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截至目前，引用Bioss產品發表的文獻共38,472篇，總影響因子196,162.07分，發表在Nature, Science, Cell, Cancer Cell以及Immunity等頂級期刊的文獻共134篇，合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等上百所國際研究機構。
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本文主要分享8篇IF≥19的文獻，它們引用了Bioss產品，分別發表在Signal Transduction and Targeted Therapy、Nature、Cell、iMeta、Materials Today、Drug Resistance Updates、Bioactive Materials、Nature Microbiology期刊上，讓我們一起學習吧。
Signal Transduction and
Targeted Therapy [IF=52.7]
文獻引用產品：
bs-10966R | Actin Rabbit pAb | WB
作者單位：四川大學華西醫院
摘要：The catabolism of glutamine is essential for living organisms, so that its first step, driven by glutaminase 1 (GLS1), generally referred to as glutaminolysis, plays important roles in physiological metabolism. However, the status and impact of glutaminolysis in pathological contexts such as aging and age-related diseases remain elusive. In this study, through metabolomics analysis and different aging models, we verified the hyperactivation status of glutaminolysis in senescent cells and aged Drosophila and mice, which we term “hyperglutaminolysis". We further confirmed the aging-promoting role of this hyperglutaminolysis by addition and removal intervention experiments. Intriguingly, a novel signaling axis connecting to senescence-associated persistent mTORC1 activation was found. This pathway begins with glutaminase-catalyzed production of ammonium and glutamate, which drives arginine biosynthesis and is subsequently sensed by CASTOR1, leading to persistent mTORC1 activation. The regulatory roles of two key enzymes within this cascade, GLS1 and argininosuccinate lyase (ASL), were specifically investigated and verified by cellular and in vivo experiments, including those using stress-promoted and naturally aged animals, combined with GLS1 and ASL knockdown, and multiple rounds of metabolite analysis. In conclusion, our work positions dysregulated glutaminolysis as a key driver of aging and delineates a previously unrecognized molecular cascade that directly links glutaminolysis, arginine biosynthesis, and mTORC1 activation. These findings significantly expand our understanding of the relationship between glutamine catabolism and aging and are valuable for identifying novel intervention targets aimed at mitigating aging-related processes.
Nature [IF=48.5]
文獻引用產品：
bs-20213R | OMPC Rabbit pAb | WB
作者單位：麻省理工學院
摘要：From mammals to bacteria, the direct recognition and cleavage of viral nucleic acids is a potent defence strategy against viral infection, but it requires mechanisms for distinguishing self from non-self In bacteria, CRISPR–Cas and restriction-modification systems achieve this discrimination by recognizing specific DNA sequences or DNA modifications, respectively. Alternative mechanisms probably remain to be discovered. Here, we characterize SNIPE, an anti-bacteriophage defence system that constitutively localizes to the bacterial cell membrane in Escherichia coli to block phage λ infection. Using radiolabelled phage DNA and time-lapse microscopy to track phage genomes, we demonstrate that SNIPE directly cleaves phage DNA during genome injection. Based on proximity labelling, we find that SNIPE associates with host proteins essential for λ genome entry and with the λ tape measure protein, which facilitates λ genome injection across the inner membrane. SNIPE also defends against diverse siphoviruses, probably through direct interactions with their tape measure proteins. Our findings establish SNIPE as a widespread bacterial defence system that exploits the spatial organization of phage genome injection to specifically target viral DNA, representing a previously unknown strategy for distinguishing self from non-self in prokaryotic immune systems.
