【25年4月文獻(xiàn)戰(zhàn)報】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

更新時間：2025-05-29 | 點擊率：105

截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共34362篇，總影響因子169875.41分，發(fā)表在Nature, Science, Cell以及Immunity等頂刊的文獻(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，請致電Bioss，我們將贈予現(xiàn)金鼓勵，金額標(biāo)準(zhǔn)請參考“發(fā)文章領(lǐng)獎金"活動頁面。

【25年4月文獻(xiàn)戰(zhàn)報】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, Nature Immunology, Cell Metabolism, Advanced Materials, Immunity, Bioactive Materials, ACS Nano等期刊的10篇IF＞15的文獻(xiàn)摘要，讓我們一起欣賞吧。

CELL [IF=45.6]

文獻(xiàn)引用產(chǎn)品：

bs-5870R | KLK6 Rabbit pAb | Other

bs-1000R | CNPase Rabbit pAb | Other

作者單位：波士頓兒童醫(yī)院

摘要：Characterizing somatic mutations in the brain is important for disentangling the complex mechanisms of aging, yet little is known about mutational patterns in different brain cell types. Here, we performed whole-genome sequencing (WGS) of 86 single oligodendrocytes, 20 mixed glia, and 56 single neurons from neurotypical individuals spanning 0.4–104 years of age and identified >92,000 somatic single-nucleotide variants (sSNVs) and small insertions/deletions (indels). Although both cell types accumulate somatic mutations linearly with age, oligodendrocytes accumulated sSNVs 81% faster than neurons and indels 28% slower than neurons. Correlation of mutations with single-nucleus RNA profiles and chromatin accessibility from the same brains revealed that oligodendrocyte mutations are enriched in inactive genomic regions and are distributed across the genome similarly to mutations in brain cancers. In contrast, neuronal mutations are enriched in open, transcriptionally active chromatin. These stark differences suggest an assortment of active mutagenic processes in oligodendrocytes and neurons.

Nature Immunology [IF=27.8]

文獻(xiàn)引用產(chǎn)品：

bs-3576R-APC-Cy7 | HBEGF Rabbit pAb, APC-Cy7 conjugated | Flow cytometry

作者單位：亞歷山大大學(xué)

摘要：Central nervous system (CNS)-resident cells such as microglia, oligodendrocytes and astrocytes are gaining increasing attention in respect to their contribution to CNS pathologies including multiple sclerosis (MS). Several studies have demonstrated the involvement of pro-inflammatory glial subsets in the pathogenesis and propagation of inflammatory events in MS and its animal models. However, it has only recently become clear that the underlying heterogeneity of astrocytes and microglia can not only drive inflammation, but also lead to its resolution through direct and indirect mechanisms. Failure of these tissue-protective mechanisms may potentiate disease and increase the risk of conversion to progressive stages of MS, for which currently available therapies are limited. Using proteomic analyses of cerebrospinal fluid specimens from patients with MS in combination with experimental studies, we here identify Heparin-binding EGF-like growth factor (HB-EGF) as a central mediator of tissue-protective and anti-inflammatory effects important for the recovery from acute inflammatory lesions in CNS autoimmunity. Hypoxic conditions drive the rapid upregulation of HB-EGF by astrocytes during early CNS inflammation, while pro-inflammatory conditions suppress trophic HB-EGF signaling through epigenetic modifications. Finally, we demonstrate both anti-inflammatory and tissue-protective effects of HB-EGF in a broad variety of cell types in vitro and use intranasal administration of HB-EGF in acute and post-acute stages of autoimmune neuroinflammation to attenuate disease in a preclinical mouse model of MS. Altogether, we identify astrocyte-derived HB-EGF and its epigenetic regulation as a modulator of autoimmune CNS inflammation and potential therapeutic target in MS.

