【2月文獻戰報】Bioss抗體新增高分文獻精彩呈現-商家動態-資訊-生物在線

【2月文獻戰報】Bioss抗體新增高分文獻精彩呈現

作者：北京博奧森生物技術有限公司 2023-05-16T11:12 (訪問量:8210)


截止目前，引用Bioss產品發表的文獻共24403篇，總影響因子113884.3分，發表在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。

我們每月收集引用Bioss產品發表的文獻。若您在當月已發表SCI文章，但未被我公司收集，請致電Bioss，我們將贈予現金鼓勵，金額標準請參考“發文章 領獎金”活動頁面。

近期收錄2023年2月引用Bioss產品發表的文獻共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]


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