【2025年6月文獻(xiàn)戰(zhàn)報(bào)】Bioss 抗體新增高分文獻(xiàn)精彩呈現(xiàn)

更新時(shí)間：2025-08-21 | 點(diǎn)擊率：651

截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共35,336篇，總影響因子176,219.79分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共126篇，合作單位覆蓋了清華、北大、復(fù)旦、華盛頓大學(xué)、麻省理工學(xué)院、東京大學(xué)以及紐約大學(xué)等上百所國(guó)際研究機(jī)構(gòu)。
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本文主要分享11篇IF＞16的文獻(xiàn)，它們引用了Bioss產(chǎn)品，分別發(fā)表在CELL、Nature Biomedical Engineering、Advanced Fiber Materials、Nature Metabolism、Bioactive Materials、Advanced Functional Materials、ACS Nano期刊上，讓我們一起學(xué)習(xí)吧。

CELL [IF=42.5]

文獻(xiàn)引用產(chǎn)品：

bs-0297P | Human IgG | IF

作者單位：首都醫(yī)科大學(xué)宣武醫(yī)院

摘要：Exercise has well-established health benefits, yet its molecular underpinnings remain incompletely understood. We conducted an integrated multi-omics analysis to compare the effects of acute vs. long-term exercise in healthy males. Acute exercise induced transient responses, whereas repeated exercise triggered adaptive changes, notably reducing cellular senescence and inflammation and enhancing betaine metabolism. Exercise-driven betaine enrichment, partly mediated by renal biosynthesis, exerts geroprotective effects and rescues age-related health decline in mice. Betaine binds to and inhibits TANK-binding kinase 1(TBK1), retarding the kinetics of aging. These findings systematically elucidate the molecular benefits of exercise and position betaine as an exercise mimetic for healthy aging.

Nature Biomedical

Engineering [IF=26.6]

文獻(xiàn)引用產(chǎn)品：

bs-20316R | QPRT/QAPRTase Rabbit pAb | IF, WB

bs-2713R | HAVCR1 Rabbit pAb | IF

bs-0189R | alpha smooth muscle Actin Rabbit pAb | IF, WB

bs-10423R | Collagen I Rabbit pAb | IF, WB

bsm-33033M | GAPDH Mouse mAb, Loading Control | WB

bs-0295G-HRP | Goat Anti-Rabbit IgG H&L, HRP conjugated | WB

bs-0296G-HRP | Goat Anti-Mouse IgG H&L, HRP conjugated | WB

作者單位：北京大學(xué)

摘要：Acute kidney injury(AKI) impairs the energy metabolism and antioxidant capacity of renal proximal tubular cells. Here we show that ultrasound-responsive liposomes integrating thylakoid fragments and encapsulating L-ascorbic acid can restore the energy supply and antioxidant capacity of the tubular cells as well as renal function in animal models of AKI. After intravenous injection, the liposomes preferentially accumulated in the injured kidneys and were internalized by proximal tubular cells. Quinolinate phosphoribosyltransferase expressed in thylakoid catalysed the biosynthesis of nicotinamide adenine dinucleotide (NAD⁺), prompting the recovery of damaged mitochondria. Local ultrasound stimulation activated electron transfer from ascorbic acid, which led to the cytoplasmic formation of NADH and to the restoration of adenosine triphosphate through the malate-aspartate shuttle. Concurrently, the enhanced pentose phosphate pathway facilitated NADPH biosynthesis and reduced the levels of reactive oxygen species. In mice and piglets with AKI, low doses of the liposomes prevented kidney damage.

Advanced Fiber

Materials [IF=21.3]

文獻(xiàn)引用產(chǎn)品：

bs-10802R | TNF alpha Rabbit pAb | IHC

bs-6761R | IL-10 Rabbit pAb | IHC

作者單位：浙江大學(xué)

摘要：Traditional antibiotic-based therapies for treating infectious wounds often face challenges in balancing long-term biosafety, promoting wound healing, and effectivelyeradicating bacteria. Herein, we introduce an innovative "top-down" approach to fabricating one-dimensional(1D) pristine silk nanofibers(SNFs) by the gradual exfoliation of silk fibers, preserving their inherent semi-crystalline structure. These SNFs functioned as a robust template for the in situ growth of two-dimensional(2D) plum blossom-like bismuth nanosheets(BiNS), whose anisotropic morphology enhances bactericidal contact efficiency. The resulting BiNS-equipped SNFs(SNF@Bi) are assembled into membranes(SNFM@Bi) via vacuum filtration, showing superior biocompatibility, photothermal efficiency, and photodynamic activity. Furthermore, the acidic wound microenvironment or near-infrared(NIR) irradiation triggered the release of Bi³⁺, exhibiting nanoenzyme-mediated catalytic activity. This multimodal mechanism allows SNFM@Bi to eliminate over 99% of Staphylococcus aureus and 100% of Escherichia coli by disrupting biofilms, inducing lysis, and causing oxidative damage. In vivo evaluations demonstrated significant bacteria clearance, accelerated angiogenesis, and enhanced collagen deposition, contributing to rapid wound healing without systemic toxicity. Notably, SNFM@Bi detaches spontaneously after healing, avoiding chronic nanomaterial retention risks. This multifunctional antimicrobial platform offers a controllable, effective, and biocompatible therapeutic strategy for antimicrobial dressing design, with potential applications in biomedicine, environmental protection, and public health.

