歡迎來到北京博奧森生物技術有限公司網站！歡迎來到北京博奧森生物技術有限公司網站！
18611424007
截至目前，引用Bioss產品發表的文獻共18868篇，總影響因子82731.02分，發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共53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2022年6月引用Bioss產品發表的文獻共227篇（圖一，綠色柱），文章影響因子(IF) 總和高達1231.317，其中，10分以上文獻15篇（圖二）。
圖一
圖二
CHEMICAL ENGINEERING JOURNAL
[IF=13.273]
文獻引用抗體：
bs-0061R
Anti-beta-Actin(Loading Control) pAb
bs-4511R
Anti-beta tubulin(Loading Control) pAb
作者單位：北京大學藥物科學學院
摘要：Most cancers recur after clinical treatment. Activation of the patient's own immunity can not only play a therapy role, but also consolidate the treatment prognosis. However, an effective immunity reconstruction strategy remains an impeding issue to be solved. Here, we report a macrophage immunity reconstruction strategy by engineering the stem cell biomimetic liposomes that carry levamisole (sLipo leva) to treat leukemia. The results demonstrated that sLipo leva was successfully constructed by incorporating the membrane of mesenchymal stem cells (MSCs). sLipo leva displayed a significant targeting effect on macrophages, induced the differentiation of them into M1 phenotype, exhibited a robust anticancer efficacy and an acceptable safety in leukemia-bearing mice. The immunity reconstruction mechanism of sLipo leva could be explained by two aspects: activation of macrophages themselves, and further activation of T cells, both of which contributed to the killing of leukemia cells. In conclusion, the present study offers a promising new strategy to activate the patient's own immunity for playing therapy efficacy and for consolidating treatment prognosis of leukemia.
CHEMICAL ENGINEERING JOURNAL
[IF=13.273]
文獻引用抗體：bs-2558R
Anti-EGFRvIII pAb
BIOMATERIALS [IF=12.479]
bs-0028R ; Anti-GSK-3 Beta pAb; WB
bs-0061R ; Anti-beta-Actin (Loading Control) pAb; WB
bs-14519R ; Anti-phospho-eIF2B epsilon (Ser539) pAb; WB
bs-14533R ; Anti-eIF2B epsilon pAb; WB
bs-17330R ; Anti-hnRNP A1 pAb; WB
bs-20611R ; Anti-PI 3 Kinase p85 alpha pAb; WB
bs-23217R ; Anti-NFKB p65 pAb; WB
bsm-33278M ; Mouse Anti-AKT mAb; WB
bs-0295P-HRP ; Rabbit IgG/HRP; WB
bs-0805R ; Anti-CD56 pAb
bs-0832R ; Anti-MICA pAb
bs-0938R ; Anti-NKG2D pAb
bs-1214R ; Anti-TRAIL pAb
bs-2411R ; Anti-NKG2A pAb
bs-2420R ; Anti-NCR2 pAb
bs-2569R ; Anti-CD226 pAb
bs-6028R ; Anti-CD16 pAb
bs-6874R ; Anti-Catalase pAb
bs-20399R ; Anti-HIF-1 Alpha pAb
bs-41214R ; Anti-NCR1 pAb
bs-0295G-AF594 ; Goat Anti-Rabbit IgG H&L/Alexa Fluor 594
作者單位：北京理工大學生命科學學院
Redox Biology [IF=11.799]
文獻引用抗體：bs-6313R
Anti-4 Hydroxynonenal pAb
Redox Biology [IF=11.799]
文獻引用抗體：bs-6313R
Clinical and Translational Medicine
[IF=11.492]
Anti-Biglycan pAb; WB
作者單位：復旦大學華山醫院骨科
摘要：Background
Toll-like receptor 4 (TLR4) participates in the initiation of neuroinflammation in various neurological diseases, including central nervous system injuries. NLR family pyrin domain containing 3 (NLRP3) inflammasome-mediated microglial pyroptosis is crucial for the inflammatory response during secondary spinal cord injury (SCI). However, the underlying mechanism by which TLR4 regulates NLRP3 inflammasome activation and microglial pyroptosis after SCI remains uncertain.
Methods
We established an in vivo mouse model of SCI using TLR4-knockout (TLR4-KO) and wild-type (WT) mice. The levels of pyroptosis, tissue damage and neurological function recovery were evaluated in the three groups (Sham, SCI, SCI-TLR4-KO)...
Gut Microbes [IF=10.711]
文獻引用抗體：
bs-2994R
Anti-IRF7 pAb; WB
bsm-34028M
Mouse Anti-ADGRE1 (F4/80) mAb; IHC
摘要：Diarrheal disease is a common health problem with complex causality. Although diarrhea is accompanied by disturbances in microbial diversity, how gut microbes are involved in the occurrence of diarrhea remains largely unknown. Here, using a pig model of post-weaning stress-induced diarrhea, we aim to elucidate and enrich the mechanistic basis of diarrhea. We found significant alterations in fecal microbiome, their metabolites, and microRNAs levels in piglets with diarrhea. Specifically, loss of ssc-miRNA-425-5p and ssc-miRNA-423-3p, which inhibit the gene expression of fumarate reductase (frd) in Prevotella genus, caused succinate accumulation in piglets, which resulted in diarrhea. Single-cell RNA sequencing indicated impaired epithelial function and increased immune response in the colon of piglet with diarrhea. Notably, the accumulated succinate increased colonic fluid secretion by regulating transepithelial Cl-secretion in the epithelial cells. Meanwhile, succinate promoted colonic inflammatory responses by activating MyD88-dependent TLR4 signaling in the macrophages. Overall, our findings expand the mechanistic basis of diarrhea and suggest that colonic accumulation of microbiota-produced succinate caused by loss of miRNAs leads to diarrhea in weanling piglets.
※ 點擊這里查看往期單月Bioss抗體產品文獻引用列表
網站首頁
