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4月文獻(xiàn)戰(zhàn)報(bào) Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)
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)等國際研究機(jī)構(gòu)上百所。
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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 Nanotechnology, Immunity, Cancer 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)未來技術(shù)學(xué)院生物醫(yī)學(xué)工程系
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]
Anti-His tag pAb | WB
作者單位:中國藥科大學(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)室和天然藥物國家重點(diǎn)實(shí)驗(yàn)室
NUCLEIC ACIDS RESEARCH
[IF=19.16]
Anti-Actin pAb | WB
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
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.