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【2月文獻戰(zhàn)報】Bioss抗體新增高分文獻精彩呈現(xiàn)

發(fā)表者：北京博奧森生物發(fā)表時間：2023-5-16

截止目前，引用Bioss產品發(fā)表的文獻共24403篇，總影響因子113884.3分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共57篇，合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等國際知名研究機構上百所。

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近期收錄2023年2月引用Bioss產品發(fā)表的文獻共301篇（圖一，綠色柱），文章影響因子(IF) 總和高達1903.359，其中，10分以上文獻30篇（圖二）。

圖一

圖二

本文主要分享引用Bioss產品發(fā)表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的5篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。

IMMUNITY [IF=43.474]

文獻引用抗體：bs-10162R

Anti-ALDH1A1 pAb | WB

作者單位：中國科學院動物模型與人類疾病機制重點實驗室

摘要：Monoamine insufficiency is suggested to be associated with depressive features such as sadness, anhedonia, insomnia, and cognitive dysfunction, but the mechanisms that cause it are unclear. We found that the acute-phase protein lipopolysaccharide-binding protein (LBP) inhibits monoamine biosynthesis by acting as an endogenous inhibitor of dopamine-β-hydroxylase (DBH) and aromatic-L-amino-acid-decarboxylase (DDC). LBP expression was increased in individuals with depression and by diverse stress challenges in mice. LBP antibodies and LBP knockdown inhibited monoamine insufficiency and depression-like features in mice, which worsened with LBP overexpression or administration. Monoamine insufficiency and depression-like symptoms were not induced by stressful stimuli in LBP-deficient mice, further highlighting a role for LBP in stress-induced depression, and a peptide we designed that blocks LBP-DBH and LBP-DDC interactions showed anti-depression effects in mice. This study reveals an important role for LBP in regulating monoamine biosynthesis and suggests that targeting LBP may have potential as a treatment for some individuals with depression.

BRAIN BEHAVIOR AND IMMUNITY [IF=19.227]

文獻引用抗體：

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
作者單位：青島大學神經再生與神經康復研究所

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]

文獻引用抗體：bs-2962R

Anti-Syncytin 1 pAb | WB

作者單位：美國貝塞斯達國立衛(wèi)生研究院尤尼斯·肯尼迪·施萊佛國立兒童健康和人類發(fā)展研究所膜生物學分部

摘要：Multinucleated osteoclasts, essential for skeletal remodeling in health and disease, are formed by the fusion of osteoclast precursors, where each fusion event raises their bone-resorbing activity. Here we show that the nuclear RNA chaperone, La protein has an additional function as an osteoclast fusion regulator. Monocyte-to-osteoclast differentiation starts with a drastic decrease in La levels. As fusion begins, La reappears as a low molecular weight species at the osteoclast surface, where it promotes fusion. La’s role in promoting osteoclast fusion is independent of canonical La-RNA interactions and involves direct interactions between La and Annexin A5, which anchors La to transiently exposed phosphatidylserine at the surface of fusing osteoclasts. Disappearance of cell-surface La, and the return of full length La to the nuclei of mature, multinucleated osteoclasts, acts as an off switch of their fusion activity. Targeting surface La in a novel explant model of fibrous dysplasia inhibits excessive osteoclast formation characteristic of this disease, highlighting La’s potential as a therapeutic target.

Nature Communications [IF=17.694]

文獻引用抗體：bs-1061R

Anti-MPO pAb | IHC

作者單位：山東大學齊魯醫(yī)學院藥學系，NMPA藥物產品技術研究和評價重點實驗室和化學生物學重點實驗室

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]

文獻引用抗體：

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：北京大學藥學院分子藥劑學與新藥傳遞系統(tǒng)重點實驗室

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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