【26年7月文献战报】博奥森高分文献精彩呈现

截至目前，引用Bioss产品发表的文献共40,905篇，总影响因子213,662.05分，发表在Nature, Science, Cell, Cancer Cell以及Immunity等顶级期刊的文献共147篇，合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等上百所国际知名研究机构。

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本文主要分享12篇IF≥18的文献，它们引用了Bioss产品，分别发表在iMeta、Molecular Cancer、Nature Nanotechnology、Advanced Materials、Bioactive Materials、Drug Resistance Updates、Journal of Extracellular Vesicles、Journal of Bioresources and Bioproducts、Nature Protocols、Nature Communications期刊上，让我们一起学习吧。

                                 

 iMeta [IF=44.4]

文献引用产品：

bs-0296G-HRP | Goat anti-Mouse IgG (H&L) pAb, HRP conj. | IHC

作者单位：北京大学第三医院

摘要：Age-related decline in endometrial function is a major cause of fertility issues in women, but effective treatments are lacking. This study aimed to investigate the impact of Bazi Bushen Capsule (BZBS) on endometrial aging and its underlying mechanisms. Using naturally aged mice and d-galactose-induced senescent human endometrial stromal cell lines, along with primary human endometrial stromal cells, we explored the effects of BZBS through single-cell RNA sequencing, transcriptome analysis, network pharmacology, and molecular dynamics simulations. Our results showed that BZBS improved endometrial receptivity, and decidualization by activating the AMPK−SIRT3 pathway. The key bioactive components of BZBS were identified as ginsenosides Rb1, Rb2, Rg5, and luteolin. Specifically, luteolin restored mitochondrial homeostasis by regulating PINK1/Parkin−mediated mitophagy and inhibiting Drp1. These findings suggested that BZBS effectively restored endometrial function and offered a promising therapeutic approach to counteract age-related endometrial dysfunction, potentially improving fertility in women of advanced maternal age.


Molecular Cancer [IF=42.2]

文献引用产品：

bs-0049R |  CASP9 | Caspase-9 Rabbit pAb | WB

作者单位：四川大学

摘要：Chemoresistance remains a major barrier in colorectal cancer (CRC) therapy. Through epigenetic compound screening in patient-derived organoids (PDOs), we identified CX6258.HCl as a potent growth inhibitor. Treatment with CX6258.HCl significantly inhibited cell mitosis and induced apoptosis in CRC cell lines. Mechanistically, CX6258.HCl binds the D687 residue within HASPIN’s kinase domain, suppressing H3T3 phosphorylation (H3T3ph). This triggers an epigenetic cascade: loss of H3T3ph upregulates demethylase KDM5B pre-mRNA, depleting H3K4me3 at promoters of Kinesin family member (KIFC1/KIF10/KIF14). Consequently, microtubule dynamics are disrupted, leading to mitotic arrest. Target specificity was validated genetically via HASPIN-D687A mutation. In vivo, CX6258.HCl suppressed CRC xenograft growth and further enhanced 5-FU-mediated tumor suppression without obvious histological injury in major organs. Clinically, elevated H3T3ph levels in human CRC tissues were associated with Ki67-positive proliferative tumor regions, suggesting that H3T3ph may represent a proliferation-associated marker in CRC. Together, our findings identify the HASPIN/H3T3ph-KDM5B-H3K4me3-KIF axis as a targetable antimitotic pathway and support therapeutic inhibition of HASPIN/H3T3ph as a potential strategy for CRC.


Nature Nanotechnology [IF=37.5]

文献引用产品：

bs-1604R | ABCB5 Rabbit pAb | FC, IF

作者单位：中国药科大学

摘要：Cancer stem-like cells contribute to innate tumour immunoresistance and an immunosuppressive tumour microenvironment, leading to poor responses to immune checkpoint inhibitors. Chemotherapeutic agents can elicit tumour immunogenicity by inducing immunogenic cell death to reinforce the therapeutic efficacies of immune checkpoint inhibitors, but suffer from inefficient immunogenic cell death activation in highly resistant cancer stem-like cells. Here we report an immunostimulatory lyotropic liquid-crystal-based lipogel for localized co-delivery of all-trans retinoic acid, a differentiation-inducing drug, and doxorubicin, an immunogenic-cell-death-inducing chemotherapeutic agent with distinct release kinetics. The lipogel is tailored to release the combinatorial drugs in a differential and sustained manner, which fulfils the requirement for enhanced drug synergism in promoting the immunogenic cell death of cancer stem-like cells. Local implantation of the immunostimulatory lipogel elicits an antitumour immune response that is further augmented by an immune checkpoint inhibitor to suppress tumour growth and metastasis, as well as to prevent post-surgical recurrence in murine models of high-stemness tumours.


