【25年2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：2025-04-08 | 點(diǎn)擊率：190

截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共33241篇，總影響因子162891.42分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共125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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【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Cell, Signal Transduction and Targeted Therapy, Cell Metabolism, Advanced Materials, nature biomedical engineering, Bioactive Materials, Nature Aging, Nucleic Acids Research, ACS Nano等期刊的11篇IF＞15的文獻(xiàn)摘要，讓我們一起欣賞吧。

CELL [IF=45.5]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-10994R-BF647 | phospho-DNA-PKcs (Ser3191) Rabbit pAb, BF647 conjugated | Flow-Cyt

作者單位：美國(guó)波士頓兒童醫(yī)院

摘要：The composition and organization of the cell surface determine how cells interact with their environment. Traditionally, glycosylated transmembrane proteins were thought to be the major constituents of the external surface of the plasma membrane. Here, we provide evidence that a group of RNA-binding proteins (RBPs) is present on the surface of living cells. These cell-surface RBPs (csRBPs) precisely organize into well-defined nanoclusters enriched for multiple RBPs and glycoRNAs, and their clustering can be disrupted by extracellular RNase addition. These glycoRNA-csRBP clusters further serve as sites of cell-surface interaction for the cell-penetrating peptide trans-activator of transcription (TAT). Removal of RNA from the cell surface, or loss of RNA-binding activity by TAT, causes defects in TAT cell internalization. Together, we provide evidence of an expanded view of the cell surface by positioning glycoRNA-csRBP clusters as a regulator of communication between cells and the extracellular environment.

Signal Transduction and

Targeted Therapy [IF=40.8]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-5913R-BF488 | Calreticulin Rabbit pAb, BF488 conjugated | ICC、IF

作者單位：四川大學(xué)華西醫(yī)院

摘要：Radiotherapy (RT) resistance in head and neck squamous cell carcinoma (HNSCC) significantly hampers local control and patient prognosis. This study investigated the efficacy and molecular mechanisms of high-energy X-ray-based ultra-high dose rate radiotherapy (UHDR-RT) in overcoming RT resistance. The established RT-resistant HNSCC cell lines and animal models were subjected to UHDR-RT or conventional RT (Conv-RT) via a high-power rhodotron accelerator. Cellular assays assessed the malignant phenotype, viability, and degree of DNA damage, whereas in vivo evaluations focused on tumor proliferation and the tumor immune microenvironment (TiME). Transcriptome sequencing and Olink proteomics were employed to explore the underlying mechanisms involved. In vitro experiments indicated that UHDR-RT suppressed radioresistant cell proliferation and invasion, while promoting apoptosis and exacerbating DNA damage. In contrast, its efficacy in radiosensitive cells was comparable to that of Conv-RT. In vivo studies using patient-derived xenograft nude mice models demonstrated that UHDR-RT only partially reversed RT resistance. Transcriptomic and proteomic analyses of C57BL/6J mice models revealed the predominant role of TiME modulating in reversing radioresistance. Immunofluorescence and flow cytometry confirmed increased CD8⁺ T cells and an increased M1/M2 macrophage ratio post-UHDR-RT. Mechanistically, UHDR-RT activated CD8⁺ T cells, which stimulated M1 macrophages through paracrine IFN-γ signaling, thereby enhancing TiME activation. Furthermore, the activated M1 macrophages secreted CXCL9, which in turn reactivated CD8⁺ T cells, forming a feedforward loop that amplified TiME activation. This study elucidates the dual role of UHDR-RT in directly inducing DNA damage and modulating the TiME, highlighting its potential in treating radioresistant HNSCC.

Cell Metabolism [IF=27.7]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-6310R | Caveolin-2 Rabbit pAb | WB

作者單位：中國(guó)科學(xué)院上海藥物研究所

摘要：Metabolic-dysfunction-associated steatohepatitis (MASH) remains a major health challenge. Herein, we identify sphingomyelin phosphodiesterase 3 (SMPD3) as a key driver of hepatic ceramide accumulation through increasing sphingomyelin hydrolysis at the cell membrane. Hepatocyte-specific Smpd3 gene disruption or pharmacological inhibition of SMPD3 alleviates MASH, whereas reintroducing SMPD3 reverses the resolution of MASH. Although healthy livers express low-level SMPD3, lipotoxicity-induced DNA damage suppresses sirtuin 1 (SIRT1), triggering an upregulation of SMPD3 during MASH. This disrupts membrane sphingomyelin-ceramide balance and promotes disease progression by enhancing caveolae-dependent lipid uptake and extracellular vesicle secretion from steatotic hepatocytes to exacerbate inflammation and fibrosis. Consequently, SMPD3 acts as a central hub integrating key MASH hallmarks. Notably, we discovered a bifunctional agent that simultaneously activates SIRT1 and inhibits SMPD3, which shows significant therapeutic potential in MASH treatment. These findings suggest that inhibition of hepatic SMPD3 restores membrane sphingolipid metabolism and holds great promise for developing novel MASH therapies.