Nature Metabolism [IF=20.8]

文獻(xiàn)引用產(chǎn)品：

bs-6313R | 4 Hydroxynonenal Rabbit pAb | IHC

作者單位：美國(guó)密歇根大學(xué)

摘要：Increased reactive oxygen species(ROS) levels are a hallmark of inflammatory bowel disease(IBD) and constitute a major mechanism of epithelial cell death. Approaches to broadly inhibit ROS have had limited efficacy in treating IBD. Here we show that lipid peroxidation contributes to the pathophysiology of IBD by promoting ferroptosis, an iron-dependent form of programmed cell death. Mechanistically, we provide evidence of heterocellular crosstalk between intestinal fibroblasts and epithelial cells. In IBD tissues and mouse models of chronic colitis, acyl-CoA synthetase long-chain family 4(ACSL4) is overexpressed in fibroblasts. ACSL4 in fibroblasts reprograms lipid metabolism and mediates intestinal epithelial cell sensitivity to ferroptosis. In mouse models, overexpressing ACSL4 in fibroblasts results in increased intestinal epithelial ferroptosis and worsened colitis, while pharmacological inhibition or deletion of fibroblast ACSL4 ameliorates colitis. Our work provides a targeted approach to therapeutic antioxidant treatments for IBD.

Bioactive Materials [IF=20.3]

文獻(xiàn)引用產(chǎn)品：

bsm-33112M | CD41/ITGA2B Mouse mAb | WB

bs-43552R | CD62p Rabbit pAb | WB

bs-20392R | GP1BA Rabbit pAb | WB

D60385 | Cyanine5 carboxylic acid | Other

作者單位：南通大學(xué)附屬醫(yī)院

摘要：Chronic nephritis management remains challenging due to the compromised therapeutic efficacy and severe systemic complications of conventional glucocorticoid therapy. Here, we developed a bioinspired platelet-mediated delivery system(LN-DEX@PLT) that leverages platelet tropism toward injured glomeruli for precision drug delivery. This system integrates lipid nanoemulsion encapsulation with platelet-mediated hitchhiking delivery to achieve three key functionalities:(1) enhanced renal targeting demonstrated by 2.2-fold higher glomerular accumulation compared to free dexamethasone via In vivo imaging, (2) effective mitigation of glucocorticoid-induced metabolic toxicity evidenced by reduced fasting plasma glucose(5.2 ± 0.3 vs 8.3 ± 0.7 mmol/L in free DEX), suppression of hepatic gluconeogenic enzymes(PEPCK expression decreased by 43 %, G-6 Pase by 51 %, both p < 0.001), and suppressed body weight (?23.1 % versus free DEX group), and(3) dual-pathway therapeutic effects through IL-6/TNF-α suppression and p53-p21^Cip1-mediated senescence delay. In Adriamycin-based chronic nephritis models, LN-DEX@PLT demonstrated superior renal protection with 81 % reduction in proteinuria (vs 33 % for free DEX). In LPS-induced and Adriamycin-based chronic nephritis models, LN-DEX@PLT demonstrated suppression of renal inflammation markers(IL-6 expression decreased to 68 %, TNF-α to 51 %) and macrophage infiltration (F4/80+ cells decreased 5.3-fold). This platelet-biohybrid system provides a clinically translatable paradigm for precision glucocorticoid therapy with reduced dosing frequency.

