截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共26390篇，總影響因子125673.17分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共62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)等國(guó)際知名研究機(jī)構(gòu)上百所。
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。
近期收錄2023年9月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共297篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1949.3，其中，10分以上文獻(xiàn)34篇（圖二）。
圖一
圖二
本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的7篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。
Nature [IF=64.8]
文獻(xiàn)引用產(chǎn)品：bs-0498R-PE
ADRB1/PE | IF、FCM
作者單位：美國(guó)索爾克生物研究所NOMIS免疫生物學(xué)和微生物發(fā)病機(jī)制中心
摘要：CD8 T?cells are essential components of the immune response against viral infections and tumours, and are capable of eliminating infected and cancerous cells. However, when the antigen cannot be cleared, T?cells enter a state known as exhaustion+1. Although it is clear that chronic antigen contributes to CD8 T?cell exhaustion, less is known about how stress responses in tissues regulate T?cell function. Here we show a new link between the stress-associated catecholamines and the progression of T?cell exhaustion through the β+1-adrenergic receptor ADRB1. We identify that exhausted CD8 T?cells increase ADRB1 expression and that exposure of ADRB1 T?cells to catecholamines suppresses their cytokine production and proliferation. Exhausted CD8 T?cells cluster around sympathetic nerves in an ADRB1-dependent manner. Ablation of β+++1-adrenergic signalling limits the progression of T?cells towards the exhausted state in chronic infection and improves effector functions when combined with immune checkpoint blockade (ICB) in melanoma. In a pancreatic cancer model resistant to ICB, β-blockers and ICB synergize to boost CD8 T?cell responses and induce the development of tissue-resident memory-like T?cells. Malignant disease is associated with increased catecholamine levels in patients+, and our results establish a connection between the sympathetic stress response, tissue innervation and T?cell exhaustion. Here, we uncover a new mechanism by which blocking β-adrenergic signalling in CD8 T?cells rejuvenates anti-tumour functions.
STTT[IF=39.3]
文獻(xiàn)引用抗體：bs-7656R
ATAD5 Rabbit pAb | WB
作者單位：四川大學(xué)華西醫(yī)院
摘要：The mineral dust-induced gene (MDIG) comprises a conserved JmjC domain and has the ability to demethylate histone H3 lysine 9 trimethylation (H3K9me3). Previous studies have indicated the significance of MDIG in promoting cell proliferation by modulating cell-cycle transition. However, its involvement in liver regeneration has not been extensively investigated. In this study, we generated mice with liver-specific knockout of MDIG and applied partial hepatectomy or carbon tetrachloride mouse models to investigate the biological contribution of MDIG in liver regeneration. The MDIG levels showed initial upregulation followed by downregulation as the recovery progressed. Genetic MDIG deficiency resulted in dramatically impaired liver regeneration and delayed cell cycle progression. However, the MDIG-deleted liver was eventually restored over a long latency. RNA-seq analysis revealed Myc as a crucial effector downstream of MDIG. However, ATAC-seq identified the reduced chromatin accessibility of OTX2 locus in MDIG-ablated regenerating liver, with unaltered chromatin accessibility of Myc locus. Mechanistically, MDIG altered chromatin accessibility to allow transcription by demethylating H3K9me3 at the OTX2 promoter region. As a consequence, the transcription factor OTX2 binding at the Myc promoter region was decreased in MDIG-deficient hepatocytes, which in turn repressed Myc expression. Reciprocally, Myc enhanced MDIG expression by regulating MDIG promoter activity, forming a positive feedback loop to sustain hepatocyte proliferation. Altogether, our results prove the essential role of MDIG in facilitating liver regeneration via regulating histone methylation to alter chromatin accessibility and provide valuable insights into the epi-transcriptomic regulation during liver regeneration.
