截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共24403篇，總影響因子113884.3分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共57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。
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近期收錄2023年2月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共301篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1903.359，其中，10分以上文獻(xiàn)30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。
IMMUNITY [IF=43.474]
Anti-ALDH1A1 pAb | WB
作者單位：中國(guó)科學(xué)院動(dòng)物模型與人類疾病機(jī)制重點(diǎn)實(shí)驗(yàn)室
BRAIN BEHAVIOR AND IMMUNITY [IF=19.227]
bs-0061R; Anti-beta-Actin (Loading Control) pAb | WB
bs-4511R; Anti-Beta tubulin (Loading Control) pAb | WB
bs-0295G-AF555; Goat Anti-Rabbit IgG H&L / AF555 | IF摘要：Acyl-CoA synthetase long-chain family member4 (ACSL4) is an important isozyme in polyunsaturated fatty acid (PUFA) metabolism. The role of ACSL4 in the lipopolysaccharide (LPS)-induced inflammation of microglia, and the effects of ACSL4-mediated inflammation on the progression of Parkinson’s disease (PD) are unknown. In this study, we found that ACSL4 expression was increased after LPS stimulation. Knocking down ACSL4 in microglia decreased proinflammatory cytokine production. Mechanistically, ACSL4 reduced vestigial-like family member 4 (VGLL4) expression to promote NF-κB signal transduction; and ACSL4 regulated lipid composition after LPS stimulation. In addition, knocking down ACSL4 alleviated neuroinflammation in a systemic LPS model and acute l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) model. These data revealed ACSL4 to be a novel regulator that promotes microglia-mediated neuroinflammation by regulating VGLL4 expression and lipid metabolism.
Nature Communications [IF=17.694]
文獻(xiàn)引用抗體：bs-2962R
Anti-Syncytin 1 pAb | WB作者單位：美國(guó)貝塞斯達(dá)國(guó)立衛(wèi)生研究院尤尼斯·肯尼迪·施萊佛國(guó)立兒童健康和人類發(fā)展研究所膜生物學(xué)分部
Nature Communications [IF=17.694]
文獻(xiàn)引用抗體：bs-1061R
Anti-MPO pAb | IHC
作者單位：山東大學(xué)齊魯醫(yī)學(xué)院藥學(xué)系，NMPA藥物產(chǎn)品技術(shù)研究和評(píng)價(jià)重點(diǎn)實(shí)驗(yàn)室和化學(xué)生物學(xué)重點(diǎn)實(shí)驗(yàn)室
摘要：Massive intra-articular infiltration of proinflammatory macrophages is a prominent feature of rheumatoid arthritis (RA) lesions, which are thought to underlie articular immune dysfunction, severe synovitis and ultimately joint erosion. Here we report an efferocytosis-informed nanoimitator (EINI) for in situ targeted reprogramming of synovial inflammatory macrophages (SIMs) that thwarts their autoimmune attack and reestablishes articular immune homeostasis, which mitigates RA. The EINI consists of a drug-based core with an oxidative stress-responsive phosphatidylserine (PtdSer) corona and a shell composed of a P-selectin-blocking motif, low molecular weight heparin (LMWH). When systemically administered, the LMWH on the EINI first binds to P-selectin overexpressed on the endothelium in subsynovial capillaries, which functions as an antagonist, disrupting neutrophil synovial trafficking. Due to the strong dysregulation of the synovial microvasculature, the EINI is subsequently enriched in the joint synovium where the shell is disassembled upon the reactive oxygen species stimulation, and PtdSer corona is then exposed. In an efferocytosis-like manner, the PtdSer-coroneted core is in turn phagocytosed by SIMs, which synergistically terminate SIM-initiated pathological cascades and serially reestablish intra-articular immune homeostasis, conferring a chondroprotective effect. These findings demonstrate that SIMs can be precisely remodeled via the efferocytosis-mimetic strategy, which holds potential for RA treatment.
Advanced Science [IF=17.521]
bs-0465R; Anti-NFKB p65 pAb | WB
bs-0982R; Anti-phospho-NFKB p65 (Ser536) pAb | WB
bs-1194R; Anti-NFkB1 pAb | WB
bs-0637R; Anti-P38 MAPK pAb | WB
bs-0636R; Anti-Phospho-P38 MAPK (Thr180 + Tyr182) pAb | WB
bs-1047R; Anti-MyD88 pAb | WB
bsm-52239R; Anti-STAT6 mAb | WB
作者單位：北京大學(xué)藥學(xué)院分子藥劑學(xué)與新藥傳遞系統(tǒng)重點(diǎn)實(shí)驗(yàn)室
摘要：Osteoarthritis (OA) is a progressive joint disease characterized by inflammation and cartilage destruction, and its progression is closely related to imbalances in the M1/M2 synovial macrophages. A two-pronged strategy for the regulation of intracellular/extracellular nitric oxide (NO) and hydrogen protons for reprogramming M1/M2 synovial macrophages is proposed. The combination of carbonic anhydrase IX (CA9) siRNA and NO scavenger in “two-in-one” nanocarriers (NAHA-CaP/siRNA nanoparticles) is developed for progressive OA therapy by scavenging NO and inhibiting CA9 expression in synovial macrophages. In vitro experiments demonstrate that these NPs can significantly scavenge intracellular NO similar to the levels as those in the normal group and downregulate the expression levels of CA9 mRNA (≈90%), thereby repolarizing the M1 macrophages into the M2 phenotype and increasing the expression levels of pro-chondrogenic TGF-β1 mRNA (≈1.3-fold), and inhibiting chondrocyte apoptosis. Furthermore, in vivo experiments show that the NPs have great anti-inflammation, cartilage protection and repair effects, thereby effectively alleviating OA progression in both monoiodoacetic acid-induced early and late OA mouse models and a surgical destabilization of medial meniscus-induced OA rat model. Therefore, the siCA9 and NO scavenger “two-in-one” delivery system is a potential and efficient strategy for progressive OA treatment.
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