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截至目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共36,126篇，總影響因子180,595.91分，發(fā)表在Nature, Science, Cell, Cancer Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共129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≥15的文獻(xiàn)，它們引用了Bioss產(chǎn)品，分別發(fā)表在CELL、Cell Metabolism、Cell Stem Cell、Bioactive Materials、Molecular Neurodegeneration、Cancer Research、Nature Communications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：
C05-02001 | BCA Protein Assay Kit | Other
作者單位：內(nèi)蒙古大學(xué)
摘要：The liver undergoes metabolic adaptations during gestation and lactation to meet evolving physiological demands, yet the precise processes, regulatory mechanisms, and functions remain unclear. Using high-resolution single-cell RNA sequencing, we systematically characterized hepatocyte adaptations in mice across pregnancy and postpartum stages. We discovered a cyclical hepatocyte trajectory (“pregnancy clock") that governs metabolic changes during gestation and postpartum recovery, reverting to pregestational states in non-lactating mice. Lactation induced a distinct branching trajectory characterized by elevated lipid synthesis and export. Deletion of glycoprotein 130 (gp130) disrupted hepatic adaptations during pregnancy, impairing fetal growth, whereas acetyl-coenzyme A (CoA) synthetase 2 (ACSS2) deficiency postpartum impaired hepatic lipid biosynthesis and export, reducing milk lipid content and compromising offspring development. Comparative analysis with sheep highlighted conserved hepatic metabolic adaptation pathways despite genetic divergence between species. These insights clarify hepatocyte plasticity during pregnancy and lactation, identifying potential therapeutic targets to optimize maternal-fetal health and lactation performance, with implications for reproductive biology and livestock management.
Cell Metabolism [IF=30.9]
文獻(xiàn)引用產(chǎn)品：
bs-12679R-PE | CD112 Rabbit pAb, PE conjugated | mIHC, FC
作者單位：上海交通大學(xué)醫(yī)學(xué)院附屬瑞金醫(yī)院
摘要：Diabetes mellitus (DM) is a known risk factor for pancreatic cancer, but the underlying mechanisms remain elusive. Here, we identify lactate-driven remodeling of tumor-associated Schwann cells (TASCs) as a key mediator of immunosuppression in diabetic pancreatic ductal adenocarcinoma (PDAC). Single-cell RNA sequencing revealed a c1-Mettl16+Cd276+Nectin2+ TASC subpopulation enriched in diabetic tumors that impairs CD8+ T cell function and promotes PD-1 resistance. Mechanistically, lactate enters TASCs via MCT1/MCT4, binds METTL16, and induces K269 lactylation, enhancing m6A-dependent CTCF stabilization and transcriptional activation of immunosuppressive ligands. Targeting METTL16 restores immune surveillance and sensitizes tumors to PD-1 blockade. Retrospective analyses confirmed therapeutic benefit in patients with diabetic PDAC receiving rosuvastatin. These findings uncover a lactate-METTL16-CTCF axis that links metabolic stress to epitranscriptomic reprogramming and immune evasion, offering a promising strategy to potentiate immunotherapy in metabolically dysregulated PDAC.
Cell Stem Cell [IF=20.4]
文獻(xiàn)引用產(chǎn)品：
作者單位：美國(guó)斯坦福大學(xué)
摘要：Skin fibrosis is driven by fibroblast activation and excessive extracellular matrix deposition. To ascertain the fibroblast subpopulation(s) responsible for instigating fibrosis, we employed an established murine bleomycin skin fibrosis model. We characterized both the fibrotic and remodeling phases of dermal fibrosis through a multi-omic approach. Using an unsupervised machine learning algorithm that quantifies 294 fiber features, we identified precise time points of fibrosis and regeneration. Single-cell transcriptomic and epigenomic sequencing then identified a Cyp26b1-expressing fibroblast subpopulation responsible for dermal fibrosis. The same fibroblast subtype was mapped to Visium spatial transcriptomic data. We further mapped the fibrotic subtypes to protein spatial data. To ascertain the functional impact of the fibroblast subpopulations, transplant delivery analysis showed their ability to drive skin fibrosis. Lastly, we identified a small molecular inhibitor of Cyp26b1 (talarozole) that prevents and rescues dermal fibrosis. Conclusively, we establish an atlas of the fibrotic and regenerative biological drivers of skin fibrosis.
