歡迎來(lái)到北京博奧森生物技術(shù)有限公司網(wǎng)站！歡迎來(lái)到北京博奧森生物技術(shù)有限公司網(wǎng)站！
18611424007
截至目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共39,179篇，總影響因子200,3.07分，發(fā)表在Nature, Science, Cell, Cancer Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共140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)。
我們每月收集引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)。若您在當(dāng)月已發(fā)表SCI文章，但未被我公司收集，請(qǐng)致電Bioss，我們將贈(zèng)予現(xiàn)金鼓勵(lì)，金額標(biāo)準(zhǔn)請(qǐng)參考“發(fā)文章 領(lǐng)獎(jiǎng)金"活動(dòng)頁(yè)面。
Nature Immunology [IF=27.6]
文獻(xiàn)引用產(chǎn)品：
bs-5977R-Cy3 | c-Maf Rabbit pAb, Cy3 conjugated | IF
作者單位：四川大學(xué)華西醫(yī)院
摘要：Fibrosis is a severe pathological outcome of many chronic diseases, yet the therapeutic potential of targeting the altered major histocompatibility complex (MHC) class I immunopeptidome remains largely unexplored. Here we characterized the MHC class I immunopeptidomes from both fibrotic foci of human idiopathic pulmonary fibrosis lung explants and bleomycin-treated mice, identifying a diverse repertoire of fibrosis-associated peptides. Parallel profiling of bleomycin-induced pulmonary fibrosis in mice enabled the computational prioritization of therapeutic targets. In vivo, therapeutic vaccination with three candidate peptides (MAF116–124, APBB270–78 and TNS3119–127) effectively mitigated fibrosis progression in bleomycin-treated mice. Furthermore, leveraging its evolutionary conservation, we found that MAF116–124 elicited specific human cytotoxic T lymphocytes that lysed human idiopathic pulmonary fibrosis-derived myofibroblasts and M2-like macrophages. This study indicates that immunopeptidome profiling provides a robust platform for discovering translatable antifibrotic immunotherapies.
Nature Immunology [IF=27.6]
文獻(xiàn)引用產(chǎn)品：
bs-0294D-BF488 | Donkey Anti-Goat IgG H&L, BF488 conjugated | IF
bs-0295D-BF594 | Donkey Anti-Rabbit IgG H&L, BF594 conjugated | IF
作者單位：北京大學(xué)
摘要：Pathogen-associated molecules can have both membrane-associated and intracellular receptors. Bacterial lipoproteins are recognized by Toll-like receptor 2, but it is unclear whether they can also be sensed by cytoplasmic receptors. Here we found that bacterial lipoproteins could be recognized in the cytoplasm of macrophages by cystathionine γ-lyase (CTH) and hydrolyzed into lipid chains containing sulfhydryl groups. The hydrolyzed lipid chains form molecules containing four acylated chains linked through disulfide bonds, which further cleave caspase-11 and activate the noncanonical inflammasome. Changing the redox environment in macrophages affects their recognition of bacterial lipoproteins. CTH-deficient primary and immortalized macrophages do not trigger activation of the noncanonical inflammasome in the presence of intracellular bacterial lipoproteins, while CTH-deficient mice exhibit attenuated immune responses to infection with Staphylococcus aureus and Listeria monocytogenes. Our findings elucidate the molecular mechanisms by which macrophages recognize intracellular bacterial lipoproteins, as well as the regulatory relationship between cellular redox levels and infection resistance.
Immunity [IF=26.3]
文獻(xiàn)引用產(chǎn)品：
作者單位：瑞士洛桑大學(xué)
摘要：Compartmentalization of secondary lymphoid organs is orchestrated by specialized fibroblastic reticular cells (FRCs), which guide immune cell migration, interaction, and function. Here, we investigated the pathways driving FRC differentiation into functionally distinct subsets. A Notch signaling signature distinguished lymph node (LN) FRCs, and deletion of Notch1 and Notch2 in FRCs restricted functional specialization, particularly for T-zone FRCs (T-zone reticular cells [TRCs]). Dendritic cell (DC)-specific deletion of the Notch ligand Jagged-1 prevented Ccl19hi TRC differentiation, with homeostatic Ccr7+ DCs also being required for their maintenance. The resulting Ccl19 chemokine expression supported formation of central T-zone sub-compartments enriched in Xcr1+ DCs and CD8+ T cells. Both the spatial organization and Notch2-Jagged1 signaling activity were conserved in human LNs. Disrupting T-zone segregation via Notch2 inactivation in FRCs impaired the generation of CD8+ T cell memory precursors. Thus, Notch2-dependent TRC programming by DCs shapes distinct T-zone niches that sustain CD8+ T cell immunity.
