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2025 CUSABIO Monthly Citation Review
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Top 1
Article Title: Neurotensin-neurotensin receptor 2 signaling in adipocytes suppresses food intake through regulating ceramide metabolism Journal Name: Cell Research Impact Factor: 28.4 CUSABIO Citation Product: Mouse neurotensin (NTS) ELISA kit; CSB-EL016136MO Research Highlights: This study reveals that neurotensin (NTS) signaling through its receptor 2 (NTSR2) in adipocytes suppresses food intake by regulating ceramide metabolism. The research shows that depletion of NTSR2 in white adipocytes increases food intake, while local administration of NTS reduces it. Mechanistically, NTS-NTSR2 signaling inhibits the phosphorylation of ceramide synthetase 2 (CerS2), decreasing the production of ceramides C20–C24 and the secretion of growth differentiation factor 15 (GDF15), thereby affecting food intake. Additionally, a positive correlation between plasma levels of ceramides C20–C24 and food intake in humans is identified. This study provides the first evidence that NTS-NTSR2 signaling controls food intake by directly regulating ceramide metabolism in adipose tissue, offering a potential new target for obesity treatment. |
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Top 2
Article Title: Exosomal circ_0006896 promotes AML progression via interaction with HDAC1 and restriction of antitumor immunity Journal Name: Molecular Cancer Impact Factor: 27.7 CUSABIO Citation Product: Human 5-hydroxyeicosatetraenoic acid(5-HETE)ELISA Kit; CSB-E17006h Research Highlights: This study investigates the role of a circular RNA (circRNA) named circ_0006896 in acute myeloid leukemia (AML). Circ_0006896 is significantly upregulated in AML cells and exosomes, correlating with poor prognosis. It binds to histone deacetylase 1 (HDAC1), inhibits histone H3 acetylation, and affects the transcription of genes involved in arachidonic acid metabolism, thereby suppressing lipid peroxidation and ferroptosis. Circ_0006896-rich AML exosomes impair CD8+ T cell function by interacting with HDAC1, inducing an immunosuppressive microenvironment and promoting AML progression. The study also shows that inhibiting circ_0006896 enhances the anti-leukemia effects of HDAC inhibitors and restores the cytotoxic function of CD8+ T cells, highlighting its potential as a therapeutic target in AML immunotherapy. |
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Top 3
Article Title: Super‐Resolution Goes Viral: T4 Virus Particles as Versatile 3D‐Bio‐NanoRulers Journal Name: Advanced Materials Impact Factor: 27.4 CUSABIO Citation Product: wac Antibody; CSB-PA319157ZA01EDZ Research Highlights: This article presents the use of T4 bacteriophage as a novel 3D bio-nano ruler in super-resolution fluorescence microscopy. The study demonstrates that the geometric structure of T4 makes it an ideal standard for precise three-dimensional imaging at the nanoscale. Using DNA point accumulation for imaging (DNA-PAINT) and optical astigmatism techniques, researchers successfully revealed the 3D structure of T4, showcasing its 120 nm length and 86 nm width icosahedral capsid and elongated viral tail. The innovation lies in the ability to directly observe the hollow structure of T4, providing high signal-to-noise ratio imaging. Additionally, the multi-target capability of T4 allows for various labeling under different experimental conditions, further enhancing its potential as a 3D bio-nano ruler. This research offers new insights and methods for super-resolution imaging in biological studies. |
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Top 4
Article Title: Dysregulation in keratinocytes drives systemic lupus erythematosus onset Journal Name: Cellular & Molecular Immunology Impact Factor: 21.8 CUSABIO Citation Product: Mouse anti-double stranded DNA antibody (IgG) ELISA Kit; CSB-E11194m Research Highlights: This article proposes a new theory that systemic lupus erythematosus (SLE) can be directly initiated by molecular alterations in keratinocytes rather than immune cell dysregulation. The study found that the level of peroxisome proliferator-activated receptor gamma (PPARγ) is significantly reduced in skin lesions of SLE patients. Mice with this reduction rapidly developed multiple hallmarks of SLE. As PPARγ decreases, interferon regulatory factor 3 occupancy at the type I interferon locus increases. Keratinocyte-secreted type I interferon activates dendritic cells (DCs), which migrate to local lymph nodes and activate CD4+ T cells in a non-MHC II-dependent manner, promoting their differentiation into effector T cells and driving disease onset. The research highlights the pivotal role of keratinocyte dysregulation in SLE pathogenesis and describes a new mouse model that mimics human SLE, emphasizing the importance of skin immunity in the onset of systemic autoimmune diseases. |
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Top 5
Article Title: Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation Journal Name: Nature Metabolism Impact Factor: 18.9 CUSABIO Citation Product: Research Highlights: This article investigates the effects of targeting fructose-1,6-bisphosphate aldolase A (ALDOA) in hepatocellular carcinoma (HCC). The study reveals that ALDOA is uniquely essential in liver cancer cells, and its depletion leads to severe energy stress and cell cycle arrest. Through metabolic flux analysis, metabolomics, and mathematical modeling, the research shows that targeting ALDOA disrupts glycolysis, causing an imbalance where the investment phase outpaces the payoff phase, leading to accumulation of fructose-1,6-bisphosphate (FBP) and ATP depletion. Additionally, ALDOA depletion extends survival and reduces cancer cell proliferation in animal models. The findings highlight the critical role of ALDOA in liver cancer and suggest that targeting ALDOA could be a novel strategy to overcome the metabolic plasticity of cancer cells. |