Advanced Materials  [IF=29.1]

文献引用产品：

bs-0296PC | Normal Mouse Control IgG | IP
作者单位：郑州大学摘要：Although nanoparticle-based PROTACs (nPROs) provide a modular strategy to improve the biological fate of PROTACs, their degradation performance was fundamentally limited by restricted intracellular diffusivity. Here, we introduced an unconventional solution: Imparting autonomous motility to nPROs to transform them from passive carriers into active protein-seeking degraders. We engineered nano-motoring PROTACs (nMPROs) through asymmetric modification of gold nanoparticles, displaying POI ligands and E3 recruiters on one hemisphere while anchoring catalase on the opposite hemisphere. Within the H2O2-rich tumor cell microenvironment, catalase-generated oxygen fueled directional propulsion, enabling nMPROs to actively navigate the intracellular space rather than relying on random diffusion. This propulsion fundamentally enhanced intracellular target-search efficiency: nMPROs function as “nanoscopic protein-sweeping robots,” autonomously interrogating a larger intracellular landscape and capturing more sparsely distributed target proteins. As a result, nMPROs achieved a threefold increase in ERα degradation potency relative to static nPROs and enabled modular, ligand exchange–based degradation of PD-L1, demonstrating platform generality. Overall, this work establishes a new mechanistic paradigm for enhancing targeted protein degradation of nPROs and lays the foundation for generalizable next-generation PROTAC nanoplatforms.
                                     

Bioactive Materials [IF=23.6]

文献引用产品：

bs-1019R | TLR2 | TIL4/CD282 Rabbit pAb | IF, WB

作者单位：复旦大学附属中山医院

摘要：Poly-lactic acid (PLA) bioresorbable scaffolds provide temporary vascular support but trigger late-stage inflammation during polymer dissolution, frequently driving neointimal hyperplasia before complete dissolution. While acute biomaterial responses are well documented, the innate immune mechanisms dictating chronic vascular remodeling remain poorly defined. We demonstrate that late-stage PLA degradation actively instructs a microenvironment dominated by neutrophil extracellular trap (NET). Combining transcriptomic profiling of stented porcine arteries, and longitudinal spatial histology, we mapped a sustained immune response directly coupled to polymer breakdown. Mechanistically, PLA degradation products induce NET extrusion via mitochondrial calcium uniporter-mediated calcium overload. These extracellular structures subsequently function as potent paracrine signals, driving human vascular smooth muscle cells (VSMCs) toward a proliferative, synthetic phenotype. We identified a toll-like receptor 2 (TLR2) signaling pathway as the primary transducer of this NET-driven VSMC reprogramming. To apply these findings therapeutically, we engineered a customized PLA scaffold coated exclusively with the selective TLR2 inhibitor C29. In a rabbit iliac artery model, this targeted immunomodulatory device successfully disrupted the local inflammatory loop, significantly reducing neutrophil accumulation and mitigating neointimal hyperplasia. This study establishes the biomaterial-driven NET-TLR2 axis as a central mechanism of adverse vascular remodeling and offers a precise bioactive strategy to preserve long-term luminal patency.


                                     

Drug Resistance Updates [IF=22]