Bioactive Materials [IF=20.3]
文獻(xiàn)引用產(chǎn)品：
摘要：Monomodal therapies often fail to eradicate tumors due to the complexity of tumorigenesis and microenvironmental resistance. Electrodynamic therapy (EDT) and cuproptosis as emerging antitumor therapies have attracted widespread attention and become the promising strategies for tumor treatment due to their unique advantages. Here, we first time present a light-cured millineedle as a tool for co-delivering a nano-pomegranate (N-PG) platform and Cu2+ by integrating EDT and cuproptosis induction for combined oral cancer treatment. This platform N-PG/NSC consists of Pt-doped dendritic mesoporous large silica nanoparticles (Pt@DLMSN) loaded copper ionophore NSC319726, enabling dual therapeutic actions: (1) N-PG/NSC-based EDT-driven generation of hydroxyl radicals (•OH) via H2O decomposition under electric fields, circumventing hypoxia-related resistance, and (2) NSC imported Cu2+-mediated cuproptosis through mitochondrial dysfunction induced by DLAT oligomerization and Fe-S cluster protein depletion. The millineedle ensures precise and weak-leakage intratumoral delivery, while simultaneously triggering immunogenic cell death (ICD) to prime antitumor immunity. When combined with the TLR7/8 agonist R848, the platform elicits systemic immune activation, effectively suppressing both primary and abscopal oral tumors. As the first reported integration of MN-assisted drug delivery, hypoxia-tolerant EDT, and cuproptosis, this work establishes a translatable paradigm for multimodal cancer therapy, merging localized cytotoxicity with immune reprogramming for enhanced clinical outcomes.
Molecular Neurodegeneration
[IF=17.5]
文獻(xiàn)引用產(chǎn)品：
摘要：To define how Aβ pathology alters microglia function in Alzheimer’s disease, we profiled the microglia surfaceome following treatment with Aβ fibrils. Our findings reveal that Aβ-associated human microglia upregulate Glypican 4 (GPC4), a GPI-anchored heparan sulfate proteoglycan (HSPG). Glial GPC4 expression exacerbates motor deficits and reduces lifespan in a Drosophila amyloidosis model, implicating GPC4 in a toxic neurodegenerative program. In cell culture, GPC4 enhances microglia phagocytosis of tau aggregates, and shed GPC4 can act in trans to facilitate tau aggregate uptake and seeding in neurons. Additionally, our data demonstrate that GPC4-mediated effects are amplified in the presence of APOE. In human Alzheimer’s disease brain, microglial GPC4 expression surrounding Aβ plaques correlates with neuritic tau pathology, supporting a pathological link between amyloid, GPC4, and tau. These studies define a mechanistic pathway by which Aβ primes microglia to promote tau pathology via HSPGs and APOE.
Cancer Research [IF=16.6]
文獻(xiàn)引用產(chǎn)品：
bs-6235R | NRG3 Rabbit pAb | IF
作者單位：美國(guó)西奈山伊坎醫(yī)學(xué)院
摘要：Despite genomic heterogeneity, most high-grade gliomas (HGG), including IDH-wildtype glioblastoma, display diffusely infiltrative growth, which impedes complete surgical resection and leads to inevitable recurrence. Understanding of HGG biology comes predominantly from studies using resected “core" tissue. Paradoxically, chemoradiation targets residual disease at the resection margin, which remains poorly defined. To address this, we generated a high-throughput single-nucleus (sn)RNA-seq and snATAC-seq multi-omic dataset from matching “core" and “margin" dissections in four distinct grade 4 HGG (EGFR-amplified, NF1-mutant, FGFR3-TACC3 fused, IDH1-mutant; n= 36,811 snRNA-seq and 30,705 snATAC-seq nuclei after filtering) and combined it with new spatial transcriptomics data from two additional HGG (EGFR-amplified, CDK4-amplifed) to evaluate “core-to-margin" transition. Computational analyses included functional enrichment, comparison to prior HGG datasets, differential analyses in core vs. margin cell types or regions-of-interest for genes, chromatin accessibility peaks, cell-cell interactions, transcription factor motif activity and associated regulon targets, and reconstruction of core-to-margin transition using RNA velocity and pseudotime. Contrasting tumor-specific biology in matching core and margin dissections defined a unique, shared “glioma infiltration" signature near the margin. EGFR was prioritized as a top differentially expressed and accessible tumor margin marker across HGG subtypes that showed dynamic expression along a core-to-margin infiltration trajectory. CRISPR/Cas9-mediated deletion of EGFR in two patient-derived models validated its role in migration, and combined snATAC-seq with ChIP-seq studies suggested a role for TEAD1 as a transcriptional regulator of EGFR at the margin. This multi-omic resource will enable further studies into residual disease biology of tumors and the microenvironment at the infiltrative margin.
Nature Communications
[IF=15.7]
文獻(xiàn)引用產(chǎn)品：
V1103 | D-Dimer Mouse mAb | ELISA
V1104 | D-Dimer Mouse mAb | ELISA
作者單位：日本三重大學(xué)
摘要：The increasing global prevalence of diabetic nephropathy poses substantial health and economic burdens. Currently, effective anti-fibrotic therapies for managing kidney fibrosis associated with chronic kidney disease are lacking. This study reveals corisin, a microbiota-derived peptide, as a central driver in the progression of diabetic kidney fibrosis. Corisin levels were found to be markedly elevated in the serum of diabetic chronic kidney disease patients relative to healthy controls, with strong correlations to advanced disease stages and declining renal function. In a murine model of kidney fibrosis, corisin levels were similarly heightened, directly contributing to increased inflammation and worsening fibrosis and renal impairment. Notably, the use of a monoclonal anti-corisin antibody significantly reduced nephropathy severity in diabetic mice. Through molecular dynamics simulations and experimental validation, we demonstrated that corisin interacts with human serum albumin, potentially enhancing its renal accumulation and pathological impact. The pathogenic mechanism of corisin involves the acceleration of cellular senescence and the induction of epithelial-mesenchymal transition and apoptosis in kidney cells. These findings underscore the critical role of corisin in progressive diabetic nephropathy and suggest a promising new target for therapeutic intervention.
