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    當(dāng)前位置:首頁(yè)  >  新聞資訊  >  4月文獻(xiàn)戰(zhàn)報(bào) Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

    4月文獻(xiàn)戰(zhàn)報(bào) Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

    更新時(shí)間:2023-06-21  |  點(diǎn)擊率:967



    截止目前,引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共24858篇總影響因子116841.414分,發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共58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4月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共288篇(圖一,綠色柱),文章影響因子(IF) 總和高達(dá)2009.871,其中,10分以上文獻(xiàn)47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 NanotechnologyImmunityCancer Cell等期刊的5篇 IF>15 的文獻(xiàn)摘要讓我們一起欣賞吧。




    Cell Discovery [IF=38.079]



    文獻(xiàn)引用抗體:bsm-41516M

    Mouse Anti- SARS-CoV-2  Spike RBD mAb | WB

    作者單位:北京大學(xué)未來(lái)技術(shù)學(xué)院生物醫(yī)學(xué)工程系

    摘要:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has elicited a worldwide pandemic since late 2019. There has been ~675 million confirmed coronavirus disease 2019 cases, leading to more than 6.8 million deaths as of March 1, 2023. Five SARS-CoV-2 variants of concern (VOCs) were tracked as they emerged and were subsequently characterized. However, it is still difficult to predict the next dominant variant due to the rapid evolution of its spike (S) glycoprotein, which affects the binding activity between cellular receptor angiotensin-converting enzyme 2 (ACE2) and blocks the presenting epitope from humoral monoclonal antibody (mAb) recognition. Here, we established a robust mammalian cell-surface-display platform to study the interactions of S-ACE2 and S-mAb on a large scale. A lentivirus library of S variants was generated via in silico chip synthesis followed by site-directed saturation mutagenesis, after which the enriched candidates were acquired through single-cell fluorescence sorting and analyzed by third-generation DNA sequencing technologies. The mutational landscape provides a blueprint for understanding the key residues of the S protein binding affinity to ACE2 and mAb evasion. It was found that S205F, Y453F, Q493A, Q493M, Q498H, Q498Y, N501F, and N501T showed a 3–12-fold increase in infectivity, of which Y453F, Q493A, and Q498Y exhibited at least a 10-fold resistance to mAbs REGN10933, LY-CoV555, and REGN10987, respectively. These methods for mammalian cells may assist in the precise control of SARS-CoV-2 in the future.

    JOURNAL OF HEPATOLOGY

    [IF=30.083]



    文獻(xiàn)引用抗體:bs-1278R

    Anti-8-OHdG (DNA/RNA Damage) pAb | IHC

    作者單位:美國(guó)明尼蘇達(dá)州羅切斯特市梅奧診所生物化學(xué)和分子生物學(xué)部

    摘要:Background & Aims

    The prevalence of non-alcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (HCC) is rising rapidly, yet its underlying mechanisms remain unclear. Herein, we aim to determine the role of hypoxia-inducible lipid droplet associated protein (HILPDA)/hypoxia-inducible gene 2 (HIG2), a selective inhibitor of intracellular lipolysis, in NASH-driven HCC.

    Methods

    The clinical significance of HILPDA was assessed in human NASH-driven HCC specimens by immunohistochemistry and transcriptomics analyses. The oncogenic effect of HILPDA was assessed in human HCC cells and in 3D epithelial spheroids upon exposure to free fatty acids and either normoxia or hypoxia. Lipidomics profiling of wild-type and HILPDA knockout HCC cells was assessed via shotgun and targeted approaches. Wild-type (Hilpdafl/fl) and hepatocyte-specific Hilpda knockout (HilpdaΔHep) mice were fed a western diet and high sugar in drinking water while receiving carbon tetrachloride to induce NASH-driven HCC.

    Results

    In patients with NASH-driven HCC, upregulated HILPDA expression is strongly associated with poor survival....



