【2月文献战报】Bioss抗体新增高分文献精彩呈现-商家动态-资讯-生物在线

截止目前，引用Bioss产品发表的文献共24403篇，总影响因子113884.3分，发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共57篇，合作单位覆盖了清华、北大、复旦、华盛顿大学、麻省理工学院、东京大学以及纽约大学等国际知名研究机构上百所。

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近期收录2023年2月引用Bioss产品发表的文献共301篇（图一，绿色柱），文章影响因子(IF) 总和高达1903.359，其中，10分以上文献30篇（图二）。

图一

图二

本文主要分享引用Bioss产品发表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的5篇 IF＞15 的文献摘要，让我们一起欣赏吧。

IMMUNITY [IF=43.474]

文献引用抗体：bs-10162R

Anti-ALDH1A1 pAb | WB

作者单位：中国科学院动物模型与人类疾病机制重点实验室

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]

文献引用抗体：

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

作者单位：青岛大学神经再生与神经康复研究所

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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