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【11月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)
截至目前,引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共23073篇,總影響因子105342.2分,發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共54篇,合作單位覆蓋了清華、北大、復(fù)旦、華盛頓大學(xué)、麻省理工學(xué)院、東京大學(xué)以及紐約大學(xué)等國(guó)際研究機(jī)構(gòu)上百所。
我們每月收集引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)。若您在當(dāng)月已發(fā)表SCI文章,但未被我公司收集,請(qǐng)致電Bioss,我們將贈(zèng)予現(xiàn)金鼓勵(lì),金額標(biāo)準(zhǔn)請(qǐng)參考“發(fā)文章 領(lǐng)獎(jiǎng)金”活動(dòng)頁(yè)面。
近期收錄2022年11月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共284篇(圖一,綠色柱),文章影響因子(IF) 總和高達(dá)1886.766,其中,10分以上文獻(xiàn)43篇(圖二)。
圖一
圖二
本文主要分享引用Bioss產(chǎn)品發(fā)表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的6篇 IF>15 的文獻(xiàn)摘要,讓我們一起欣賞吧。
ADVANCED MATERIALS
[IF=32.086]
作者單位:廣東省傳感器技術(shù)與生物醫(yī)學(xué)儀器重點(diǎn)實(shí)驗(yàn)室中山大學(xué)生物醫(yī)學(xué)工程學(xué)院深圳校區(qū)中山大學(xué)深圳分校
JOURNAL OF MEDICAL VIROLOGY
[IF=20.693]
文獻(xiàn)引用抗體:
bsk11014; Human TNF-α ELISA KIT; ELISA
bsk11007; Human IL-6 ELISA KIT; ELISA
摘要:Lots of epidemiological and clinical studies have shown that human cytomegalovirus (HCMV) is related to the pathogenesis of atherosclerosis. Released by inflammatory cells and vascular smooth muscle cell (VSMCs), metalloproteinases are observed in many pathological vessel conditions, including atherosclerosis and restenosis. This study was designed to investigate the effect of HCMV infection on the expression of metalloproteinases and their involvements in the HCMV-induced functional changes of VSMCs. Differential metalloproteinase after HCMV infection was assayed using reverse transcription-polymerase chain reaction (RT-PCR) microarray.
MOLECULAR CELL
[IF=19.328]
Anti-MDH1 pAb; WB
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體:bs-11462R
Anti-BCAS1 pAb; IF
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體:
bs-0296G-FITC; Goat Anti-Mouse IgG H&L / FITC antibody; IF
bs-0521R-FITC; Anti-CD44/FITC pAb;IF
C05-07004; BiossECL Plus WB Substrate
作者單位:中國(guó)南京東南大學(xué)生物科學(xué)與醫(yī)學(xué)工程學(xué)院生物電子學(xué)國(guó)家重點(diǎn)實(shí)驗(yàn)室
摘要:Cancer vaccine, which can promote tumor-specific immunostimulation, is one of the most important immunotherapeutic strategies and holds tremendous potential for cancer treatment/prevention. Here, we prepare a series of nanoparticles composed of doxorubicin- and tyrosine kinase inhibitor-loaded and hyaluronic acid-coated dendritic polymers (termed HDDT nanoparticles) and find that the HDDT nanoparticles can convert various cancer cells to micrometer-sized vesicles (1.6−3.2 μm; termed HMVs) with ~100% cell-to-HMV conversion efficiency. We confirm in two tumor-bearing mouse models that the nanoparticles can restrain tumor growth, induce robust immunogenic cell death, and convert the primary tumor into an antigen depot by producing HMVs in situ to serve as personalized vaccines for cancer immunotherapy. Furthermore, the HDDT-healed mice show a strong immune memory effect and the HDDT treatment can realize long-term protection against tumor rechallenge. Collectively, the present work provides a general strategy for the preparation of tumor-associated antigen-containing vesicles and the development of personalized cancer vaccines.
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體:bs-0437P-AF555
Streptavidin / AF555
作者單位:北京大學(xué)口腔醫(yī)學(xué)院老年牙科系
摘要:RIG-I/DDX58 plays a key role in host innate immunity. However, its therapeutic potential for inflammation-related cancers remains to be explored. Here we identify frameshift germline mutations of RIG-I occurring in patients with colon cancer. Accordingly, Rig-ifs/fs mice bearing a frameshift mutant Rig-i exhibit increased susceptibility to colitis-related colon cancer as well as enhanced inflammatory response to chemical, virus or bacteria. In addition to interruption of Rig-i mRNA translation, the Rig-i mutation changes the secondary structure of Rig-i pre-mRNA and impairs its association with DHX9, consequently inducing a circular RNA generation from Rig-i transcript, thereby, designated as circRIG-I. CircRIG-I is frequently upregulated in colon cancers and its upregulation predicts poor outcome of colon cancer. Mechanistically, circRIG-I interacts with DDX3X, which in turn stimulates MAVS/TRAF5/TBK1 signaling cascade, eventually activating IRF3-mediated type I IFN transcription and aggravating inflammatory damage. Reciprocally, all-trans retinoic acid acts as a DHX9 agonist, ameliorates immunopathology through suppression of circRIG-I biogenesis. Collectively, our results provide insight into mutant RIG-I action and propose a potential strategy for the treatment of colon cancer.