    ADVANCED FUNCTIONAL 

    MATERIALS [IF=19.924]


    文獻(xiàn)引用抗體:bs-0287R

    Anti-His tag pAb | WB

    作者單位:中國(guó)藥科大學(xué)生命科學(xué)與技術(shù)學(xué)院江蘇省生物藥物可提取性重點(diǎn)實(shí)驗(yàn)室和天然藥物國(guó)家重點(diǎn)實(shí)驗(yàn)室

    摘要:The efficient delivery of biologics into cells provide unique opportunities to modulate intracellular targets not druggable by conventional small molecules. The supercharged polypeptide (SCP) has become a novel intracellular delivery system due to their special advantages, including enhanced delivery efficiency and serum tolerance. However, owing to their cationic charge and non-specificity characteristics, the in vivo application of SCP is limited. Here, an activatable SCP (ASCP) with a pH-sensitive charge shielding sequence (CSS), a protease cleavage site, and SCP are engineered. This system shows the potential to reduce the non-specific binding and effectively deliver various cargo (peptide, protein, small molecule, and siRNA) into the cytosol not only in vitro but also in vivo. Furthermore, an ASCP fusion protein is designed to co-delivery of peptide (KLA)/siRNA (IKBKE) with different tumorigenesis pathways to triple negative breast cancer (TNBC) for optimal therapeutic outcomes. It is believed that ASCP delivery system will facilitate the development of bioactive molecules for use against intracellular targets. This simple yet versatile delivery system can also pave the way for the co-delivery of multiple therapeutic cargos to address the emerging needs of combination cancer therapy.


    NUCLEIC ACIDS RESEARCH

     [IF=19.16]


    文獻(xiàn)引用抗體bs-10966R

    Anti-Actin pAb | WB

    作者單位:中國(guó)廣東廣州中山大學(xué)附屬第一醫(yī)院兒科

    摘要:CST (CTC1-STN1-TEN1) is a telomere associated complex that binds ssDNA and is required for multiple steps in telomere replication, including termination of G-strand extension by telomerase and synthesis of the complementary C-strand. CST contains seven OB-folds which appear to mediate CST function by modulating CST binding to ssDNA and the ability of CST to recruit or engage partner proteins. However, the mechanism whereby CST achieves its various functions remains unclear. To address the mechanism, we generated a series of CTC1 mutants and studied their effect on CST binding to ssDNA and their ability to rescue CST function in CTC1?/? cells. We identified the OB-B domain as a key determinant of telomerase termination but not C-strand synthesis. CTC1-ΔB expression rescued C-strand fill-in, prevented telomeric DNA damage signaling and growth arrest. However, it caused progressive telomere elongation and the accumulation of telomerase at telomeres, indicating an inability to limit telomerase action. The CTC1-ΔB mutation greatly reduced CST-TPP1 interaction but only modestly affected ssDNA binding. OB-B point mutations also weakened TPP1 association, with the deficiency in TPP1 interaction tracking with an inability to limit telomerase action. Overall, our results indicate that CTC1-TPP1 interaction plays a key role in telomerase termination.



    ACS Nano [IF=18.027]



    文獻(xiàn)引用抗體:bs-0295G-HRP

    Goat Anti-Rabbit IgG H&L / HRP | WB
    作者單位:北京理工大學(xué)生命科學(xué)學(xué)院

    摘要:The intrinsic features and functions of platelets and mesenchymal stem cells (MSCs) indicate their great potential in the treatment of intracerebral hemorrhage (ICH). However, neither of them can completely overcome ICH because of the stealth process and the complex pathology of ICH. Here, we fabricate hybrid cells for versatile and highly efficient ICH therapy by fusing MSCs with platelets and loading with lysophosphatidic acid-modified PbS quantum dots (LPA-QDs). The obtained LPA-QDs@FCs (FCs = fusion cells) not only inherit the capabilities of both platelets and MSCs but also exhibit clearly enhanced proliferation activated by LPA. After systemic administration, many proliferating LPA-QDs@FCs rapidly accumulate in ICH areas for responding to the vascular damage and inflammation and then efficiently prevent both the primary and secondary injuries of ICH but with no obvious side effects. Moreover, the treatment process can be tracked by near-infrared II fluorescence imaging with highly spatiotemporal resolution, providing a promising solution for ICH therapy.

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