Materials Today [IF=22]
文獻(xiàn)引用產(chǎn)品：
摘要：Invasive Aspergillus fumigatus infection poses a serious threat to immunocompromised individuals, characterized by high morbidity and mortality. Given the challenges of time-consuming diagnosis, limited therapeutic options, and the increasing emergence of drug resistance, there is an urgent need to develop novel and effective preventive strategies. Circular RNA (CircRNA) vaccines represent an emerging vaccine platform that exhibits high stability in vivo, enables sustained antigen expression, and can elicit robust and durable immune responses. Consequently, they hold considerable potential for the prevention of infectious diseases. In this study, we designed and constructed two circRNA vaccines, each encoding a fusion antigen derived from non-transmembrane regions of the iron ion permease FtrA located in the cell membrane of A. fumigatus. The circRNA vaccines were prepared using a group I intron-based cis-acting ribozyme system (CARS) and delivered via lipid nanoparticles (LNPs) in a murine model. The results revealed that the circRNAFtrA2 vaccine could effectively induce both cellular and humoral immune responses. Following challenge with A. fumigatus, vaccinated mice, particularly those receiving circRNAFtrA2, exhibited a significant reduction in fungal burden in the lungs compared with the unvaccinated controls. Furthermore, lung pathology was markedly alleviated, and survival rate was notably improved. Collectively, these findings highlight a promising and innovative vaccine for combating invasive A. fumigatus infection.
Cell Stem Cell [IF=20.4]
文獻(xiàn)引用產(chǎn)品：
bs-0924D-BF647 | Donkey Anti-Goat IgG H&L, BF647 conjugated | Other
摘要：The clinical application of human stem cell-derived islet organoids (SC-islets) is hindered by immaturity and ischemia-induced dysfunction post-transplantation. Hypoxia-driven angiogenesis is a common adaptation, but the metabolic fragility of SC-islet β cells leads to early functional damage and suppressed vascular endothelial growth factor A (VEGFA) expression, thereby delaying vascularization and causing graft loss. The key challenge in SC-islet transplantation is how to prevent hypoxia-induced stress and promote rapid angiogenesis. We found that excessive zinc in SC-islet β cells induces oxidative modification that inhibits AMP-activated protein kinase (AMPK) activity. Chemical inhibition of zinc transportation activates AMPK, enhances functional maturation, improves hypoxia resistance, and increases hypoxia-inducible factor 1α (HIF1A)-independent VEGFA expression to facilitate endothelial cell integration. In diabetic animal models, this approach significantly improved hypoxia resistance, accelerated angiogenesis, and enhanced glycemic control. Our findings demonstrate that chemical inhibition of zinc transportation boosts SC-islet functional competence, offering a potential strategy to advance pre-adaptation to stress in regenerative medicine.
