BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS生物化学与生物物理研究通讯
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS(英文缩写 BIOCHEM BIOPH RES CO),ISSN 0006-291X,eISSN 1090-2104,中文译名:生物化学与生物物理研究通讯 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.322 | Q3 |
| 2022 | 3.100 | Q2 |
| 2023 | 2.500 | Q3 |
| 2024 | 2.200 | Q3 |
| 2025 | 2.500 | Q3 |
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 最新收录文献
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6. Characteristics of plasma-activated water and its effect on apoptosis of malignant melanoma cells.
PMID:日期:2026-10-15Plasma-activated water (PAW) has emerged as a promising indirect cold atmospheric plasma modality for cancer therapy due to its rich reactive oxygen and nitrogen species (RONS) content, yet its effects on malignant melanoma and the underlying mechanisms require further elucidation. In this study, deionized water was irradiated with a helium atmospheric pressure plasma jet (APPJ) for 1, 2, 3, 4, and 5 min to generate five PAWs (PAW1, PAW2, PAW3, PAW4, PAW5). Physicochemical analysis of PAWs revealed progressive increases in conductivity, decreases in pH, and accumulation of hydrogen peroxide (HO), nitrite (NO), and nitrate (NO) with prolonged APPJ irradiation. Compared to control group, PAWs treatment reduced malignant melanoma cell (B16) viability in a time-dependent manner, concomitant with increased apoptosis and elevated lactate dehydrogenase release. Oxidative stress markers demonstrated an obvious increase in malondialdehyde (MDA) content and a progressive decline in superoxide dismutase (SOD) activity. PAW5 treatment exerted the strongest cytotoxic effect on B16 cells. Western blotting analysis revealed significant downregulation of anti-apoptotic Bcl-2, accompanied by a sustained upregulation of pro-apoptotic Bax. This was followed by significant activation of cleaved caspase-9 and cleaved caspase-3, indicating the induction of the mitochondrial apoptotic pathway. These findings demonstrated that PAW-induced oxidative stress triggered the mitochondrial apoptotic pathway in melanoma cells, supporting the potential of PAW as a novel therapeutic strategy for malignant melanoma.
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7. A novel DNA-protective function of Escherichia coli thioredoxin 2 mediated by its N-terminal zinc-binding domain.
PMID:日期:2026-10-15Thioredoxins are ubiquitous thiol-disulfide oxidoreductases that maintain intracellular redox homeostasis. In addition to its conserved catalytic domain, Escherichia coli thioredoxin 2 (EcTrx2) possesses a unique N-terminal zinc-binding domain whose physiological function remains largely unknown. Here, we identify a previously unrecognized DNA-binding activity of EcTrx2 and demonstrate its role in protecting DNA during oxidative stress. Electrophoretic mobility shift assays showed that EcTrx2 bound plasmid DNA in a concentration-dependent and GST-tag-independent manner, whereas EcTrx1 exhibited no detectable DNA-binding activity. DNA binding was abolished by deletion of the N-terminal zinc-binding domain and was blocked by zinc occupancy, indicating that this unique domain is essential for DNA interaction. Consistent with these findings, EcTrx2 significantly protected plasmid DNA from DNase I digestion and hydroxyl radical-mediated oxidative damage in vitro. Furthermore, EcTrx2 enhanced bacterial tolerance to the DNA-damaging agents zeocin and diamide, supporting the physiological relevance of its DNA-binding activity. Our results reveal a DNA-binding role for EcTrx2 and identify its N-terminal zinc-binding domain as a key determinant of DNA binding and protection against oxidative DNA damage.
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8. {"_":"Activation of lipid synthesis following glycolysis is required for CD8 T cells to acquire antitumor immune activity.","sup":["+"]}
PMID:日期:2026-10-15Activated CD8 T cells undergo metabolic reprogramming and shift to aerobic glycolysis to fulfill their energy and biosynthetic demands. However, the downstream pathways linking glycolytic flux to potent antitumor immunity remain unclear. In this study, we used a T-cell-specific phosphoglycerate mutase 1 (Pgam1)-deficient mouse model to demonstrate that accelerated lipid synthesis induced by glycolysis is necessary for CD8 T cells to acquire antitumor activity. Pgam1 deficiency severely impaired antitumor activity and intratumoral infiltration in the MC38-OVA tumor model. Transcriptomic profiling of Pgam1-deficient CD8 T cells activated in vitro revealed that Pgam1 deficiency caused a marked reduction in the lipid biosynthetic program and altered lipid composition. We found that in Pgam1-deficient CD8 T cells, TCR stimulation dose not induce the upregulation of the Srebf1 and Srebf2 genes, which encode the master transcription factors Srebp1 and Srebp2, respectively, that regulate lipid synthesis. Pharmacological inhibition of SREBPs by fatostatin attenuated effector functions, such as TCR-induced proliferation, cytokine production, and cytotoxicity. These findings indicate that the activation of SREBP-dependent lipid synthesis pathways, which follow glycolysis, is important for the acquisition of antitumor activity by CD8 T cells.