Advanced Materials [IF=27.4]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-5913R | Calreticulin Rabbit pAb | IF、Flow-Cyt

bs-0295G-BF555 | Goat Anti-Rabbit IgG H&L, BF555 conjugated | IF、Flow-Cyt

bs-0295G-BF488 | Goat Anti-Rabbit IgG H&L, BF488 conjugated | IF、Flow-Cyt

作者單位：南方醫(yī)科大學(xué)

摘要：Immune checkpoint blockade (ICB) therapy has achieved remarkable benefits in the treatment of malignant tumors, but the clinical response rates are unsatisfied due to the low tumor immunogenicity and the abundant immunosuppressive cells. Herein, a plasma membrane targeted photodynamic nanoagonist (designated as PMTPN) is developed to potentiate ICB therapy by initiating tumor cell pyroptosis and depleting infiltrating B cells. PMTPN is composed of a rationally designed chimeric peptide sequence loaded with Bruton's tyrosine kinase inhibitor (Ibrutinib). Notably, PMTPN is capable of sequentially targeting tumor and tumor cell membrane to trigger immunogenic pyroptosis and cause overwhelming release of cytokines, promoting dendritic cells maturation, and cytotoxic T lymphocytes (CTLs) activation. Meanwhile, PMTPN can also deplete infiltrating B cells and reduce the secretion of interleukin-10 to decrease immunosuppressive regulatory T cells and enhance CTLs infiltration. Beneficially, the synergistic immune modulating characteristics of PMTPN potentiate ICB therapy to simultaneously eliminate primary and distant tumors. This study offers a promising strategy to elevate the immunotherapeutic response rate in consideration of the complex immunosuppressive factors.

Nature biomedical

engineering [IF=26.8]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-8660R | Silent protein UshA(0) Rabbit pAb | IF

作者單位：上海交通大學(xué)

摘要：The efficacy of bacteriophages in treating bacterial infections largely depends on the phages’ vitality, which is impaired when they are naturally released from their hosts, as well as by culture media, manufacturing processes and other insults. Here, by wrapping phage-invaded bacteria individually with a polymeric nanoscale coating to preserve the microenvironment on phage-induced bacterial lysis, we show that, compared with naturally released phages, which have severely degraded proteins in their tail, the vitality of phages isolated from polymer-coated bacteria is maintained. Such latent phages could also be better amplified, and they more efficiently bound and lysed bacteria when clearing bacterial biofilms. In mice with bacterially induced enteritis and associated arthritis, latent phages released from orally administered bacteria coated with a polymer that dissolves at neutral pH had higher bioavailability and led to substantially better therapeutic outcomes than the administration of uncoated phages.

Bioactive Materials [IF=18]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-1134R | RUNX2 Rabbit pAb | WB
bs-0195R | CD31 Rabbit pAb | IF

作者單位：中山大學(xué)

摘要：The divalent metal cations promote new bone formation through modulation of sensory and sympathetic nervous systems (SNS) activities. In addition, acetylcholine (Ach), as a chief neurotransmitter released by the parasympathetic nervous system (PNS), also affects bone remodeling, so it is of worth to investigate if the divalent cations influence PNS activity. Of note, these cations are key co-enzymes modulating glucose metabolism. Aerobic glycolysis rather than oxidative phosphorylation favors osteogenesis of mesenchymal stem cells (MSCs), so it is of interest to study the effects of these cations on glucose metabolic pathway. Prior to biological function assessment, the tolerance limits of the divalent metal cations (Mg²⁺, Zn²⁺, and Ca²⁺) and their combinations were profiled. In terms of direct effects, these divalent cations potentially enhanced migration and adhesion capability of MSCs through upregulating Tgf-β1 and Integrin-β1 levels. Interestingly, the divalent cations alone did not influence osteogenesis and aerobic glycolysis of undifferentiated MSCs. However, once the osteogenic differentiation of MSCs was initiated by neurotransmitters or osteogenic differentiation medium, the osteogenesis of MSCs could be significantly promoted by the divalent cations, which was accompanied by the improved aerobic glycolysis. In terms of indirect effects, the divalent cations significantly upregulated levels of sensory nerve derived CGRP, PNS produced choline acetyltransferase and type H vessels, while significantly tuned down sympathetic activity in the defect zone in rats, thereby contributing to significantly increased bone formation relative to the control group. Together, the divalent cations favor bone regeneration via modulation of sensory-autonomic nervous systems and promotion of aerobic glycolysis-driven osteogenesis of MSCs after osteogenic initiation by neurotransmitters.

