycle (G0) yet remain responsive to the environment. In the first step of adult neurogenesis, quiescent NSCs (qNSCs) receive a signal and activate, exiting quiescence and re-entering the cell cycle.

Glial progenitor cells (GPCs) are a class of neural precursor cells characterized by self-renewal capacity and multi-lineage differentiation potential, primarily giving rise to the three major glial cell types of the central nervous system (CNS): astrocytes, oligodendrocytes, and ependymal cells.

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.

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).