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当前位置：首页  >  新闻资讯  >  【9月文献战报】Bioss抗体新增高分文献精彩呈现

【9月文献战报】Bioss抗体新增高分文献精彩呈现

更新时间：2022-11-10  |  点击率：527

 


截至目前，引用Bioss产品发表的文献共20640篇，总影响因子93542.19分，发表在Nature, Science, Cell以及Immunity等期刊的文献共53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研究机构上百所。

我们每月收集引用Bioss产品发表的文献。若您在当月已发表SCI文章，但未被我公司收集，请致电Bioss，我们将赠予现金鼓励，金额标准请参考“发文章 领奖金”活动页面。

近期收录2022年9月引用Bioss产品发表的文献共291篇（图一，绿色柱），文章影响因子(IF) 总和高达1897.06，其中，10分以上文献34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7篇 IF＞15 的文献摘要，让我们一起欣赏吧。

 

NATURE METHODS

 [IF=47.99]



文献引用抗体：bs-6970R

Anti-FOXN1 pAb; IF

作者单位：美国宾夕法尼亚州匹兹堡，阿勒格尼健康网络，细胞治疗研究所

摘要：Hematopoietic humanized (hu) mice are powerful tools for modeling the action of human immune system and are widely used for preclinical studies and drug discovery. However, generating a functional human T cell compartment in hu mice remains challenging, primarily due to the species-related differences between human and mouse thymus. While engrafting human fetal thymic tissues can support robust T cell development in hu mice, tissue scarcity and ethical concerns limit their wide use. Here, we describe the tissue engineering of human thymus organoids from inducible pluripotent stem cells (iPSC-thymus) that can support the de novo generation of a diverse population of functional human T cells. T cells of iPSC-thymus-engrafted hu mice could mediate both cellular and humoral immune responses, including mounting robust proinflammatory responses on T cell receptor engagement, inhibiting allogeneic tumor graft growth and facilitating efficient Ig class switching. Our findings indicate that hu mice engrafted with iPSC-thymus can serve as a new animal model to study human T cell-mediated immunity and accelerate the translation of findings from animal studies into the clinic.

 

Military Medical Research

 [IF=34.915]


文献引用抗体：bs-9267R
Anti-USP10 pAb; IHC

作者单位：总医院第五医疗中心肿瘤内科、高级肿瘤科

摘要：Background

Melatonin, a natural hormone secreted by the pineal gland, has been reported to exhibit antitumor properties through diverse mechanisms of action. However, the oncostatic function of melatonin on esophageal squamous cell carcinoma (ESCC) remains elusive. This study was conducted to investigate the potential effect and underlying molecular mechanism of melatonin as single anticancer agent against ESCC cells.

Methods

ESCC cell lines treated with or without melatonin were used in this study. In vitro colony formation and EdU incorporation assays, and nude mice tumor xenograft model were used to confirm the proliferative capacities of ESCC cells. RNA-seq, qPCR, Western blotting, recombinant lentivirus-mediated target gene overexpression or knockdown, plasmids transfection and co-IP were applied to investigate the underlying molecular mechanism by which melatonin inhibited ESCC cell growth.

 

 

 


ADVANCED MATERIALS

 [IF=32.086]


文献引用抗体：bs-0666R

Anti-Fibronectin/FN1 pAb; IF

作者单位：德国肺研究中心，亥姆霍兹慕尼黑，肺健康与免疫研究所和综合肺病学中心

摘要：Lung fibrosis, one of the major post-COVID complications, is a progressive and ultimately fatal disease without a cure. Here, an organ- and disease-specific in vitro mini-lung fibrosis model equipped with noninvasive real-time monitoring of cell mechanics is introduced as a functional readout. To establish an intricate multiculture model under physiologic conditions, a biomimetic ultrathin basement (biphasic elastic thin for air–liquid culture conditions, BETA) membrane (<1 µm) is developed with unique properties, including biocompatibility, permeability, and high elasticity (<10 kPa) for cell culturing under air–liquid interface and cyclic mechanical stretch conditions. The human-based triple coculture fibrosis model, which includes epithelial and endothelial cell lines combined with primary fibroblasts from idiopathic pulmonary fibrosis patients established on the BETA membrane, is integrated into a millifluidic bioreactor system (cyclic in vitro cell-stretch, CIVIC) with dose-controlled aerosolized drug delivery, mimicking inhalation therapy. The real-time measurement of cell/tissue stiffness (and compliance) is shown as a clinical biomarker of the progression/attenuation of fibrosis upon drug treatment, which is confirmed for inhaled Nintedanib—an antifibrosis drug. The mini-lung fibrosis model allows the combined longitudinal testing of pharmacodynamics and pharmacokinetics of drugs, which is expected to enhance the predictive capacity of preclinical models and hence facilitate the development of approved therapies for lung fibrosis.

 

JOURNAL OF CLINICAL 

INVESTIGATION [IF=19.456]


文献引用抗体：bs-3195R

Anti-Phospho-IRF3 (Ser396) pAb; WB

作者单位：台北医科大学医学科学研究所

摘要：Diabetes mellitus (DM) is highly comorbid with severe dengue diseases; however, the underlying mechanisms are unclear. Patients with DM have a 1.61-fold increased risk of developing dengue hemorrhagic fever. In search of host factors involved in dengue virus (DENV) infection, we used high-glucose (HG) treatment and showed that HG increased viral protein expression and virion release but had no effects on the early stages of viral infection. After HG stimulation, DENV–firefly luciferase–transfected assay and cellular replicon–based assay indicated increased viral translation, whereas using the glucose uptake inhibitor phloretin blocked this effect. HG treatment increased the translational factor poly(A)-binding protein (PABP) in a glucose transporter–associated, PI3K/AKT-regulated manner. Silencing PABP significantly decreased HG-prompted virion production. HG enhanced the formation of the PABP–eukaryotic translation initiation factor 4G complex, which is regulated by protein–disulfide isomerase. Hyperglycemia increased PABP expression, mortality rate, viral protein expression, and viral loads in streptozotocin-induced DM mice. Overall, hyperglycemic stress facilitates DENV infection by strengthening PABP-mediated viral translation.

