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當前位置:首頁  >  新聞資訊  >  【8月文獻戰報】Bioss抗體新增高分文獻精彩呈現

【8月文獻戰報】Bioss抗體新增高分文獻精彩呈現

更新時間:2023-10-17  |  點擊率:138




截止目前,引用Bioss產品發表的文獻共26093篇,總影響因子123723.87分,發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共60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2023年8月引用Bioss產品發表的文獻共304篇(圖一,綠色柱),文章影響因子(IF) 總和高達1925.1,其中,10分以上文獻36篇(圖二)。

圖一


圖二




本文主要分享引用Bioss產品發表文章至Nature NanotechnologyImmunityCancer Cell等期刊的4篇 IF>15 的文獻摘要,讓我們一起欣賞吧。




Nature [IF=64.8]



文獻引用產品:bs-0737R-AF488

HIF-1 Alpha/AF488 pAb | FCM

作者單位:哈佛大學醫學院

摘要:Dendritic cells (DCs) have a role in the development and activation of self-reactive pathogenic T cells. Genetic variants that are associated with the function of DCs have been linked to autoimmune disorders, and DCs are therefore attractive therapeutic targets for such diseases. However, developing DC-targeted therapies for autoimmunity requires identification of the mechanisms that regulate DC function. Here, using single-cell and bulk transcriptional and metabolic analyses in combination with cell-specific gene perturbation studies, we identify a regulatory loop of negative feedback that operates in DCs to limit immunopathology. Specifically, we find that lactate, produced by activated DCs and other immune cells, boosts the expression of NDUFA4L2 through a mechanism mediated by hypoxia-inducible factor 1α (HIF-1α). NDUFA4L2 limits the production of mitochondrial reactive oxygen species that activate XBP1-driven transcriptional modules in DCs that are involved in the control of pathogenic autoimmune T cells. We also engineer a probiotic that produces lactate and suppresses T cell autoimmunity through the activation of HIF-1α–NDUFA4L2 signalling in DCs. In summary, we identify an immunometabolic pathway that regulates DC function, and develop a synthetic probiotic for its therapeutic activation.


Nature Communications

[IF=16.6]



文獻引用抗體:bs-0086R

TGF beta 1 Rabbit pAb | IF

作者單位:夕法尼亞大學

摘要:The desmoplastic stroma in solid tumors presents a formidable challenge to immunotherapies that rely on endogenous or adoptively transferred T cells, however, the mechanisms are poorly understood. To define mechanisms involved, here we treat established desmoplastic pancreatic tumors with CAR T cells directed to fibroblast activation protein (FAP), an enzyme highly overexpressed on a subset of cancer-associated fibroblasts (CAFs). Depletion of FAP+ CAFs results in loss of the structural integrity of desmoplastic matrix. This renders these highly treatment-resistant cancers susceptible to subsequent treatment with a tumor antigen (mesothelin)-targeted CAR T cells and to anti-PD-1 antibody therapy. Mechanisms include overcoming stroma-dependent restriction of T cell extravasation and/or perivascular invasion, reversing immune exclusion, relieving T cell suppression, and altering the immune landscape by reducing myeloid cell accumulation and increasing endogenous CD8+ T cell and NK cell infiltration. These data provide strong rationale for combining tumor stroma- and malignant cell-targeted therapies to be tested in clinical trials.



Nature Communications

 [IF=16.6]


文獻引用抗體:D10746

Fibrinogen (from Rat plasma)

作者單位:川大學

摘要:Clinical use of intraoperative auto-transfusion requires the removal of platelets and plasma proteins due to pump-based suction and water-soluble anticoagulant administration, which causes dilutional coagulopathy. Herein, we develop a carboxylated and sulfonated heparin-mimetic polymer-modified sponge with spontaneous blood adsorption and instantaneous anticoagulation. We find that intrinsic coagulation factors, especially XI, are inactivated by adsorption to the sponge surface, while inactivation of thrombin in the sponge-treated plasma effectively inhibits the common coagulation pathway. We show whole blood auto-transfusion in trauma-induced hemorrhage, benefiting from the multiple inhibitory effects of the sponge on coagulation enzymes and calcium depletion. We demonstrate that the transfusion of collected blood favors faster recovery of hemostasis compared to traditional heparinized blood in a rabbit model. Our work not only develops a safe and convenient approach for whole blood auto-transfusion, but also provides the mechanism of action of self-anticoagulant heparin-mimetic polymer-modified surfaces.

BRAIN BEHAVIOR AND

IMMUNITY [IF=15.1]


文獻引用產品:bs-0480R

IFN gamma Rabbit pAb | IF

作者單位:康涅狄格大學

摘要:

Background

Alzheimer’s disease (AD) is the most common cause of dementia in older adults and characterized by progressive loss of memory and cognitive functions that are associated with amyloid-beta (Aβ) plaques and neurofibrillary tangles. Immune cells play an important role in the clearance of Aβ deposits and neurofibrillary tangles. T cells are the major component of the immune system. The thymus is the primary organ for T cell generation. T cell development in the thymus depends on thymic epithelial cells (TECs). However, TECs undergo both qualitative and quantitative loss over time. We have previously reported that a recombinant (r) protein containing FOXN1 and a protein transduction domain can increase the number of TECs and subsequently increases the number of T cells in mice. In this study we determined the ability of rFOXN1 to affect cognitive performance and AD pathology in mice.

Methods

Aged 3xTg-AD and APP/PS1 AD mice were injected with rFOXN1 or control protein. Cognitive performance, AD pathology, the thymic microenvironment and immune cells were then analyzed.

Results

Administration of rFOXN1 into AD mice improves cognitive performance and reduces Aβ plaque load and phosphorylated tau in the brain...

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