Cell Biology

This practical ICC protocol describes fixation, permeabilization, blocking, antibody incubation, counterstaining, mounting and fluorescence imaging for cultured adherent and suspension cells. It compares direct and indirect immunostaining, outlines essential controls for single‑ and multicolor experiments, provides image acquisition guidelines, common troubleshooting and reporting requirements to localize target proteins inside or on the surface of cells.

This review explores how cell cycle regulation and DNA repair cooperate to maintain genome stability. It outlines major repair pathways, checkpoint signaling, and cell fate decisions, highlighting their implications for cancer therapy and the interpretation of experimental biomarkers.

In cell culture experiments, besides culture media and cytokines, the microenvironment where cells reside also deserves attention. This product encodes an important extracellular matrix (ECM) glycoprotein that participates in cell adhesion, migration, and interactions between cells and their surroundings.

UMR‑106 is an osteogenic osteosarcoma cell line derived from Sprague‑Dawley (SD) rats. Originally cloned from primary rat osteosarcoma, it was established alongside UMR 104, 105, 108 for morphological and biochemical characterization. These clones exhibit high alkaline phosphatase activity and can activate adenylate cyclase upon parathyroid hormone (PTH) stimulation, showing typical osteoblastic phenotypes that can be stably maintained during serial subculture. UMR‑106 cell line is available from the American Type Culture Collection (ATCC).

Compare cell lysis methods and buffers for western blot, co-IP, DNA, RNA and mass spectrometry, with sample-specific selection tips.

Obesity arises from an imbalance between energy intake and expenditure, accompanied by adipose tissue dysfunction, and is closely linked to metabolic disorders such as diabetes, cardiovascular disease, non‑alcoholic fatty liver disease, and certain cancers. Adipose tissue expansion mainly involves hypertrophy of white adipocytes or hyperplasia from precursor cells. Adipogenic induction is pivotal for mechanistic research and drug development against obesity‑related diseases. The 3T3‑L1 cell line is the most widely used model for adipogenic differentiation, with Oil Red O staining as the standard detection method. This paper elaborates on the characteristics of white and brown adipose tissue, the pros and cons of commonly used cells (3T3‑L1, hMSCs, hADSCs), and provides a detailed protocol for adipogenic differentiation of 3T3‑L1 cells using reagent RC0044. Common issues including insufficient lipid droplet formation, excessive background staining, and massive cell death are analyzed with corresponding troubleshooting strategies, offering a reliable reference for adipogenic induction experiments.

Diabetic nephropathy (DN), one of the most devastating complications of diabetes, has been increasing in prevalence globally. Approximately 40% of patients with type 2 diabetes and 30% of patients with type 1 diabetes will suffer from kidney damage, which may eventually progress to end-stage renal disease. However, its pathogenesis has not been fully elucidated, and there is still a lack of effective targeted therapies in clinical practice. Is there a key molecule that plays a central role in the development of diabetic nephropathy and could become a potential therapeutic target? In July 2025, researchers published a study titled "Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice" in Advanced Science. Through multi-model and multi-dimensional experiments in vivo and in vitro, the study for the first time revealed the pathogenic role and regulatory mechanism of GOLM1 in podocytes during the progression of diabetic nephropathy, providing novel insights for clinical treatment.

The reagent contains the water-soluble tetrazolium salt WST-8 [chemical name: 2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium monosodium salt]. Under the mediation of an electron carrier—1-methoxy-5-methylphenazinium methylsulfate (1-Methoxy PMS)—this salt is reduced by mitochondrial dehydrogenases within viable cells into a highly water-soluble yellow formazan dye. The amount of formazan produced is directly proportional to the number of viable cells. By measuring the optical density (OD) value at a wavelength of 450 nm using a microplate reader, one can indirectly quantify the number of viable cells.

Literature Sharing: Microglia-specific Regulation of Lipid Metabolism in Alzheimer's Disease I. Research Background Alzheimer's disease (AD), as the most common neurodegenerative disease and major cause of dementia, is characterized by severe disruption of brain homeostasis as one of its core pathological features. The role of abnormal lipid metabolism in disease progression has long been insufficiently recognized. In recent years, with the development of lipidomics technology, studies have found that imbalances in lipids such as phospholipids, sphingolipids, and cholesterol may be initiating factors in AD pathogenesis, rather than mere pathological byproducts. These lipid disorders can promote amyloidogenesis through mechanisms such as regulating membrane fluidity, secretase compartmentalization, and Aβ aggregation kinetics. The study "Microglia-specific regulation of lipid metabolism in Alzheimer's disease revealed by microglial depletion in 5xFAD Mice" focuses on microglia—the brain's resident immune cells. Combining the 5xFAD transgenic mouse model with human post-mortem brain tissue samples, the study investigates the specific regulatory role of microglia in lipid metabolism disorders in AD. The aim is to decipher the association between abnormal lipid metabolism in AD and different brain cell types and molecular pathways, providing new therapeutic targets for the disease. Previous studies have confirmed that lipid metabolism risk genes enriched in microglia (such as TREM2, PLCG2, GRN, etc.) are involved in Aβ clearance and neuroinflammation regulation. However, the specific impact of microglial depletion on brain lipid metabolism has been widely overlooked, with only one study focusing on its necessity for leukotriene synthesis, which became the core entry point for this study.

Literature Sharing: Tumor Immune Evasion Mechanisms and Counterstrategies