 

JOURNAL OF CLINICAL 

INVESTIGATION [IF=19.456]


文献引用抗体：bs-4089R

Anti-phospho-AKT2 (Ser474) pAb; IF

作者单位：北京大学口腔医学院和口腔医院和口腔疼痛中心

摘要：Early-stage temporomandibular joint osteoarthritis (TMJOA) is characterized by excessive subchondral bone loss. Emerging evidence suggests that TMJ disc displacement is involved, but the pathogenic mechanism remains unclear. Here, we established a rat model of TMJOA that simulated disc displacement with a capacitance-based force-sensing system to directly measure articular surface pressure in vivo. Micro-CT, histological staining, immunofluorescence staining, IHC staining, and Western blot were used to assess pathological changes and underlying mechanisms of TMJOA in the rat model in vivo as well as in RAW264.7 cells in vitro. We found that disc displacement led to significantly higher pressure on the articular surface, which caused rapid subchondral bone loss via activation of the RANTES–chemokine receptors–Akt2 (RANTES-CCRs-Akt2) axis. Inhibition of RANTES or Akt2 attenuated subchondral bone loss and resulted in improved subchondral bone microstructure. Cytological studies substantiated that RANTES regulated osteoclast formation by binding to its receptor CCRs and activating the Akt2 pathway. The clinical evidence further supported that RANTES was a potential biomarker for predicting subchondral bone loss in early-stage TMJOA. Taken together, this study demonstrates important functions of the RANTES-CCRs-Akt2 axis in the regulation of subchondral bone remodeling and provides further knowledge of how disc displacement causes TMJOA.


 

Advanced Science 

[IF=17.521]


文献引用抗体：

bs-0397R; Anti-MMP9 pAb

bs-1313R; Anti-VEGFA pAb

bs-10802R; Anti-TNF alpha pAb

bs-1407R; Anti-HIF1 beta pAb

bs-4593R; Anti-MMP9 pAb

bs-0782R; Anti-IL-6 pAb

bs-6761R; Anti-IL-10 pAb

bsm-33188M; Mouse Anti-alpha smooth muscle Actin mAb
作者单位：西北大学研究院陕西省可降解生物医用材料重点实验室陕西省生物材料与发酵工程生物技术研发中心

摘要：In addition to oxidative stress and impaired angiogenesis, the overexpression of metalloproteinases (MMPs) and proinflammatory cytokines, which are promoted by hyperglycemia, causes chronic inflammation in diabetic wounds. Herein, TA-siRNA nanogels are prepared for the first time on the basis of the self-assembling interaction between tannic acid (TA) and short interfering RNA (siRNA). The efficient, biodegradable nanogels are cross-linked with poly(vinyl alcohol) (PVA), human-like collagen (HLC), TA, and borax to prepare adaptive, conductive PHTB (TA-siRNA) hydrogels. In response to high levels of reactive oxygen species (ROS), the ROS-responsive borate ester bonds in the hydrogels are oxidized and broken, and TA-siRNA nanogels are released into cells to reduce the expression of the MMP-9. Moreover, the TA and HLC promote collagen expression, reduce inflammation, and ROS level. It is found that electrical stimulation (ES) promotes the in vivo release of TA-siRNA nanogels from PHTB (TA-siRNA) hydrogels and endocytosis of the nanogels. The combination therapy using ES and PHTB (TA-siRNA) hydrogels accelerates the healing of diabetic wounds by reducing the levels of ROS and MMP-9 and promoting the polarization of macrophages, production of collagen, and angiogenesis. This study provides insights on the design of functional gene-delivery and efficient therapeutic strategies to promote the repair of diabetic chronic wounds.


 

CHEMICAL ENGINEERING 

JOURNAL [IF=16.744]


文献引用抗体：bs-0470R
Anti-Osteocalcin pAb; IHC

作者单位：上海交通大学医学院,上海市第九人民医院口腔种植科

摘要：Metabolic energy to steer osteoblastic differentiation of bone marrow mesenchymal stem cells (BMSCs) could be a promising therapeutic target for bone tissue engineering (BTE), but prior knowledge of this issue is limited. To address bone defects with BTE, we customized a three-dimensional (3D)-printed composite scaffold (Cur@MS) to allow the controlled release of curcumin, which could facilitate the “switch-on” mode of Glucose transporter 1 (GLUT1) in BMSCs. Consequently, bioenergetic channels, i.e. glucose uptake, were “switched on” to activate GLUT1-RUNX2 crosstalk, which was closely orchestrated with bone regeneration. Furthermore, curcumin-induced cholesterol/lipid raft (Cho/LR) was a “sensor” to trigger the “switch” (GLUT1) by directing its spatial distribution into clusters. In contrast, selective inhibition of Cho/LR and GLUT1 led to a “switch-off” mode and compromised bone regeneration in vivo. Overall, the results suggest Cho/LR is a potential target to steer BMSCs and Cur@MS is an ideal BTE material for stimulating rapid bone regeneration.
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