文献引用产品：

SV2000 | anti-ZDHHC16 antiobody | WB, IHC, IF

bs-13396R | GPX2 | GPx-GI Rabbit pAb | CoIP, IHC, IF

作者单位：中国医科大学盛京医院

摘要：S-palmitoylation is a common and reversible post-translational modification. This study aims to elucidate the functional role and mechanism of S-palmitoylation in lenvatinib resistance and lenvatinib-induced immunogenic cell death (ICD) in hepatocellular carcinoma (HCC). Using small interfering RNA (siRNA) screening in HCC cells, zinc finger DHHC-type palmitoyltransferase 16 (ZDHHC16) was identified as a lenvatinib resistance-associated palmitoyl acyltransferase. ZDHHC16 was abnormally overexpressed in both lenvatinib-resistant tissues and cells. ZDHHC16 knockdown improved the sensitivity of HCC cells to lenvatinib. Furthermore, ZDHHC16 knockdown boosted lenvatinib-induced ICD of HCC cells, characterized by an increase in the release of danger associated molecular patterns (DAMPs), including calreticulin (CRT) exposure on the tumor cell surface, high mobility group box 1 (HMGB1), annexin A1 (ANXA1), and adenosine-5′-triphosphate (ATP), as well as an increase in reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, and the secretion of cytotoxic cytokines (tumor necrosis factor (TNF)-α and interferon (IFN)-γ). Mechanistically, ZDHHC16 catalyzed the S-palmitoylation of glutathione peroxidase 2 (GPX2) at C67, which prevented ubiquitination-proteasome degradation of GPX2, thereby enhancing its protein stability. Targeting the ZDHHC16-mediated GPX2 S-palmitoylation improved lenvatinib-induced ICD and antitumor immunity, thereby enhancing the efficacy of lenvatinib. Collectively, our findings reveal that ZDHHC16-induced GPX2 S-palmitoylation plays a crucial role in modulating lenvatinib resistance and lenvatinib-induced ICD in HCC. Targeting this pathway is a promising approach to improve lenvatinib’s antitumor activity.

                                     

Journal of Extracellular [IF=21.7]

文献引用产品：

bs-2489R | CD9 Rabbit pAb | WB

作者单位：捷克科学院生物技术研究所

摘要：Extracellular vesicles (EVs) are small membrane-bound structures that facilitate intercellular communication in the reproductive system, modulating gamete maturation, capacitation, immunomodulation and fertilization. Despite pigs’ high relevance as a biomedical model, many aspects of EV biology remain poorly understood. EVs from boar seminal plasma (SP-EVs) are relatively well studied, whereas epididymosomes remain largely uncharacterized. Therefore, this study aimed to isolate and characterize EVs from the caput, corpus and cauda regions of boar epididymis, as well as from SP, with their further precise analysis towards their interaction with sperm. We successfully obtained EVs from all studied fluids with sufficient purity. Importantly, our isolation protocol preserved the EVs’ ability to interact with sperm, demonstrated by lipophilic dye staining and biotin labelling experiments, confirming precisely their interaction and cargo transfer to sperm cells. Well-established EV markers, such as Alix and tetraspanins, were detected in the EVs, and additionally, phosphorylated, ubiquitinated and sialylated proteins were uniquely identified. Furthermore, we employed a proteomic approach to characterize EV proteins (mass spectrometry data are available via ProteomeXchange with identifier PXD074929) and investigate their functional roles using the Gene Ontology (GO) database. This study contributes valuable insights into the molecular composition and functional properties of EVs from the male reproductive tract. It may provide a solid framework for further basic and translational research in reproductive biology and biomedicine.
                                     

Journal of Bioresources and 

Bioproducts [IF=19.9]

文献引用产品：

bs-0295G-BF488 | Goat anti-Rabbit IgG (H&L) pAb, BF488 conj. | IF

作者单位：西安交通大学

摘要：The development of robust biomimetic interfaces remains challenging due to the inherent instability of native cell membranes when integrated into functional devices. Herein, we reported a bio-based functional composite in which a chitosan-derived conductive hydrogel served as a multifunctional matrix to achieve unprecedented stabilization of red blood cell membranes (RBCMs). Leveraging the three-dimensional polycationic network and abundant amino groups of this natural polysaccharide, the hydrogel electrostatically anchored RBCMs while preserving their native fluidity and membrane-bound acetylcholinesterase conformation-overcoming a long-standing bottleneck in biomembrane-based material engineering. Integration of carboxylated multi-walled carbon nanotubes endowed the composite with efficient electron transfer capability without compromising biocompatibility. The resulting biomimetic interface retained 85.8% of its initial electrochemical response after 7 days of continuous operation and enabled sensitive detection of organophosphate pesticides in real agricultural samples (apples, oranges, and tomatoes). This work established chitosan hydrogel as a versatile bio-based platform for constructing stable biomembrane composites, expanding the application scope of natural polysaccharides in functional material design for environmental monitoring.

