发表者：北京博奥森生物      发表时间：2022-8-18

截止目前，引用Bioss产品发表的文献共19603篇，总影响因子87327.086分，发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共53篇，合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等国际知名研究机构上百所。

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近期收录2022年7月引用Bioss产品发表的文献共247篇（图一，绿色柱），文章影响因子(IF) 总和高达1703.345，其中，20分以上文章3篇，10分以上文献39篇（图二）。

图一

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本文主要分享引用Bioss产品发表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的8篇 IF＞10的文献摘要，让我们一起欣赏吧。

Molecular Cancer [IF=41.444]

文献引用抗体：bs-1152R

Anti-ATPase Na+/ K+ beta 2(Loading Control) pAb; WB

作者单位：美国纽约西奈山伊坎医学院医学系

摘要：Background

Long Interspersed Nuclear Element-1 (LINE-1, L1) is increasingly regarded as a genetic risk for lung cancer. Transcriptionally active LINE-1 forms a L1-gene chimeric transcript (LCTs), through somatic L1 retrotransposition (LRT) or L1 antisense promoter (L1-ASP) activation, to play an oncogenic role in cancer progression.

Methods

Here, we developed Retrotransposon-gene fusion estimation program (ReFuse), to identify and quantify LCTs in RNA sequencing data from TCGA lung cancer cohort (n = 1146) and a single cell RNA sequencing dataset then...

Signal Transduction and Targeted 

Therapy [IF=38.104]

文献引用抗体：bs-20694RAnti-Beta tubulin pAb; IF

作者单位：中山大学生命科学学院

摘要：SARS-CoV-2, the culprit pathogen of COVID-19, elicits prominent immune responses and cytokine storms. Intracellular Cl− is a crucial regulator of host defense, whereas the role of Cl− signaling pathway in modulating pulmonary inflammation associated with SARS-CoV-2 infection remains unclear. By using human respiratory epithelial cell lines, primary cultured human airway epithelial cells, and murine models of viral structural protein stimulation and SARS-CoV-2 direct challenge, we demonstrated that SARS-CoV-2 nucleocapsid (N) protein could interact with Smad3, which downregulated cystic fibrosis transmembrane conductance regulator (CFTR) expression via microRNA-145. The intracellular Cl− concentration ([Cl−]_i) was raised, resulting in phosphorylation of serum glucocorticoid regulated kinase 1 (SGK1) and robust inflammatory responses. Inhibition or knockout of SGK1 abrogated the N protein-elicited airway inflammation. Moreover, N protein promoted a sustained elevation of [Cl−]_i by depleting intracellular cAMP via upregulation of phosphodiesterase 4 (PDE4). Rolipram, a selective PDE4 inhibitor, countered airway inflammation by reducing [Cl−]_i. Our findings suggested that Cl− acted as the crucial pathological second messenger mediating the inflammatory responses after SARS-CoV-2 infection. Targeting the Cl− signaling pathway might be a novel therapeutic strategy for COVID-19.

Cell Stem Cell [IF=25.269]

文献引用抗体：

bs-3155R;Anti-Phospho-GCN2 (Thr899) pAb

bs-2469R;Anti-PERK pAb

作者单位：中山大学中山纪念医院RNA生物医学研究所

摘要：Hematopoietic stem cells (HSCs) adapt their metabolism to maintenance and proliferation; however, the mechanism remains incompletely understood. Here, we demonstrated that homeostatic HSCs exhibited high amino acid (AA) catabolism to reduce cellular AA levels, which activated the GCN2-eIF2α axis, a protein synthesis inhibitory checkpoint to restrain protein synthesis for maintenance. Furthermore, upon proliferation conditions, HSCs enhanced mitochondrial oxidative phosphorylation (OXPHOS) for higher energy production but decreased AA catabolism to accumulate cellular AAs, which inactivated the GCN2-eIF2α axis to increase protein synthesis and coupled with proteotoxic stress. Importantly, GCN2 deletion impaired HSC function in repopulation and regeneration. Mechanistically, GCN2 maintained proteostasis and inhibited Src-mediated AKT activation to repress mitochondrial OXPHOS in HSCs. Moreover, the glycolytic metabolite, NAD⁺precursor nicotinamide riboside (NR), accelerated AA catabolism to activate GCN2 and sustain the long-term function of HSCs. Overall, our study uncovered direct links between metabolic alterations and translation control in HSCs during homeostasis and proliferation.

Nature Communications

[IF=17.694]

文献引用抗体：

bs-12702R-HRP;Anti-phospho-DRP1 (Ser616)/HRP pAb; IHC,IF

bs-0080R;Anti-CD20 pAb; IHC,IF

作者单位：中国中山大学中山纪念医院口腔颌面外科

摘要：Mitochondrial dynamics can regulate Major Histocompatibility Complex (MHC)-I antigen expression by cancer cells and their immunogenicity in mice and in patients with malignancies. A crucial role in the mitochondrial fragmentation connection with immunogenicity is played by the IRE1α-XBP-1s axis. XBP-1s is a transcription factor for aminopeptidase TPP2, which inhibits MHC-I complex cell surface expression likely by degrading tumor antigen peptides. Mitochondrial fission inhibition with Mdivi-1 upregulates MHC-I expression on cancer cells and enhances the efficacy of adoptive T cell therapy in patient-derived tumor models. Therefore mitochondrial fission inhibition might provide an approach to enhance the efficacy of T cell-based immunotherapy.