[IF=19.0]Advanced Functional Materials[IF=19.0]
文獻(xiàn)引用抗體：
bsk12001; IFN-γ ELISA KIT | ELISA
bsk12002; TNF-α ELISA KIT | ELISA
bsk12016; IL-2 ELISA KIT | ELISA
bsk12017; IL-12p70 ELISA KIT | ELISA
bs-0081R; Caspase-3 Rabbit pAb | WB
bs-0664R; HMGB1 Rabbit pAb | WB
bs-0784R; IFNB1 Rabbit pAb | WB
bs-8766R; HAVCR2/TIM-3 Rabbit pAb | WB
bs-9278R; phospho-IRF3 (Ser386) Rabbit pAb | WB
bs-41373R; GAPDH Rabbit pAb | WB
作者單位：南方醫(yī)科大學(xué)附屬第十醫(yī)院
摘要：CRISPR/Cas13a is a powerful genome editing system for RNA knockdown that holds enormous potential for cancer treatment by targeting currently undruggable oncogenes or immune checkpoints. However, the precise intratumoral activation of CRISPR/Cas13a to maximize the therapeutic efficiency while guaranteeing biosafety remains a daunting challenge. Here, a cascade self-uncloaking nanoassembly (SRC) based on a dual-prodrug comprising SN38 and Cas13a/RNP is developed, and the external encapsulation is performed by coating with a ROS-responsive probe, which is stimulated by the tumor microenvironment to achieve the efficient NIR-II imaging by CH10055 due to disaggregation into single molecules, while the second release of prodrug in the hypoxic environment enables targeted controlled release. SN38 not only induces immunogenic cell death (ICD), but significantly combats the immunosuppressive microenvironment of colorectal cancer in combination with the RNA editing targeting the novel immune checkpoint TIM3 to regulate the cGAS-STING pathways, resulting in synergistic activation of both innate and adaptive immunity. The treatment of SRC exhibits a tenfold increase in tumor regression of α-PD-L1 in PD-L1-resistant orthotopic and xenograft models by inducing effective tumor immune infiltration. These results demonstrate the feasibility of using CRISPR/Cas13a in cancer treatment, and SRC holds immense promise as a neoadjuvant strategy for enhancing CRC immunotherapy.
Advanced Functional Materials[IF=19.0]
文獻(xiàn)引用產(chǎn)品：bs-4587R
IL-6 Rabbit pAb | IHC
作者單位：四川大學(xué)生物質(zhì)科學(xué)與工程學(xué)院、成都大三創(chuàng)新醫(yī)療科技有限公司、重慶醫(yī)科大學(xué)附屬第一醫(yī)院泌尿外科
摘要：Hydrophilic lubricant coatings with antifouling properties are commercially applied to urological devices, such as ureteral stents (USs), to inhibit biofilm formation and reduce the likelihood of infectious encrustation. However, their long-term effectiveness is limited due to the lack of active and precise antibacterial activity. Herein, this work reports a hydrophilic lubricant (defined as SA-PU/PVP) coating with smart urease-responsive antibiotic release functionality, achieved by incorporating the antibiotic sulfanilamide-conjugated polyurethane (SA-PU) polymers into a commercial lubricant coating agent containing hydrophilic polyvinylpyrrolidone (PVP). During the initial implantation period, the hydrophilic PVP chains rapidly absorb urine on the coating interface, forming a lubricating layer with the desired antifouling activities that reduce the attachment of host proteins, bacteria, and urate crystals by over 90%. As time progresses and the bacteria proliferates and produces urease, the urease enzymatically degrades the urea linkages in the SA-PU/PVP coating, actively releasing SA antibiotics on demand to prevent biofilm formation and encrustation. Benefiting from this synergistic antifouling and smart antibacterial activities, the SA-PU/PVP-coated US exhibits superior performance in preventing infectious encrustation in a porcine model over a 7-week period, surpassing the effectiveness of a commercial hydrophilic lubricant US. This coating strategy offers a practical solution for inhibiting urological device-associated complications.