                                  

Nature Protocols [IF=18.4]

文献引用产品：

bs-1012R | BMP2 Rabbit pAb | IF, IHC

作者单位：四川大学华西口腔医院

摘要：The selective capture of endogenous cells and proteins holds immense potential in regenerative medicine, single-cell analysis, biosensing and cell therapy. However, conventional multivalent platforms suffer from uncontrolled ligand distribution and poor spatial alignment, limiting capture efficiency. Here we provide a protocol for a programmable tetrahedral DNA nanostructure (TDN) platform that enables precise spatial control of capture ligands through site-specific editability. This protocol describes two distinct capture systems: (1) an aptamer-functionalized TDN for the selective capture of mesenchymal stem cells, which increases binding affinity 2.25-fold and achieves ~90% capture efficiency, and (2) a peptide-functionalized TDN–hydrogel for sequestering endogenous growth factors, which enhances capture efficiency from <40% with conventional methods to nearly 90%. The complete protocol, from computational design and nanostructure assembly to in vitro functional validation, can be completed in ~10–20 d, with subsequent in vivo studies extending over several weeks. This versatile platform enables the rational design of high-efficiency capture agents for diverse biological targets, providing a powerful and adaptable tool for tissue engineering, cell sorting and biosensing.


Nature Communications [IF=18.1]

文献引用产品：

bs-1310R | ITGAV | CD51 Rabbit pAb | IF

作者单位：西班牙马德里国家心血管研究中心

摘要：Thoracic aortic aneurysms and dissections (TAAD), a life-threatening complication of Marfan syndrome (MFS), lack curative therapies. Our previous studies revealed that versican accumulation drives MFS aortopathy through AKT-NO pathway overactivation, but the upstream mechanisms remained unclear. Here, we show that versican-driven fibronectin (FN) accumulation activates an αVβ3-PI3K-PIP3-PDK1-ILK signaling cascade leading to AKT-NOS2 upregulation and aortic disease. FN accumulates in aortas of MFS patients and mice of both sexes and correlates with increased αVβ3 integrin and ILK expression. Disrupting FN assembly or inhibiting αVβ3, PI3K, PIP3, PDK1 or ILK prevents FN-induced AKT activation and NOS2 upregulation, restores vascular contractility, and limits aortic dilation in MFS mice. Inhibition of ILK or PDK1, aortic silencing of Ilk, or smooth muscle-specific deletion of Ilk reverses or prevents aortic growth. Together, these findings define a mechanistically integrated FN-αVβ3-PI3K-PIP3-PDK1-ILK-AKT-NOS2 signaling cascade in MFS and support its causative role in human TAAD, highlighting its components as potential targets for therapeutic intervention.


Nature Communications [IF=18.1]

文献引用产品：

bsm-60920R | CD33 Recombinant Rabbit mAb | Other

作者单位：英国剑桥

摘要：Mechanisms linking CD33 variants to Alzheimer Disease (AD) are poorly defined. Here, we combine structural, cellular, and genetic analyses to delineate how the CD33M splice isoform, upregulated in carriers of CD33 risk alleles, modulates microglial function. We show that CD33M ectodomain dimerizes, enabling binding of large multi-sialylated molecules. We demonstrate that another AD risk protein - clusterin (CLU) ± Aβ oligomers (but not ApoE) binds with nanomolar avidity to CD33M, but not CD33m. We show that in human monocytes CD33M:CLU binding induces CD33M ITIM phosphorylation, recruits SHP-1, suppresses Aβ phagocytosis, and impairs clearance of amyloid plaques. We identify a soluble CD33M ectodomain fragment (sCD33M) - absent from CD33m-expressing cells - which could contribute to the role of CD33M in AD. Genetic analyses confirm that CD33:CLU interaction modulates amyloid burden, cognition, and disease risk. These findings define a mechanistic CLU:Aβ:CD33M axis, highlighting CD33M dimerization and ligand-binding sites as potential therapeutic targets.


Nature Communication[IF=18.1]

文献引用产品：

bs-0297G |  Goat anti-Human IgG (H&L) pAb | ELISA

作者单位：山西医科大学

摘要：Ribozyme-based approaches have been extensively employed for in vitro circular RNA (circRNA) synthesis. However, several critical challenges are impeding the progress in this field, including the relatively low ribozyme utilization efficiency, limited synthetic flexibility, and complicated downstream purification procedures. Here, we introduce a split intron-exon (SIE) system for circRNA synthesis by physically separating the ribozyme from its substrates. This design ensures efficient circRNA synthesis by overcoming the inherent limitations of current ribozyme-based techniques, in which each ribozyme can only catalyse the synthesis of at most one circRNA molecule. Moreover, the SIE system enables the efficient synthesis of both unmodified and chemically modified circRNAs. Furthermore, the recyclability and immobilization of the ribozyme within the SIE system reduce reaction impurities and improves circRNA enrichment and yield. Overall, the SIE system holds great potential to advance the diversification and large-scale development of circRNA therapeutics.