截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共22023篇，總影響因子100843.61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)際知名研究機(jī)構(gòu)上百所。
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近期收錄2022年10月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共207篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1372.784，其中，10分以上文獻(xiàn)22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7篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。
Molecular Cancer
[IF=41.444]
作者單位：德國(guó)馬爾堡菲利普斯大學(xué)德國(guó)肺研究中心，吉森大學(xué)和馬爾堡肺中心分子腫瘤研究所
摘要：
Background
In vivo gene editing of somatic cells with CRISPR nucleases has facilitated the generation of autochthonous mouse tumors, which are initiated by genetic alterations relevant to the human disease and progress along a natural timeline as in patients. However, the long and variable, orthotopic tumor growth in inner organs requires sophisticated, time-consuming and resource-intensive imaging for longitudinal disease monitoring and impedes the use of autochthonous tumor models for preclinical studies.
Methods
To facilitate a more widespread use, we have generated a reporter mouse that expresses a Cre-inducible luciferase from Gaussia princeps (GLuc), which is secreted by cells in an energy-consuming process and can be measured quantitatively in the blood as a marker for the viable tumor load...
Cell Metabolism
[IF=31.373]
摘要：The underlying cellular events driving kidney fibrogenesis and metabolic dysfunction are incompletely understood. Here, we employed single-cell combinatorial indexing RNA sequencing to analyze 24 mouse kidneys from two fibrosis models. We profiled 309,666 cells in one experiment, representing 50 cell types/states encompassing epithelial, endothelial, immune, and stromal populations. Single-cell analysis identified diverse injury states of the proximal tubule, including two distinct early-phase populations with dysregulated lipid and amino acid metabolism, respectively. Lipid metabolism was defective in the chronic phase but was transiently activated in the very early stages of ischemia-induced injury, where we discovered increased lipid deposition and increased fatty acid β-oxidation. Perilipin 2 was identified as a surface marker of intracellular lipid droplets, and its knockdown in vitro disrupted cell energy state maintenance during lipid accumulation. Surveying epithelial cells across nephron segments identified shared and unique injury responses. Stromal cells exhibited high heterogeneity and contributed to fibrogenesis by epithelial-stromal crosstalk.
JOURNAL OF CLINICAL INVESTIGATION
[IF=19.456]
MOLECULAR CELL
[IF=19.328]
文獻(xiàn)引用抗體：bs-8170R；Anti-KMT3B pAb; IF
作者單位：美國(guó)哥倫比亞大學(xué)歐文醫(yī)學(xué)中心遺傳與發(fā)育系
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體：bs-11040R；Anti-Bestrophin pAb; IHC
作者單位：美國(guó)賓夕法尼亞州匹茲堡市匹茲堡大學(xué)醫(yī)學(xué)院眼科學(xué)系
摘要：The retinal pigment epithelium (RPE) plays an important role in the development of diabetic retinopathy (DR), a leading cause of blindness worldwide. Here we set out to explore the role of Akt2 signaling—integral to both RPE homeostasis and glucose metabolism—to DR. Using human tissue and genetically manipulated mice (including RPE-specific conditional knockout (cKO) and knock-in (KI) mice), we investigate whether Akts in the RPE influences DR in models of diabetic eye disease. We found that Akt1 and Akt2 activities were reciprocally regulated in the RPE of DR donor tissue and diabetic mice. Akt2 cKO attenuated diabetes-induced retinal abnormalities through a compensatory upregulation of phospho-Akt1 leading to an inhibition of vascular injury, inflammatory cytokine release, and infiltration of immune cells mediated by the GSK3β/NF-κB signaling pathway; overexpression of Akt2 has no effect. We propose that targeting Akt1 activity in the RPE may be a novel therapy for treating DR.
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體：
bs-3420R；Anti-Phospho-Smad2 (Ser245 + Ser250 + Ser255) pAb;FCM
bs-3425R；Anti-Phospho-Smad3 (Ser423 + Ser425) pAb;FCM
作者單位：首爾國(guó)立大學(xué)醫(yī)學(xué)院生物醫(yī)學(xué)科學(xué)系解剖與細(xì)胞生物學(xué)
摘要：Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year overall survival rate. Patients with PDAC display limited benefits after undergoing chemotherapy or immunotherapy modalities. Herein, we reveal that chemotherapy upregulates placental growth factor (PlGF), which directly activates cancer-associated fibroblasts (CAFs) to induce fibrosis-associated collagen deposition in PDAC. Patients with poor prognosis have high PIGF/VEGF expression and an increased number of PIGF/VEGF receptor-expressing CAFs, associated with enhanced collagen deposition. We also develop a multi-paratopic VEGF decoy receptor (Ate-Grab) by fusing the single-chain Fv of atezolizumab (anti-PD-L1) to VEGF-Grab to target PD-L1-expressing CAFs. Ate-Grab exerts anti-tumor and anti-fibrotic effects in PDAC models via the PD-L1-directed PlGF/VEGF blockade. Furthermore, Ate-Grab synergizes with gemcitabine by relieving desmoplasia. Single-cell RNA sequencing identifies that a CD141+ CAF population is reduced upon Ate-Grab and gemcitabine combination treatment. Overall, our results elucidate the mechanism underlying chemotherapy-induced fibrosis in PDAC and highlight a combinatorial therapeutic strategy for desmoplastic cancers.
Nature Communications
[IF=17.694]
文獻(xiàn)引用抗體：bs-4682R；Anti-Klrb1c pAb; IHC
作者單位：韓國(guó)科學(xué)技術(shù)高等學(xué)院(KAIST)醫(yī)學(xué)科學(xué)與工程研究生院
摘要：Infiltrating tumor-associated macrophages (TAM) are known to impede immunotherapy against glioblastoma (GBM), however, TAMs are heterogeneous, and there are no clear markers to distinguish immunosuppressive and potentially immune-activating populations. Here we identify a subset of CD169+ macrophages promoting an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we find that CD169+ macrophages in human and mouse gliomas produce pro-inflammatory chemokines, leading to the accumulation of T cells and NK cells. CD169 expression on macrophages facilitates phagocytosis of apoptotic glioma cells and hence tumor-specific T cell responses. Depletion of CD169+ macrophages leads to functionally impaired antitumor lymphocytes and poorer survival of glioma-bearing mice. We show that NK-cell-derived IFN-γ is critical for the accumulation of blood monocyte-derived CD169+ macrophages in gliomas. Our work thus identifies a well-distinguished TAM subset promoting antitumor immunity against GBM, and identifies key factors that might shift the balance from immunosuppressive to anti-tumor TAM.