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Top 6
Article Title: Intestinal TM6SF2 protects against metabolic dysfunction-associated steatohepatitis through the gut–liver axis Journal Name: Nature metabolism Impact Factor: 18.9 CUSABIO Citation Product: Mouse Lipopolysaccharides(LPS) ELISA Kit; CSB-E13066m Research Highlights: This article reveals the crucial role of intestinal TM6SF2 in metabolic dysfunction-associated steatohepatitis (MASH). The study found that mice with specific knockout of Tm6sf2 in intestinal epithelial cells (Tm6sf2ΔIEC) developed MASH spontaneously, characterized by impaired intestinal barrier function and gut microbiota dysbiosis. Mechanistically, Tm6sf2-deficient intestinal cells interact with fatty acid-binding protein 5 (FABP5) to secrete more free fatty acids, leading to intestinal barrier dysfunction, enrichment of pathobionts, and elevated levels of lysophosphatidic acid (LPA). LPA translocates from the gut to the liver, contributing to lipid accumulation and inflammation. Fecal microbiota transplantation experiments further confirmed the key role of gut microbiota in MASH development in Tm6sf2ΔIEC mice. Additionally, pharmacological inhibition of the LPA receptor or modulation of the gut microbiota effectively alleviated MASH symptoms. These findings not only elucidate the mechanism of intestinal TM6SF2 in MASH but also provide a theoretical basis for developing new therapeutic strategies. |
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Top 7
Article Title: A tailored phytosomes based nose-to-brain drug delivery strategy: Silver bullet for Alzheimer's disease Journal Name: Bioactive Materials Impact Factor: 18 CUSABIO Citation Product: DCX Antibody; CSB-PA006576DA01HU Research Highlights: This article presents a novel nose-to-brain drug delivery strategy for Alzheimer’s disease (AD) using phytosome-based nasal spray to co-deliver ginsenoside Rg3 (GRg3) and rivastigmine hydrogen tartrate (RHT). By employing a viscosity control strategy, the nasal spray was optimized to enhance drug deposition in the olfactory region, effectively bypassing the blood-brain barrier and improving brain delivery efficiency. In an AD rat model, GRg3@RHT nasal spray significantly improved learning and memory abilities, alleviated behavioral dysfunctions, and delayed neurodegenerative processes. The study also established the correlation between viscosity and spray performance, further confirmed by in vivo pharmacokinetic and pharmacodynamic experiments. This research offers new insights into AD treatment and innovative ideas for drug delivery targeting nervous system disorders. |
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Top 8
Article Title: Methylcobalamin protects against liver failure via engaging gasdermin E Journal Name: Nature Communications Impact Factor: 14.7 CUSABIO Citation Product: Recombinant Human Gasdermin-E (GSDME); CSB-EP006766HU Research Highlights: This study identifies methylcobalamin (MeCbl), an endogenous form of vitamin B12, as a specific inhibitor of Gasdermin E (GSDME) cleavage, effectively combating cholestatic liver failure. Through high-throughput screening, MeCbl was found to directly bind to GSDME, preventing its recognition and cleavage by caspase-3 or granzyme B (GzmB), thereby inhibiting GSDME-mediated pyroptosis. In various mouse models of liver failure, MeCbl significantly reduced serum transaminase activities and inflammatory cytokines, alleviated hepatocyte death, and decreased mortality. The study also revealed that the conserved Cys180 residue in GSDME is essential for caspase-3/GzmB recognition, and MeCbl acts by binding to this site. This research not only provides a new potential therapeutic option for liver failure but also offers a new approach for drug development based on endogenous metabolites. |
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Top 9
Article Title: Brucella abortus impairs T lymphocyte responsiveness by mobilizing IL-1RA-secreting omental neutrophils Journal Name: Nature communications Impact Factor: 14.7 CUSABIO Citation Product: Research Highlights: This study reveals that Brucella abortus impairs T cell responsiveness by mobilizing IL-1RA-secreting neutrophils in the mouse omentum, promoting chronic infection. The research shows that B. abortus can replicate within omental macrophages and persist over time, leading to the accumulation of macrophages, monocytes, and neutrophils in the omentum. These cells express immunosuppressive markers PD-L1 and Sca-1, which depend on the core structure of Brucella LPS. The study also finds that brucellosis patients exhibit upregulated PDL1 and LY6E genes and elevated IL-1RA levels in serum, consistent with the mouse model. This work not only uncovers a new mechanism of chronic infection involving the omentum but also provides potential therapeutic targets for treating chronic bacterial infections. |
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Top 10
Article Title: CHAC1 Mediates Endoplasmic Reticulum Stress‐Dependent Ferroptosis in Calcium Oxalate Kidney Stone Formation Journal Name: Advanced Science Impact Factor: 14.3 CUSABIO Citation Product: Mouse Kidney injury molecule 1,Kim-1 ELISA Kit; CSB-E08809m Research Highlights: This study investigates the role of CHAC1 in calcium oxalate kidney stone formation, revealing the mechanism of endoplasmic reticulum (ER) stress-dependent ferroptosis. CHAC1 is found to play a crucial role in ER stress and ferroptosis by regulating glutathione metabolism, thereby affecting cell injury. In experiments, treatment with 4-phenylbutyric acid (4-PBA) and CHAC1 deficiency reduced oxidative damage, improved renal function, and decreased crystal deposition. The study also shows that CHAC1 is a key downstream target gene of ATF4, and ATF4 depletion inhibits the upregulation of CHAC1 and the ferroptotic response. CHAC1 degrades glutathione, weakening GPX4 activity and promoting ferroptosis. This research offers new potential strategies for preventing and treating calcium oxalate kidney stones. |