Cell Metabolism [IF=27.7]

【25年4月文獻(xiàn)戰(zhàn)報】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

C0103 | PBS (1×, powder, 2L) | Other

作者單位：武漢大學(xué)中南醫(yī)院

摘要：Bacteria-based metabolic therapy has been acknowledged as a promising strategy for tumor treatment. However, the insufficient efficiency of wild-type bacteria severely restricts their therapeutic efficacy. Here, we elaborately develop an ?-cyst(e)ine-addicted bacteria-nanodrug biohybrid for metabolic therapy through a dual-selection directed evolution strategy. Our evolved strain exhibits a 36-fold increase in ?-cystine uptake and a 23-fold improvement in total activity of cysteine desulfhydrases compared with the wild-type strain. By conjugating with DMXAA-loaded liposomes, the engineered bacteria-nanodrug biohybrid not only prevents the influx of nutrients into the tumor by blocking neovasculature but also achieves efficient and durable CySS catabolism locally. The unavailable of Cys species disrupts redox homeostasis and strikingly increases intracellular ROS level, achieving favorable therapeutic outcomes in multiple tumor models. Our study not only highlights the promise of directed evolution strategy in enhancing the stability and efficiency of bacteria-based living biocatalyst but also provides new opportunities for antitumor metabolic therapy.

Advanced Materials [IF=27.4]

文獻(xiàn)引用產(chǎn)品：

BA00208 | Cell Counting Kit-8 | Other

作者單位：山西大學(xué)

摘要：Tailored photophysical properties and chemical activity is the ultimate pursuit of functional dyes for in vivo biomedical theranostics. In this work, the independent regulation of the absorption and fluorescence emission wavelengths of heptamethine cyanines is reported. These dyes retain near-infrared fluorescence emission (except a nitro-modified dye) while feature variable absorption wavelengths ranging from 590 to 860 nm. This enables to obtain customized functional dyes that meet the excitation and fluorescence wavelength requirements defined by the optical properties of tissues for in vivo biomedical applications. Typically, a nitro-modified photothermal active derivative Cy-Mu-7-9 is used, which features strong absorption at 810 nm in PBS, a wavelength that balanced the tissue penetration depth and non-specific photothermal effect, to realize non-destructive inflammatory bowel disease (IBD) therapy via photothermal induced up-regulation of heat shock protein 70 in the intestinal epithelial cells. The corresponding amino-modified dye Cy-Mu-7-9-NH₂, which can be formed in health enteric cavity by Cy-Mu-7-9 after oral administration, is a fluorescence compound with the emission of 800 nm in PBS. Based on the IBD sensitive transformation of Cy-Mu-7-9 and Cy-Mu-7-9-NH₂, in vivo IBD theranostic and therapeutic effect evaluation is realized via the synergy of fluorescence imaging and photothermal therapy for the first time.

Immunity [IF=25.5]

【25年4月文獻(xiàn)戰(zhàn)報】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-1927R | PLAUR Rabbit pAb | ICC

作者單位：德國慕尼黑大學(xué)

摘要：Thrombotic diseases remain the major cause of death and disability worldwide, and the contribution of inflammation is increasingly recognized. Thromboinflammation has been identified as a key pathomechanism, but an unsupervised map of immune-cell states, trajectories, and intercommunication at a single-cell level has been lacking.

Here, we reveal innate leukocyte substates with prominent thrombolytic properties by employing single-cell omics measures on human stroke thrombi. Using in vivo and in vitro thrombosis models, we propose a pro-resolving monocyte-neutrophil axis, combining two properties: (1) NR4A1^hi non-classical monocytes acquire a thrombolytic and neutrophil-chemoattractive phenotype, and (2) blood neutrophils are thereby continuously recruited to established thrombi through CXCL8-CXCR1 and CXCR2 and adopt a hypoxia-induced thrombus-resolving urokinase receptor (PLAUR)⁺ phenotype. This immunothrombolytic axis results in thrombus resolution. Together, with this immune landscape of thrombosis, we provide a valuable resource and introduce the concept of “immunothrombolysis" with broad mechanistic and translational implications at the crossroad of inflammation and thrombosis.

Bioactive Materials [IF=18]

【25年4月文獻(xiàn)戰(zhàn)報】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

文獻(xiàn)引用產(chǎn)品：

bs-0195R | CD31 Rabbit pAb | IF

bs-5884R-PE | Endomucin Rabbit pAb, PE conjugated | IF

作者單位：南方醫(yī)科大學(xué)