Nature Communications

[IF=17.694]

文献引用抗体：

bs-2641R;Anti-Integrin alpha 6 pAb; IF

作者单位：美国俄亥俄州克利夫兰诊所癌症生物学系

摘要：Therapeutic targeting of angiogenesis in glioblastoma has yielded mixed outcomes. Investigation of tumor-associated angiogenesis has focused on the factors that stimulate the sprouting, migration, and hyperproliferation of the endothelial cells. However, little is known regarding the processes underlying the formation of the tumor-associated vessels. To address this issue, we investigated vessel formation in CD31⁺ cells isolated from human glioblastoma tumors. The results indicate that overexpression of integrin α3β1 plays a central role in the promotion of tube formation in the tumor-associated endothelial cells in glioblastoma. Blocking α3β1 function reduced sprout and tube formation in the tumor-associated endothelial cells and vessel density in organotypic cultures of glioblastoma. The data further suggest a mechanistic model in which integrin α3β1-promoted calcium influx stimulates macropinocytosis and directed maturation of the macropinosomes in a manner that promotes lysosomal exocytosis during nascent lumen formation. Altogether, our data indicate that integrin α3β1 may be a therapeutic target on the glioblastoma vasculature.

Nature Communications

[IF=17.694]

文献引用抗体：

bs-4573R;Anti-APOA1 pAb

作者单位：中国科学技术大学合肥国家微尺度物理科学研究中心

摘要：Nanoparticle elasticity is crucial in nanoparticles’ physiological fate, but how this occurs is largely unknown. Using core-shell nanoparticles with a same PEGylated lipid bilayer shell yet cores differing in elasticity (45 kPa – 760 MPa) as models, we isolate the effects of nanoparticle elasticity from those of other physiochemical parameters and, using mouse models, observe a non-monotonic relationship of systemic circulation lifetime versus nanoparticle elasticity. Incubating our nanoparticles in mouse plasma provides protein coronas varying non-monotonically in composition depending on nanoparticle elasticity. Particularly, apolipoprotein A-I (ApoA1) is the only protein whose relative abundance in corona strongly correlates with our nanoparticles’ blood clearance lifetime. Notably, similar results are observed when above nanoparticles’ PEGylated lipid bilayer shell is changed to be non-PEGylated. This work unveils the mechanisms by which nanoparticle elasticity affects nanoparticles’ physiological fate and suggests nanoparticle elasticity as a readily tunable parameter in future rational exploiting of protein corona.

Genome Medicine [IF=15.266]

文献引用抗体：bs-5720R

Anti-GDF10 pAb; IF

作者单位：希腊瓦里“亚历山大·弗莱明”生物医学科学研究中心基础生物医学研究所

摘要：Background

Synovial fibroblasts (SFs) are specialized cells of the synovium that provide nutrients and lubricants for the proper function of diarthrodial joints. Recent evidence appreciates the contribution of SF heterogeneity in arthritic pathologies. However, the normal SF profiles and the molecular networks that govern the transition from homeostatic to arthritic SF heterogeneity remain poorly defined.

Methods

We applied a combined analysis of single-cell (sc) transcriptomes and epigenomes (scRNA-seq and scATAC-seq) to SFs derived from naïve and hTNFtg mice (mice that overexpress human TNF, a murine model for rheumatoid arthritis), by employing the Seurat and ArchR packages...

Science Advances [IF=14.957]

文献引用抗体：

bs-10232R; Anti-CD93 pAb

作者单位：第四军医大学口腔医学院口腔颌面外科、军事口腔医学国家重点实验室、国家口腔疾病临床研究中心、陕西省口腔医学重点实验室

摘要：Matching material degradation with host remodeling, including endothelialization and muscular remodeling, is important to vascular regeneration. We fabricated 3D PGS-PCL vascular grafts, which presented tunable polymer components, porosity, mechanical strength, and degrading rate. Furthermore, highly porous structures enabled 3D patterning of conjugated heparin-binding peptide, dimeric thymosin β4 (DTβ4), which played key roles in antiplatelets, fibrinogenesis inhibition, and recruiting circulating progenitor cells, thereafter contributed to high patency rate, and unprecedentedly acquired carotid arterial regeneration in rabbit model. Through single-cell RNA sequencing analysis and cell tracing studies, a subset of endothelial progenitor cells, myeloid-derived CD93⁺/CD34⁺ cells, was identified as the main contributor to final endothelium regeneration. To conclude, DTβ4-inspired porous 3DVGs present adjustable physical properties, superior anticoagulating, and re-endothelializing potentials, which leads to the regeneration of small-caliber artery, thus offering a promising tool for vessel replacement in clinical applications.

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