Cell [IF=42.5]
文獻引用產品：
作者單位：復旦大學附屬腫瘤醫院
摘要：Innervation is critical in tumor progression. However, the involvement of sensory neurons in the ecosystem of triple-negative breast cancer (TNBC) remains poorly elucidated. Here, we decipher that sensory neurons, the dominant neuron type in the TNBC ecosystem, drive the immune-excluded tumor microenvironment (TME) by stimulating a dense extracellular matrix. Mechanistically, a high concentration of nerve growth factor (NGF) in TME triggers sensory neurons to secrete the neuropeptide calcitonin gene-related peptide (CGRP), thereby activating cancer-associated fibroblasts (CAFs) to secrete collagen. Specifically, CGRP binds to its receptor RAMP1 (receptor activity modifying protein 1), which is expressed mainly on CAFs, and subsequently activates cyclic AMP (cAMP)/protein kinase A (PKA)/cAMP-response element binding protein 1 (CREB1) signaling to increase collagen deposition. Clinically, targeting sensory neurons remodels the disordered TME and synergizes with anti-programmed cell death protein 1 (PD-1) immunotherapy in TNBC. Collectively, our findings reveal a connection between sensory neurons and CAFs that obstructs antitumor immunity in TNBC. The CGRP antagonist rimegepant thus has clinical translational potential as an immuno-sensitizer to augment tumor immunotherapy.
iMeta [IF=33.2]
文獻引用產品：
摘要：The early discovery of covalent drugs is frequently inspired by, or derived from, natural sources, with such compounds often showing favorable safety profiles and a comparatively lower risk of clinical failure. However, a straightforward, high-throughput technique for screening covalent-binding molecules directly from complex medicinal plant extracts remains unavailable. In this study, we introduce an integrated strategy that combines protein microarrays with bioorthogonal click chemistry (Ccc-Chip). This platform includes a differential scanning fluorimetry (DSF)-based pre-screening step to enhance efficiency, with the Ccc-Chip serving as the core confirmation tool. It provides simple and intuitive readouts, enabling synchronous, high-throughput screening of covalent ligands targeting multiple proteins through detection of their competitive binding with cysteine-reactive probes. To validate the approach, we constructed a mutant isocitrate dehydrogenase 1 (mIDH1) protein microarray and used the integrated workflow to screen 110 medicinal plants. Our results led to the identification of flavokawain C (Flc), a covalent inhibitor of mIDH1, from Piper methysticum Forst. Subsequent in vivo experiments showed that Flc significantly reduced 2-hydroxyglutarate (2-HG) levels in an mIDH1-driven orthotopic tumor model and enhanced CD8+ T cell activity. Notably, when combined with a programmed cell death protein 1 (PD-1) blocking antibody, Flc synergistically augmented antitumor immunity, resulting in suppressed tumor growth. This work not only supports the high-throughput utility of the Ccc-Chip strategy but also provides a practical framework for combining bioorthogonal labeling with protein microarray technology, facilitating the discovery of bioactive covalent molecules from plant sources for challenging therapeutic targets.
Materials Today [IF=22]
文獻引用產品：
摘要：The regimen of combining anthracyclines with immune checkpoint inhibitors (ICIs) has been recommended for the treatment of triple-negative breast cancer (TNBC), but the clinical outcomes fall short of estimates. Our analysis of clinical patient samples reveals that this is highly correlated with hypoxia-related immune resistance. To achieve an integrated immunosuppression relief, we elaborately exploit an oxygen-carrying nanomodulator co-assembled by a redox-responsive fluorinated prodrug (DSSF) of doxorubicin (DOX) and a PD-L1 inhibitor (JQ1). The fluorinated DOX prodrug not only confers stable co-assembly with JQ1, but also endows the nanomodulator with outstanding oxygen-carrying capacity (~80 mg L-1). Moreover, redox-responsive prodrug activation in tumor cells triggers synchronous release of JQ1 to downregulate the PD-L1 on tumor cells. As expected, the nanomodulator significantly alleviates hypoxia and relieves immunosuppression, displaying striking effects in immunogenic chemotherapy, tumor recurrence and metastasis prevention against TNBC. This study offers a facile and feasible solution to potentiate chemo-immunotherapy of TNBC.
Drug Resistance
Updates [IF=21.7]
文獻引用產品：
bs-7510R | stabilin1 Rabbit pAb | WB
bs-2386R | CD47 Rabbit pAb | WB
作者單位：同濟大學醫學院腫瘤研究所
Lipid-associated macrophages are a specific subpopulation of macrophages that play a crucial role in cancer progression and treatment resistance. However, the functional impact of lipid-associated macrophages in lung adenocarcinoma (LUAD) remains poorly understood. This study aims to investigate the role and underlying mechanisms of lipid-associated macrophages in LUAD liver metastasis and resistance to osimertinib, a third-generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI).