摘要：The treatment of refractory bone defects is a major clinical challenge, especially in steroid-associated osteonecrosis (SAON), which is characterized by insufficient osteogenesis and angiogenesis. Herin, a microenvironment responsiveness scaffold composed of poly-L-lactide (PLLA), and manganese dioxide (MnO₂) nanoparticles is designed to enhance bone regeneration by scavenging endogenous reactive oxygen species (ROS) and modulating immune microenvironment in situ. A catalase-like catalytic reaction between MnO₂ and endogenous hydrogen peroxide (H₂O₂) generated at the bone defect area, which typically becomes acidic and ROS-rich, triggers on-demand release of oxygen and Mn²⁺, significantly ameliorating inflammatory response by promoting M2-type polarization of macrophages, reprograming osteoimmune microenvironment conducive to angiogenesis and osteogenesis. Furthermore, the fundamental mechanisms were explored through transcriptome sequencing analysis, revealing that PLLA/MnO₂ scaffolds (PMns) promote osteogenic differentiation by upregulating the TGF-β/Smad signaling pathway in human bone marrow mesenchymal stem cells (hBMSCs). Overall, the PMns exhibit superior immunomodulatory, excellent osteogenic-angiogenic properties and promising candidates as bone graft substitutes for therapy clinical refractory bone defects.

ACS Nano [IF=15.8]

文獻(xiàn)引用產(chǎn)品：

bs-1712R | Pan Cytokeratin Rabbit pAb | mIHC

作者單位：中山大學(xué)

摘要：Head and neck squamous cell carcinoma (HNSCC) frequently develops resistance to immune checkpoint blockade (ICB) therapy, resulting from an immune-excluded microenvironment. Immunogenic cell death (ICD) can increase tumor immunogenicity and further augment immune-cell infiltration by releasing immunogenic molecules. Hence, inducing ICD within tumors might be a promising strategy to restore antitumor immunity and sensitize HNSCC to ICB. Herein, we developed shikonin (SHK)-loaded, CGKRK-modified lipid nanoparticles (C-SNPs) and demonstrated that C-SNPs could enrich in tumor cells and induce necroptosis in vitro and in vivo. Transcriptomic profiling revealed that C-SNPs suppressed tumor-cell mismatch repair, which later activated the cGAS-mediated IFN response and further increased the expression of PD-L1. Combining C-SNPs with an anti-PD-1 antibody increased the infiltration of DCs and CD8⁺ T cells, yet the response was limited. Modifying C-SNPs with Mn²⁺ (C-SMNPs) enhanced the activation of cGAS-STING signaling and further boosted the maturation of DCs and the differentiation of cytotoxic T cells within ICB-treated tumors. Importantly, compared to C-SNPs, the combination of C-SMNPs with ICB resulted in more sustained tumor suppression in vivo. Together, we developed a versatile nanoparticle that delivered SHK and Mn²⁺ which sensitized HNSCC to ICB by disrupting tumor-cell mismatch repair and boosting the cGAS-STING-mediated IFN response. This nanosized ICD inducer-based strategy holds therapeutic potential in synergizing with anti-PD-1 immunotherapy to enhance treatment efficacy in HNSCC.

ACS Nano [IF=15.8]

文獻(xiàn)引用產(chǎn)品：

bs-4631R | Beta galactosidase Rabbit pAb | IHC
bs-1110R | SP7/Osterix Rabbit pAb | IHC

作者單位：華南理工大學(xué)

摘要：Aging-related bone degeneration and impaired healing capacity remain significant challenges in regenerative medicine, necessitating innovative, efficient, and targeted strategies to restore bone health. Here, we engineered extracellular vesicles (EVs) derived from the serum of pretreated juvenile mice, with the goals of reversing aging, enhancing osteogenic potential, and increasing bioavailability to rejuvenate the aging bone environment. First, we established bone healing models representing different phases of healing to identify the EV type with the highest potential for improving the bone microenvironment in older individuals. Second, we employed DSS6 for bone targeting to enhance the biological effects of the selected EVs in vivo. The engineered EVs effectively targeted bone repair sites and promoted fracture healing more effectively than unmodified EVs in older mice. RNA sequencing revealed that the translocase of outer mitochondrial membrane 7 (Tomm7) is crucial for the underlying mechanism. Silencing Tomm7 significantly diminished the positive regulatory effects of the EVs. Specifically, the engineered EVs may enhance mitochondrial function in aging cells by activating the Tomm7-mediated Pink1/Parkin mitophagy pathway, promoting stemness recovery in aging bone marrow stromal cells (BMSCs) and reversing the adverse conditions of the aging bone microenvironment. Overall, the developed engineered EVs derived from serum from juvenile mice offer an alternative approach for treating aging bones. The identified underlying biological mechanisms provide a valuable reference for precision treatment of aging bones in the future.