Bioactive Materials [IF=18]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-23103R | Ki-67 Rabbit pAb | IHC

作者單位：武漢大學(xué)

摘要：Dental pulp stem cells (DPSCs) have demonstrated remarkable potential in enhancing peripheral nerve regeneration, though the precise mechanisms remain largely unknown. This study investigates how DPSCs alleviate Schwann cell pyroptosis and restore mitochondrial homeostasis through intercellular mitochondrial transfer. In a crab-eating macaque model, we first observed that DPSC-loaded nerve conduits significantly promoted long-term nerve regeneration, facilitating tissue proliferation and myelin recovery. We further established a rat facial nerve injury (FNI) model and found that DPSC treatment reduced pyroptosis and mitochondrial ROS production in Schwann cells. A pivotal mitochondrial protective mechanism, resembling the effects of a ROS-targeted inhibitor, involved the transfer of mitochondria from DPSCs to pyroptosis-induced Schwann cells via tunneling nanotubes, while blocking intercellular junctions or mitochondrial function diminished the therapeutic effects. TNFα secreted by pyroptosis-induced Schwann cells activated the NF-κB pathway in DPSCs, enhancing mitochondrial transfer and adaptive stress responses, thereby promoting mitochondrial protection against pyroptosis in Schwann cells, as reflected in the improved therapeutic efficacy of TNFα-preconditioned DPSCs in the FNI model. These findings unveil a mechanism through which DPSCs foster nerve regeneration via mitochondrial transfer, presenting a promising strategy for enhancing stem cell-based therapies for nerve injuries.

Nature Aging [IF=17]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

作者單位：德國(guó)呂貝克大學(xué)

摘要：Blood-borne factors are essential to maintain neuronal synaptic plasticity and cognitive resilience throughout life. One such factor is osteocalcin (OCN), a hormone produced by osteoblasts that influences multiple physiological processes, including hippocampal neuronal homeostasis. However, the mechanism through which this blood-borne factor communicates with neurons remains unclear. Here we show the importance of a core primary cilium (PC) protein–autophagy axis in mediating the effects of OCN. We found that the OCN receptor GPR158 is present at the PC of hippocampal neurons and mediates the regulation of autophagy machinery by OCN. During aging, autophagy and PC core proteins are reduced in neurons, and restoring their levels is sufficient to improve cognitive impairments in aged mice. Mechanistically, the induction of this axis by OCN is dependent on the PC-dependent cAMP response element-binding protein signaling pathway. Altogether, this study demonstrates that the PC–autophagy axis is a gateway to mediate communication between blood-borne factors and neurons, and it advances understanding of the mechanisms involved in age-related cognitive decline.

Nucleic Acids Research [IF=16.6]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-20430R | Semaphorin 5A Rabbit pAb | ChIP-seq、WB