Single-cell RNA sequencing (scRNA-seq) was performed on human lung tumor tissues from patients with primary LUAD and those with LUAD liver metastasis, which identified a novel subpopulation of stabilin-1 (STAB1)+ lipid-associated macrophages. The influence of STAB1+ lipid-associated macrophages on LUAD liver metastasis and osimertinib resistance was evaluated in vitro and in vivo. An in vitro co-culture system was established to investigate the interaction between LUAD cells and lipid-associated macrophages, and the mechanisms were analyzed by RNA-seq, Luminex multi-factor detection, Co-IP, in vivo, and rescue experiments.
The subpopulation of STAB1+ lipid-associated macrophages was more abundant in liver metastatic LUAD tumors than in primary tumors. This lipid-associated macrophage subpopulation exhibited a stronger ability of lipid uptake from tumors and lipid droplet accumulation. We found that C-X-C motif ligand 12 (CXCL12) chemokine secreted by liver metastatic LUAD cells was responsible for recruiting circulating monocytes and subsequently inducing their differentiation into STAB1+ lipid-associated macrophages. STAB1 overexpression impaired the phagocytic ability of macrophage towards dying tumor cells by upregulating the signal regulatory protein α (SIRPα)-CD47 “don’t eat me" signal. In tumor xenograft models, inhibition of STAB1+ lipid-associated macrophages effectively suppressed LUAD osimertinib resistance and liver metastasis....
Bioactive Materials [IF=20.3]
文獻引用產品：
作者單位：四川大學華西口腔醫院
摘要：Enhancing the cellular infiltration and mineralization capacity of bone scaffolds can effectively address the challenges of bone nonunion and the prolonged osteogenic repair cycle, particularly in the treatment of critical-sized bone defects. Conventional bone scaffolds, whether composed of inorganic materials or fabricated via 3D-printed titanium alloy, frequently hinder seamless cellular integration due to inherent structural discontinuities, such as granular interfaces or layer-by-layer striations. Here, we address this limitation by employing graphene, not merely as a filler, but as a continuous surface modifier within a 3D scaffold. Through an in-situ reduction-induced phase separation technique, we engineered a long-range, frost-like graphene surface at a low graphene concentration of 3.4 wt% in fabricated scaffold. The resulted unique architecture establishes a continuous pathway for cell migration, leading to significantly enhanced cellular adhesion, accelerated infiltration, rapid calcium deposition and bone ingrowth. We demonstrate that these pro-osteogenic effects are mediated through the modulation of genetic pathways related to ion channels and cell-extracellular matrix interactions. Furthermore, the scaffolds show excellent biocompatibility, integrating seamlessly into nascent bone tissue without eliciting inflammation or immune rejection. Thus, this strategy of constructing continuous cell-migration surfaces presents a promising and scalable platform for the regeneration of critical-sized bone defects.
Nature Micribiology [IF=19.4]
文獻引用產品：
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：中南大學湘雅醫學院
摘要：Intestinal motility is a function of the enteric nervous system involving secretion of the excitatory neurotransmitter acetylcholine (ACh). Although gut commensal bacteria are key regulators of intestinal physiology, the molecular mechanisms underlying microbial influence on intestinal peristalsis and constipation remain unclear. Here we report a link between microbial nitrogen metabolism and intestinal motility regulation via ammonia production. We observed compensatory elevation of intestinal ammonia levels and urease activity in mouse models of intestinal dysmotility, induced by ACh deficiency, and in patients with constipation. Ammonia supplementation or intervention in mice with the urease-positive Lysinibacillus fusiformis isolated from patient stool, or engineered urease-expressing bacteria, effectively restored colonic ACh levels. In vitro, ammonia upregulated the expression of voltage-gated calcium channels on enteric neurons, driving Ca2+ influx to potentiate ACh secretion. Our study reveals a microbial compensatory mechanism that responds to fluctuating ACh levels in the intestine and provides microbial targets for intestinal motility disorders.
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