【3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

【3月文献战报】Bioss抗体新增高分文献精彩呈现

作者:北京博奥森生物技术有限公司 2023-05-24T14:03 (访问量:4169)


截止目前,引用Bioss产品发表的文献共24676篇总影响因子115653.06分,发表在Nature, Science, Cell以及Immunity等顶级期刊的文献共58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307篇(图一,绿色柱),文章影响因子(IF) 总和高达2073.152,其中,10分以上文献42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8IF>15 的文献摘要让我们一起欣赏吧。


CELL [IF=66.85]



文献引用抗体:bs-2735R

Anti-GSTP1 pAb

作者单位:北京大学化学与分子工程学院,北京分子科学国家实验室,合成与功能生物分子中心

摘要:A generalizable strategy with programmable site specificity for in situ profiling of histone modifications on unperturbed chromatin remains highly desirable but challenging. We herein developed a single-site-resolved multi-omics (SiTomics) strategy for systematic mapping of dynamic modifications and subsequent profiling of chromatinized proteome and genome defined by specific chromatin acylations in living cells. By leveraging the genetic code expansion strategy, our SiTomics toolkit revealed distinct crotonylation (e.g., H3K56cr) and β-hydroxybutyrylation (e.g., H3K56bhb) upon short chain fatty acids stimulation and established linkages for chromatin acylation mark-defined proteome, genome, and functions. This led to the identification of GLYR1 as a distinct interacting protein in modulating H3K56cr′s gene body localization as well as the discovery of an elevated super-enhancer repertoire underlying bhb-mediated chromatin modulations. SiTomics offers a platform technology for elucidating the “metabolites-modification-regulation” axis, which is widely applicable for multi-omics profiling and functional dissection of modifications beyond acylations and proteins beyond histones.

Signal Transduction and

Targeted Therapy [IF=38.104]


文献引用抗体:bs-1570R

Anti-APOH pAb

作者单位:北京大学基础医学院生理学和病理生理学系,分子心血管科学教育部重点实验室

摘要:Hyperhomocysteinemia (HHcy) is a risk factor for chronic kidney diseases (CKDs) that affects about 85% CKD patients. HHcy stimulates B cells to secrete pathological antibodies, although it is unknown whether this pathway mediates kidney injury. In HHcy-treated 2-kidney, 1-clip (2K1C) hypertensive murine model, HHcy-activated B cells secreted anti-beta 2 glycoprotein I (β2GPI) antibodies that deposited in glomerular endothelial cells (GECs), exacerbating glomerulosclerosis and reducing renal function. Mechanistically, HHcy 2K1C mice increased phosphatidylethanolamine (PE) (18:0/20:4, 18:0/22:6, 16:0/20:4) in kidney tissue, as determined by lipidomics. GECs oxidative lipidomics validated the increase of oxidized phospholipids upon Hcy-activated B cells culture medium (Hcy-B CM) treatment, including PE (18:0/20:4 + 3[O], PE (18:0a/22:4 + 1[O], PE (18:0/22:4 + 2[O] and PE (18:0/22:4 + 3[O]). PE synthases ethanolamine kinase 2 (etnk2) and ethanolamine-phosphate cytidylyltransferase 2 (pcyt2) were increased in the kidney GECs of HHcy 2K1C mice and facilitated polyunsaturated PE synthesis to act as lipid peroxidation substrates. In HHcy 2K1C mice and Hcy-B CM-treated GECs, the oxidative environment induced by iron accumulation and the insufficient clearance of lipid peroxides caused by transferrin receptor (TFR) elevation and down-regulation of SLC7A11/glutathione peroxidase 4 (GPX4) contributed to GECs ferroptosis of the kidneys. In vivo, pharmacological depletion of B cells or inhibition of ferroptosis mitigated the HHcy-aggravated hypertensive renal injury. Consequently, our findings uncovered a novel mechanism by which B cell-derived pathogenic anti-β2GPI IgG generated by HHcy exacerbated hypertensive kidney damage by inducing GECs ferroptosis. Targeting B cells or ferroptosis may be viable therapeutic strategies for ameliorating lipid peroxidative renal injury in HHcy patients with hypertensive nephropathy.


ACS Nano [IF=18.027]


文献引用抗体:

bs-3884R; Anti-GPX4 pAb | WB

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