Advanced Functional Materials[IF=19.0]
文獻(xiàn)引用產(chǎn)品：bs-0295G-PE
Goat Anti-Rabbit IgG H&L / PE | IF
作者單位：中國(guó)科學(xué)技術(shù)大學(xué)中國(guó)科學(xué)技術(shù)大學(xué)附屬第一醫(yī)院
摘要：Impaired antigen presentation either in dendritic cells (DCs) or tumor cells impedes the triggering of antitumor immunity or tumor cell killing, resulting in failures of multiple types of cancer immunotherapy. Herein, the strategy of using dual-targeting nanomedicines to simultaneously improve the presentation of tumor antigens by both DCs and tumor cells is proposed. It is shown that tuning of surface charge of nanoparticles (NPs) by incorporating different amounts of cationic lipids alters the in vivo NP tissue accumulation and cellular targeting profiles. NPs with moderately positive surface charge (≈20 mV) achieve efficient accumulation in tumors and lymph nodes and dual-targeting to both DCs and tumor cells. As a proof-of-concept demonstration, siRNA against YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) is delivered by the dual-targeting NPs to inhibit excessive antigen degradation in both DCs and tumor cells. For DCs, YTHDF1 downregulation promotes tumor antigen cross-presentation and cross-priming of antigen-specific T cells. For tumor cells, it enhances the presentation of endogenous tumor antigens and hence improves both the recognition and killing of tumor cells by primed antigen-specific T cells. The dual-targeting nanomedicines generate efficient antitumor immunity.
ACS Nano[IF=17.1]
文獻(xiàn)引用抗體：
bs-7525R; TNMD Rabbit pAb | WB、IHCbs-20124R; Collagen alpha-1(I) chain Rabbit pAb | IHC
作者單位：上?？萍即髮W(xué)物理科學(xué)與技術(shù)學(xué)院、復(fù)旦大學(xué)附屬中山醫(yī)院
摘要：Replicating the controlled nanofibrillar architecture of collagenous tissue represents a promising approach in the design of tendon replacements that have tissue-mimicking biomechanics─outstanding mechanical strength and toughness, defect tolerance, and fatigue and fracture resistance. Guided by this principle, a fibrous artificial tendon (FAT) was constructed in the present study using an engineering strategy inspired by the fibrillation of a naturally spun silk protein. This bioinspired FAT featured a highly ordered molecular and nanofibrillar architecture similar to that of soft collagenous tissue, which exhibited the mechanical and fracture characteristics of tendons. Such similarities provided the motivation to investigate FAT for applications in Achilles tendon defect repair. In vitro cellular morphology and expression of tendon-related genes in cell culture and in vivo modeling of tendon injury clearly revealed that the highly oriented nanofibrils in the FAT substantially promoted the expression of tendon-related genes combined with the Achilles tendon structure and function. These results provide confidence about the potential clinical applications of the FAT.
Nature Communications[IF=16.6]
文獻(xiàn)引用抗體：D10060
pNP-β-D-glucopyranoside
作者單位：上海交通大學(xué)生命科學(xué)與生物技術(shù)學(xué)院
摘要：：Viruses are ubiquitous in the oceans, exhibiting high abundance and diversity. Here, we systematically analyze existing genomic sequences of marine prokaryotes to compile a Marine Prokaryotic Genome Dataset (MPGD, consisting of over 12,000 bacterial and archaeal genomes) and a Marine Temperate Viral Genome Dataset (MTVGD). At least 40% of the MPGD genomes contain one or more proviral sequences, indicating that they are lysogens. The MTVGD includes over 12,900 viral contigs or putative proviruses, clustered into 10,897 viral genera. We show that lysogens and proviruses are abundant in marine ecosystems, particularly in the deep sea, and marine lysogens differ from non-lysogens in multiple genomic features and growth properties. We reveal several virus-host interaction networks of potential ecological relevance, and identify proviruses that appear to be able to infect (or to be transferred between) different bacterial classes and phyla. Auxiliary metabolic genes in the MTVGD are enriched in functions related to carbohydrate metabolism. Finally, we experimentally demonstrate the impact of a prophage on the transcriptome of a representative marine Shewanella bacterium. Our work contributes to a better understanding of the ecology of marine prokaryotes and their viruses.