ACS Nano [IF=15.8]

文獻(xiàn)引用產(chǎn)品：

bs-0295G-FITC | Goat Anti-Rabbit IgG H&L, FITC conjugated | ICC

作者單位：南方醫(yī)科大學(xué)

摘要：Adoptive T cell therapy (ACT) is an emerging cancer immunotherapy undergoing clinical evaluation, showing significant promise in the treatment of solid tumors. However, the clinical translation of ACT is hindered by its time-, labor-, and financial-consuming procedures, heterogeneity of cytotoxic T lymphocytes (CTLs), and immunosuppressive tumor microenvironment. Herein, we have developed a bionic cytotoxic T lymphocyte-inspiring microscale system (CTLiMS) composed of mesoporous silica dioxide microspheres containing membrane-disrupting boron clusters (BICs) and proapoptotic monomethyl auristatin E (MMAE) peptides. The BICs were found to disrupt the integrity of cancer cell membranes and enhance the internalization of MMAE, effectively mimicking the biological functions of perforin and granzymes released by CTLs to destroy cancer cells. As expected, the CTLiMSs demonstrated exceptional in vitro anticancer activity, inducing cancer cell apoptosis and exhibiting strong antiproliferative effects. Notably, CTLiMS treatment was demonstrated to induce immunogenic cell death of cancer cells as a result of Ca²⁺ and MMAE influx and subsequent production of reactive oxygen species. The animal studies demonstrated that the CTLiMS treatment led to efficient repression of the tumor growth. Furthermore, the CTLiMS administration resulted in favorable antitumor immunotherapeutic effects, as shown by significant inhibition of distant tumors, increased immune cell infiltration, and elevated plasma levels of pro-inflammatory cytokines. This pilot study using CTLiMSs for cancer immunotherapy offers an innovative bionic strategy for the future advancement of adoptive T cell therapy.

ACS Nano [IF=15.8]

文獻(xiàn)引用產(chǎn)品：

bs-52240R | GLUT1 Recombinant Rabbit mAb | WB

作者單位：吉林大學(xué)第一醫(yī)院

摘要：Disulfidptosis and ferroptosis are recently identified programmed cell deaths for tumor therapy, both of which highly depend on the intracellular cystine/cysteine transformation on the cystine transporter solute carrier family 7 member 11/glutathione/glutathione peroxidase 4 (SLC7A11/GSH/GPX4) antioxidant axis. However, disulfidptosis and ferroptosis are usually asynchronous due to the opposite effect of cystine transport on them. Herein, systematic glucose deprivation, by both inhibiting upstream glucose uptake and promoting downstream glucose consumption, is proposed to synchronously evoke disulfidptosis and ferroptosis. As an example, Au nanodots and Fe-apigenin (Ap) complexes coloaded FeOOH nanoshuttles (FeOOH@Fe-Ap@Au NSs) are employed to regulate the SLC7A11/GSH/GPX4 axis for performing disulfidptosis- and ferroptosis-mediated tumor therapy synchronously. In this scenario, Au nanodots exhibit glucose oxidase-like activity when consuming massive glucose. Meanwhile, Ap can inhibit glucose uptake by downregulating glucose transporter 1, depriving glucose fundamentally. The systematical glucose deprivation limits the supplement of NADPH and suppresses cystine/cysteine transformation on the SLC7A11/GSH/GPX4 axis, thus solving the contradiction of cystine transport on disulfidptosis and ferroptosis. In addition, the efficient delivery of exogenous iron ions by FeOOH@Fe-Ap@Au NSs and self-supplied H₂O₂ through Au nanodots-catalytic glucose oxidation facilitate intracellular Fenton reaction and therewith help to amplify ferroptosis. As a result of synchronous occurrence of disulfidptosis and ferroptosis, FeOOH@Fe-Ap@Au NSs exhibit good efficacy in an ovarian cancer therapeutic model.

上一篇：蛋白標(biāo)記在疫苗研發(fā)中的作用

下一篇：Bioss | 掃碼立領(lǐng)！秒到賬的暑期科研驚喜