文獻(xiàn)引用產(chǎn)品：
bs-20160R | NFKB p65 Rabbit pAb | IF, WB
bs-1287R | IKB alpha Rabbit pAb | WB
bs-3614R | PPAR alpha Rabbit pAb | WB
作者單位：西南交通大學(xué)
Cellular & Molecular
Immunology [IF=19.8]
文獻(xiàn)引用產(chǎn)品：
作者單位：中山大學(xué)第一附屬醫(yī)院
摘要：Keratinocytes are increasingly recognized as central regulators of cutaneous immune responses and key contributors to maintaining immune homeostasis. However, whether and how epidermal stem and progenitor cells (EPSCs) actively suppress proinflammatory signaling pathways to prevent excessive inflammation and maintain epidermal immune quiescence remains unclear. Here, we generated a conditional knockout mouse model (K14-CreERT; Supt6fl/fl) to investigate the role of SPT6, a transcription elongation factor, in epidermal and immune homeostasis. Loss of SPT6 in basal keratinocytes led to spontaneous, psoriasis-like skin inflammation, characterized by epidermal hyperplasia, immune cell infiltration, parakeratosis, and hyperkeratosis. SPT6-deficient mice also exhibited significantly delayed wound healing accompanied by impaired Wnt signaling. Moreover, single-cell RNA sequencing revealed distinct keratinocyte subpopulations with inflammatory signatures, elevated NF-κB signaling, and suppressed Wnt signaling. Mechanistically, SPT6 suppresses NF-κB signaling by binding to an enhancer of the RELA gene and preventing its positive transcriptional feedback loop. These findings support a new paradigm in which the default state of the skin may be primed for inflammation, and active suppression by factors such as SPT6 is required to maintain epidermal homeostasis. Taken together, the results of our study reveal a previously unrecognized role for SPT6 as a key regulator of epidermal immune quiescence and tissue integrity.
Nature Aging [IF=19.4]
文獻(xiàn)引用產(chǎn)品：
作者單位：福建醫(yī)科大學(xué)附屬協(xié)和醫(yī)院
摘要：Malignant tumors are the leading cause of death in individuals over 65 years old, with metastasis as the primary driver. Emerging evidence suggests that age-related metabolic changes and secreted factors increase the risk of metastasis, but the underlying mechanisms remain unclear. Here we demonstrate in mice that extracellular vesicles (EVs) from senescent hepatocytes promote metastasis across tumor types. We show that aged liver tissue exhibits elevated expression of P2X purinoceptor 7 (P2RX7), which is associated with increased EV biogenesis. We identify EV-encapsulated miRNAs (miR-25, miR-92a, miR-30c and miR-30d) that reach primary tumors through the circulation and enhance tumor invasiveness and metastatic potential. Similarly, clinical samples from older patients show reduced expression of the miRNA target genes PTEN and LATS2, as well as enhanced epithelial–mesenchymal transition in metastatic tumors. Therapeutically, targeting senescence with dasatinib and quercetin (D?+?Q), inhibiting P2RX7, or silencing EV-associated miRNAs considerably reduces metastasis in aged mice. Together, our study uncovers a mechanism by which senescent hepatocyte-derived EVs drive tumor metastasis during aging and highlights potential strategies to mitigate this process.
Advanced Functional
Materials [IF=19]
文獻(xiàn)引用產(chǎn)品：
作者單位：韓國(guó)首爾延世大學(xué)
摘要：Extracellular matrix (ECM) of the heart exhibits highly organized anisotropy, which is essential for directing cellular alignment, force transmission, and tissue function. However, mechanistic pathways linking ECM alignment to nuclear and epigenetic remodeling remain poorly defined, especially in the context of direct cardiac reprogramming. Here, a 3D anisotropically aligned decellularized heart ECM (HEM) is engineered to investigate how structural and biochemical cues modulate maturation of chemically induced cardiomyocyte-like cells (CiCMs). The alignment of HEM enhances cytoskeletal organization and perinuclear actin assembly, leading to nuclear elongation and intermembrane redistribution of emerin from the inner to the outer nuclear membrane. These changes are accompanied by upregulation of SUN1/2, key components of the LINC complex, and by a transient increase in nuclear YAP/TAZ localization. Chromatin condensation is reduced under aligned conditions, with corresponding increases in H3K4me3 and decreases in H3K9me3, indicative of a more transcriptionally permissive chromatin state. Functionally, CiCMs in aligned HEM exhibit improved sarcomere structure and t-tubule development, enhanced responsiveness to β-adrenergic and muscarinic stimulation, and increased contractile force under electrical pacing. These findings reveal a mechanotransductive cascade linking cardiac ECM alignment to nuclear and chromatin remodeling, ultimately promoting functional maturation of reprogrammed cardiomyocytes in a biomimetic 3D microenvironment.
網(wǎng)站首頁(yè)