Nature Communications
[IF=15.7]
文獻(xiàn)引用產(chǎn)品：
作者單位：中山大學(xué)孫逸仙紀(jì)念醫(yī)院
摘要：Diabetic foot ulcers are severe diabetic complications, and promoting impaired angiogenesis is essential for wound healing. Pro-angiogenic galectin-3 is elevated in diabetic serum and promotes systemic insulin resistance that may impair wound healing. However, the exact role of galectin-3 in the regulation of diabetic wound healing remains unclear. Here, we demonstrate that galectin-3 promotes skin wound healing and angiogenesis via binding to its receptor integrin α5β1, and enhances downstream focal adhesion kinase phosphorylation by forming a liquid-liquid phase separation with integrin α5β1. Under diabetic conditions, aberrant accumulated advanced glycation end-products bind to galectin-3, blocking its interaction with integrin α5β1 and impairing angiogenesis. Topical treatment of recombinant galectin-3 in hydrogels promotes diabetic wound healing in rodents without causing systemic insulin resistance and synergizes with insulin. This study clarifies the binding of galectin-3 to integrin α5β1, instead of advanced glycation end-products, forming phase separation to promote angiogenesis and diabetic wound healing, laying the foundation for local galectin-3 therapy to treat diabetic foot ulcers.
Nature Communications
[IF=15.7]
文獻(xiàn)引用產(chǎn)品：
作者單位：中山大學(xué)腫瘤防治中心
摘要：Heat nociception involves thermosensors like transient receptor potential channel V1 in dorsal root ganglion (DRG) neurons, but their loss only partially impairs heat sensing, suggesting other mechanisms. Autism frequently involves abnormal pain perception, but its mechanisms remain unclear. Here we show that dedicator of cytokinesis 4 (Dock4), an autism susceptibility gene, is decreased in DRG neurons across multiple pain models via histone H4K8 lactylation. DOCK4 deficiency in sensory neurons increases heat nociception in mice. Mechanistically, DOCK4 interacts with sodium channel Nav1.7 and mediates its trafficking from the membrane to the cytoplasm in DRG neurons. Acting an adaptor protein, DOCK4 binds the motor protein Dynein to form a Dynein/DOCK4/Nav1.7 complex, where Dynein provides the mechanical force for Nav1.7 trafficking. DOCK4 knockdown in sensory neurons also enhances heat nociception in male nonhuman primates. Thus, the Dynein/DOCK4/Nav1.7 complex represents a thermosensor-independent mechanism regulating heat nociception and provides insights into abnormal pain in autism.
Nature Communications
[IF=15.7]
文獻(xiàn)引用產(chǎn)品：
作者單位：暨南大學(xué)第一附屬醫(yī)院
摘要：Clear elucidation of the connection between chemical structure and biological action mechanisms is the key issue preventing the successful development of nanomedicines. Herein, employing essential trace element selenium (Se) as an example, we fabricate organic-inorganic covalent Se hybrid by anchoring Se atom to polyethylene glycol chain during carbonization to form organic Se-C and inorganic Se-Se bonds in one system to integrate the advantages of both species. The weak covalent Se-Se bond breaks down in response to redox stimuli, thus releases organic Se with stronger electron transfer ability to scavenge free radicals, and forms highly active inorganic Se, which further releases free Se atom to trigger selenoprotein synthesis and activation, ultimately reverses reperfusion injury in male-mice ischemic stroke, and improves neurological restoration. This work provides a unique Se atom reprogramming strategy to design highly bioactive hybrid Se species with clear chemical nature and action mechanisms.
Nature Communications
[IF=15.7]
文獻(xiàn)引用產(chǎn)品：
作者單位：沈陽(yáng)藥科大學(xué)
摘要：Ligand-targeted nanomedicines provide precise delivery, enhance drug accumulation, and reduce side effects, but their clinical translation is hindered by challenges like protein corona formation, which can mask targeting ligands and impair functionality, and complex manufacturing processes. Here we develop galloylated liposomes (GA-lipo) by incorporating gallic acid-modified lipids into lipid bilayers, enabling the stable and controlled adsorption of targeting ligands through non-covalent physical interactions. This approach preserves ligand orientation and functionality, ensuring that binding sites remain exposed even in the presence of a protein corona. As a proof of concept, a weakly basic derivative of DXd (DXdd) is remotely loaded into liposomes, followed by trastuzumab adsorption, achieving 95% encapsulation efficiency for DXdd in 100?nm liposomes (with each trastuzumab molecule delivering approximately 580 DXdd molecules). These trastuzumab-functionalized immunoliposomes exhibit improved tumor inhibition in an SKOV3 tumor model, demonstrating the potential of GA-lipo as a simple and effective approach for constructing targeted nanomedicine delivery systems. This method overcomes key challenges in targeted drug delivery technologies, providing a scalable solution with broad clinical applicability.
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