作者單位：上海交通大學(xué)醫(yī)學(xué)院附屬仁濟(jì)醫(yī)院

摘要：Polycomb repressive complex 2 (PRC2) is responsible for depositing H3K27me3 and plays essential roles in gene silencing during development and cancer. Meanwhile, the nuclear exosome targeting (NEXT) complex facilitates the degradation of numerous noncoding RNAs in the nucleoplasm. Here we find that the functional deficiency of the NEXT complex leads to an overall decrease in H3K27me3 levels. Specifically, ZCCHC8 depletion results in significant upregulation of nascent long noncoding RNAs (lncRNAs) containing G-quadruplex (G4) and U-Rich motifs (G4/U-Rich lncRNAs). The G4 motif binds to EZH2, blocking the chromatin recruitment of PRC2, while the U-Rich motif is specifically recognized by the NEXT complex for RNA exosome-mediated degradation. In tumor tissues with high ZCCHC8 expression in clear cell renal cell carcinoma (ccRCC) and lung adenocarcinoma (LUAD) patients, the NEXT complex excessively degrades nascent G4/U-Rich lncRNAs. Consequently, PRC2 core subunits are released and recruited to neighboring genomic loci, resulting in increased H3K27me3 levels and downregulation of adjacent genes, including tumor suppressors like SEMA5A and ARID1A. Notably, the EZH2 inhibitor Tazemetostat (EPZ-6438) exhibits greater sensitivity in cells with higher ZCCHC8 expression. Altogether, our findings demonstrate a novel mechanism that the NEXT complex regulates H3K27me3 levels by degrading nascent G4/U-Rich lncRNAs in cancer cells.

ACS Nano [IF=15.8]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-1036R-PE | CD62L Rabbit pAb, PE conjugated | Flow-Cyt
bs-4916R-APC | CD44 Rabbit pAb, APC conjugated | Flow-Cyt

作者單位：中國(guó)科學(xué)院生物醫(yī)學(xué)與生物技術(shù)研究所

摘要：“Living therapeutic carriers" present a promising avenue for cancer research, but it is still challenging to achieve uniform and durable distribution of payloads throughout the solid tumor owing to the tumor microenvironment heterogeneity. Herein, a living drug sprinkle biohybrid (YB1–HCNs) was constructed by hitching acid/enzyme-triggered detachable nanoparticles (HCNs) backpack on the surface of metabolic oligosaccharide-engineered oncolytic bacteria YB1. Along with the process of tumor penetration by bacterial hypoxia navigation, YB1–HCNs responsively and continuously release HCNs, achieving a uniform distribution of loaded agents throughout the tumor. Upon successive irradiation of laser and ultrasound (US), the HCNs can separately generate type II and type I ROS for superior sono–photodynamic therapy (SPDT), which enables HCNs to synergize with YB1 for a satisfactory therapeutic effect in both superficial normoxic and deep hypoxic regions of the tumor. After a single dose, this efficient combination realized 98.3% primary tumor inhibition rate and prolonged survival of mice for 90 days with no recurrence, further inducing a powerful immunological memory effect to completely suppress tumor rechallenge in cured mice. Such a bacterial hybridization vector enables optimization of the spatial distribution of YB1 and HCNs, providing an innovative strategy to maximize therapeutic outcomes and evoke durable antitumor immunity.

ACS Nano [IF=15.8]

【25年2月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-6313R | 4 Hydroxynonenal Rabbit pAb | IF

作者單位：首都醫(yī)科大學(xué)附屬北京友誼醫(yī)院

摘要：Ferroptosis is a classic type of programmed cell death characterized by iron dependence, which is closely associated with many diseases such as cancer, intestinal ischemic diseases, and nervous system diseases. Transferrin (Tf) is responsible for ferric-ion delivery owing to its natural Fe³⁺ binding ability and plays a crucial role in ferroptosis. However, Tf is not considered as a classic druggable target for ferroptosis-associated diseases since systemic perturbation of Tf would dramatically disrupt blood iron homeostasis. Here, we reported a nonpharmaceutical, noninvasive, and Tf-targeted electromagnetic intervention technique capable of desensitizing ferroptosis with directivity. First, we revealed that the THz radiation had the ability to significantly decrease binding affinity between the Fe³⁺ and Tf via molecular dynamics simulations, and the modulation was strongly wavelength-dependent. This result provides theoretical feasibility for the THz modulation-based ferroptosis intervention. Subsequent extracellular and cellular chromogenic activity assays indicated that the THz field at 8.7 μm (i.e., 34.5 THz) inhibited the most Fe³⁺ bound to the Tf, and the wavelength was in good agreement with the simulated one. Then, functional assays demonstrated that levels of intracellular Fe²⁺, lipid peroxidation, malondialdehyde (MDA) and cell death were all significantly reduced in cells treated with this 34.5 THz wave. Furthermore, the iron deposition, lipid peroxidation, and MDA in the ferroptosis disease model induced by ischemia-reperfusion injury could be nearly eliminated by the same radiation, validating THz wave-induced desensitization of ferroptosis in vivo. Together, this work provides a preclinical exemplar for electromagnetic irradiation-stimulated desensitization of ferroptosis and predicts an innovative, THz wave-based therapeutic method for ferroptosis-associated diseases in the

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