Bioactive Materials [IF=20.3]

文獻(xiàn)引用產(chǎn)品：

bs-10900R | GAPDH Rabbit pAb, Loading Control | WB

作者單位：中山大學(xué)

摘要：The ligamentization process of the tendon graft in anterior cruciate ligament(ACL) reconstruction is crucial for graft healing quality, thereby affecting knee joint function. Excessive scar tissue, caused by activation of trans-differentiation of fibroblasts to myofibroblasts, rather than orientated collagen fibers with normal composition and structure in the graft mid-substance seriously impacts ligamentization. The elucidation of the underlying mechanism behind the graft fibrosis may facilitate modulation of tendon graft ligamentization. Here, we show that transforming growth factor beta 1(TGF-β1) was significantly upregulated with ligamentization process, contributing to fibroblast to myofibroblast trans-differentiation and thereby leading to impaired collagen orientation with overproduction of collagen type III. Of note, we verified that prostaglandin E2(PGE2), a principal mediator of inflammation secreted by macrophages, significantly reversed TGF-β1-induced trans-differentiation of fibroblasts to myofibroblasts. Importantly, magnesium(Mg) ions were found to upregulate PGE2 production in macrophages, ultimately favoring inhibition of scar tissue formation and promoting expression of ligament-like phenotype in the graft mid-substance in rats. Consistently, the rats, with injection of the sodium alginate containing Mg ions into knee joint cavity, exhibited significantly improved gait performance and failure load relative to the control group. These results demonstrate the feasibility of using Mg ions to modulate tendon ligamentization in patients after ACL reconstruction.

Advanced Functional

Materials [IF=19]

文獻(xiàn)引用產(chǎn)品：

bsm-60761R | CD206 Recombinant Rabbit mAb | IF

作者單位：同濟(jì)大學(xué)

摘要：Optimal healing of diabetic chronic wound requires a well-organized cascade integration of bacterial death, cell migration and proliferation, and extracellular remodeling. However, such biological progress is usually impaired in chronic diabetic wound and traditional antibacterial hydrogels unmatched for ordered repair needs. Herein, an iron-coordinated glycopeptide hydrogel(Fe-GP gel) that could effectively treat MRSA-infected chronic diabetic wounds within 11 days by reprogramming healing process is developed. This Fe-GP hydrogel is formed based on glucomannan-decorated peptide nanofibers framework and then loaded with tannic acid/Fe nanocomplexes. The burst release of nanocomplexes is achieved to conduct the first healing stage, which could induce the ferroptosis-like death of methicillin-resistant Staphylococcus aureus (MRSA) for eliminating over 98% of MRSA bacteria by metabolism disrupting within 6 h. In the second healing stage, sustained release of glucomannan promotes M2 macrophage polarization(five times higher than control group) through extracellular signal-regulated kinase and signal transducer and activator of transcription 6(ERK/STAT6) pathway within 2 days. After the elimination of MRSA and restoration of immune microenvironment, the remaining 3D peptide nanofibers framework is able to facilitate extracellular remodeling through anchoring fibroblast cells as the third healing stage within weeks. Overall, this glycopeptide hydrogel has demonstrated a promising approach to realize the orderly progression during healing process for enhanced treatment of drug-resistant bacteria-infected chronic wounds.

Advanced Functional

Materials [IF=19]

文獻(xiàn)引用產(chǎn)品：

bs-0061R | beta-Actin Rabbit pAb, Loading Control | WB

作者單位：AIR FORCE MEDICAL CENTER, PLA

摘要：Monoclonal antibodies demonstrate significant potential in the clinical management of Human Epidermal Growth Factor Receptor 2/Estrogen Receptor-positive(HER2/ER+) breast cancer. However, the therapeutic outcomes of antitumor drugs are significantly hampered by challenges such as inter-pathway crosstalk, the restricted efficacy of single-pathway mechanisms, and suboptimal drug targeting. Herein, this study developed a Zr/Fe bimetallic MOF loaded with Cyclin-dependent kinases 4 and 6(CDK4/6) inhibitor ribociclib and surface-functionalized with trastuzumab (Herceptin). Under the acidic tumor microenvironment(TME), this nanomaterial degrades, releasing trastuzumab, ribociclib, and Fe³⁺. Trastuzumab enhances tumor targeting, reduces normal tissue toxicity, and inhibits Cyclin D1-CDK4/6 activation to decrease retinoblastoma(RB) phosphorylation, while ribociclib suppresses CDK4/6 enzymatic activity, synergistically blocking RB phosphorylation, inducing G1-phase arrest, and halting tumor proliferation. Additionally, Fe³⁺ catalyzes the conversion of H₂O₂ into highly cytotoxic hydroxyl radicals (·OH) through the Fenton reaction, leading to oxidative stress-induced cellular damage. Together, these three components synergistically inhibit the proliferation of HER2/ER+ breast cancer cells by disrupting cell cycle progression and cellular homeostasis. In vivo studies demonstrated that Zr-Fe MOF@Ribociclib@Herceptin(ZFRH) not only significantly inhibits the growth of orthotopic tumors but also effectively suppresses the formation of lung-metastatic tumors. These findings suggest a promising strategy for the precision-targeted therapy of HER2/ER+ breast cancer.