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9. Comparative antidiabetic effects of Cymbopogon citratus leaf extract, derived silver nanoparticles, and their combination in alloxan-induced diabetic mice.
PMID:日期:2026-10-15Plant-mediated nanoparticles are being investigated for metabolic disorders, but therapeutic gains from full-dose co-administration should be distinguished from true pharmacological synergy. This study compared the antidiabetic effects of Cymbopogon citratus leaf ethanolic extract (LEE), biosynthesized silver nanoparticles (AgNPs), and their combination in alloxan-induced diabetic mice. AgNPs were synthesized using LEE as a reducing and capping agent and characterized by UV-Vis spectroscopy, dynamic light scattering, zeta potential analysis, transmission electron microscopy, Fourier-transform infrared spectroscopy, and X-ray diffraction. The AgNPs showed a surface plasmon resonance peak at 432 nm, mean hydrodynamic diameter of 38.2 ± 4.6 nm, zeta potential of -28.4 ± 3.1 mV, and predominantly spherical morphology. Diabetic mice received metformin, LEE, AgNPs, or LEE + AgNPs for 28 days, followed by evaluation of glycaemic, oxidative, lipid, hepatorenal, haematological, pancreatic histopathological, and integrated biomarker recovery responses. The combination group recorded fasting blood glucose of 128.0 ± 3.0 mg/dL and HbA1c of 6.5 ± 0.1%, compared with 141.0 ± 5.7 mg/dL and 7.3 ± 0.1%, respectively, in the AgNP group. Although combined administration produced the highest integrated biomarker recovery index (80.61 ± 0.61%), additional improvements over AgNP monotherapy were limited or nonsignificant across several endpoints. Pancreatic histopathology also showed improved islet area, cellular density, and lesion scores following treatment. Co-administration produced endpoint-specific additional benefits but did not demonstrate pharmacological synergy. Further route-matched dose-response studies, mechanistic validation, nanoparticle biodistribution, and long-term biosafety assessment are required.
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10. {"_":"Monomeric hapten dissociates FcεRI-evoked STIM1-Orai1 interaction and immediately terminates Ca influx in rat basophilic leukemia cells.","sup":["2+"]}
PMID:日期:2026-10-15Crosslinking of the high affinity IgE receptor (FcεRI) by multivalent antigen increases intracellular Ca concentration ([Ca]) through two sequential steps: (i) Ca release from the endoplasmic reticulum (ER) and (ii) store-operated Ca entry (SOCE) mediated by stromal interaction molecule 1 (STIM1)-Orai1 interaction. This process is essential for basophil and mast cell activation. We previously showed that FcεRI disaggregation by monomeric hapten rapidly and persistently inhibited [Ca] increase although upstream signal disruption was transient in rat basophilic leukemia cells. However, the underlying inhibitory mechanisms remain unclear. In this study, we found that monomeric hapten dissociates STIM1-Orai1 interaction by promoting Orai1 re-phosphorylation. Although Ca release from ER, the first step in [Ca] increase, was blocked by monomeric hapten addition, phosphorylation of phospholipase Cγ1, a critical step for Ca release from the ER, was inhibited only when the monomeric hapten was added immediately after multivalent antigen stimulation, but not when added several minutes later. However, STIM1-Orai1 interaction was dissociated by the monomeric hapten, regardless of the timing of its addition. Multivalent antigen induced Orai1 dephosphorylation, which is necessary for SOCE. In contrast, monomeric hapten addition promoted its re-phosphorylation. These results suggest that cessation of [Ca] increase following FcεRI disaggregation primarily arises from immediate suppression of SOCE via STIM1-Orai1 dissociation.