ACS Nano [IF=16]

文獻(xiàn)引用產(chǎn)品：

C5084 | Rehydragel@LV Alum Adjuvant | Other

作者單位：中國(guó)科學(xué)院武漢病毒研究

摘要：Nipah virus(NiV) is a serious hazard to human health since it can cause severe respiratory infections and viral encephalitis with a high fatality rate. Given the lack of a licensed NiV vaccine, there is an urgent need to develop one to protect public health. Previously, we developed NiV G protein nanoparticle vaccines by loading G protein onto ferritin nanoparticles(FeNP) via SpyCatcher/SpyTag technology, resulting in nanoparticles with three layers(FeNP-SC/ST-G_head), including the inner core of ferritin(20 kDa), the intermediate layer of covalently linked SpyCatcher/SpyTag(11.2 kDa) and the outer layer of G protein. The intermediate layer is unnecessary in terms of immunization and occupies immune resources in the body. In this study, we used a split-intein to conjugate NiV G_head onto FeNP, yielding FeNP-G_head with two layers. In BALB/c mice, FeNP-G_head could avoid immune response against SpyCatcher, elicit high levels of specific humoral immune responses for up to 217 days and long-lasting Th1-biased cellular immune responses. Furthermore, FeNP-G_head showed potent protection efficacy in the hamster model, with immunization of 1 μg providing 100% protection against challenge with 1000 LD₅₀ of NiV, and even as low as 0.2 μg being partially protective(83% survival). Since FeNP-G_head has a lower protein content than FeNP-SC/ST-G_head, it will occupy fewer immune resources in vivo, thereby reduce the potential for adverse immune side effect.

ACS Nano [IF=16]

文獻(xiàn)引用產(chǎn)品：

D-9110 | DiD perchlorate | Other

作者單位：重慶醫(yī)科大學(xué)

摘要：To overcome the limitations of conventional oral drugs and nanocarrier-dependent delivery systems in atherosclerosis(AS) therapy, our work proposes an "integration of Chinese and Western medicine" approach to develop a new biomimetic traditional Chinese and Western medicine components coassembled nanoparticles(NPs), termed as MMVs/RPNPs, for targeted AS therapy. In this work, we demonstrated that ginsenoside Rb1 can coassemble with probucol without excipients to form stable carrier-free NPs, termed RPNPs. To impart the specific targeting property to atherosclerotic sites, macrophage microvesicles(MMVs) were utilized to coat the RPNPs to obtain the MMVs/RPNPs. Developed MMVs/RPNPs exhibited excellent capabilities in eliminating intracellular ROS, suppressing pro-inflammatory factor secretion, and inhibiting intracellular lipid deposition in vitro. In a mouse model of AS, MMVs/RPNPs efficiently accumulated at atherosclerotic sites following intravenous injection and effectively retarded atherosclerotic plaque formation through synergistic effects of antioxidative stress, anti-inflammation, and inhibition of lipid deposition. Additionally, MMVs/RPNPs did not cause any adverse effects with long-term treatment. Our work presents simple, effective, and safe NPs against AS and underscores the potential of the "integration of Chinese and Western medicine" strategy for treating other cardio-cerebrovascular diseases.

ACS Nano [IF=16]

文獻(xiàn)引用產(chǎn)品：

bs-41210P | Recombinant human CK-MB protein | Other

bs-41107P | Human Purified Myoglobin | Other

bs-10877P | Recombinant human TNNI3 protein, His | Other

作者單位：東南大學(xué)

摘要：Timely diagnosis of acute myocardial infarction(AMI) during the prehospital phase is crucial to decrease mortality rates. Given that certain patients may not exhibit typical alterations in their electrocardiogram(ECG) patterns during the initial phases, the diagnosis of AMI is typically achieved by simultaneously assessing ECG results and myocardial injury biomarkers. This procedure requires the use of specialized equipment and trained personnel that are only available in hospitals, which may lead to possible delays of several hours. The development of a device that can detect both ECG and acute myocardial injury markers in the prehospital setting remains a significant challenge. In this study, a wearable dual-modal patch that combines a surface-enhanced Raman scattering(SERS) microneedle array with flexible electronics is introduced for the prehospital diagnosis of AMI. The patch allows for the noninvasive and rapid monitoring of both ECG and the levels of three myocardial injury markers in the interstitial fluid(ISF) by a portable Raman spectrometer, in accordance with the established clinical standard. This strategy was validated through experiments conducted on rats induced with AMI. The time required for diagnosing ischemia was significantly reduced to 50 min after its onset. The patch is optimally integrated into a stamp-sized band-aid, accompanied by a smartphone app for data visualization and real-time analysis. This initiative aims to facilitate the prompt delivery of interventions to reduce ischemic events.

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