【文獻戰報】Bioss抗體新增高分文獻精彩呈現-商家動態-資訊-生物在線

【文獻戰報】Bioss抗體新增高分文獻精彩呈現

作者:北京博奧森生物技術有限公司 2022-03-16T10:18 (訪問量:5396)

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文獻戰報


我們每月定期收集引用 Bioss產品發表的文獻。截止目前,引用Bioss產品發表的文獻共16533篇,總影響因子70371.348分,發表在Nature / Science / Cell 以及 Immunity 頂級期刊的文獻共47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知名研究機構上百所。
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,也請致電我們,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。

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近期收錄 2022 年2 月引用 Bioss 產品發表的文獻211篇(圖一,綠色柱),文章影響因子 (IF) 總和:1189.69,25分以上文獻:1篇,10分以上文獻:19篇(圖二)。

圖一


圖二

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本文分享來自 Nature Nanotechnology / Immunity / Cancer Cell 等期刊的10篇 IF>10的文獻摘要,讓我們一起欣賞這些文章吧。

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文獻 1

[IF=25.606] Nature Immunology
DOI: 10.1038/s41590-022-01145-x
文獻引用抗體: bs-3330R | Anti-p-PERK(T980) pAb | FCM
Institution: 美國俄亥俄州克利夫蘭凱斯西儲大學醫學院病理學系
Abstract: Chronic inflammation triggers compensatory immunosuppression to stop inflammation and minimize tissue damage. Studies have demonstrated that endoplasmic reticulum (ER) stress augments the suppressive phenotypes of immune cells; however, the molecular mechanisms underpinning this process and how it links to the metabolic reprogramming of immunosuppressive macrophages remain elusive. In the present study, we report that the helper T cell 2 cytokine interleukin-4 and the tumor microenvironment increase the activity of a protein kinase RNA-like ER kinase (PERK)-signaling cascade in macrophages and promote immunosuppressive M2 activation and proliferation. Loss of PERK signaling impeded mitochondrial respiration and lipid oxidation critical for M2 macrophages. PERK activation mediated the upregulation of phosphoserine aminotransferase 1 (PSAT1) and serine biosynthesis via the downstream transcription factor ATF-4. Increased serine biosynthesis resulted in enhanced mitochondrial function and α-ketoglutarate production required for JMJD3-dependent epigenetic modification. Inhibition of PERK suppressed macrophage immunosuppressive activity and could enhance the efficacy of immune checkpoint programmed cell death protein 1 inhibition in melanoma. Our findings delineate a previously undescribed connection between PERK signaling and PSAT1-mediated serine metabolism critical for promoting immunosuppressive function in M2 macrophages.






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文獻 2

[IF=17.173] Neuron
DOI: 10.1016/j.neuron.2022.01.012
文獻引用抗體bs-11410R | Anti-mPRβ (PAQR8) pAb | Other
Institution : 法國巴黎索邦大學,巴黎腦研究所
Abstract : Optimizing reproductive fitness in mammalians requires behavioral adaptations during pregnancy. Maternal preparatory nesting is an essential behavior for the survival of the upcoming litter. Brain-wide immediate early gene mapping in mice evoked by nesting sequences revealed that phases of nest construction strongly activate peptidergic neurons of the Edinger-Westphal nucleus in pregnant mice. Genetic ablation, bidirectional neuromodulation, and in vitro and in vivo activity recordings demonstrated that these neurons are essential to modulate arousal before sleep to promote nesting specifically. We show that these neurons enable the behavioral effects of progesterone on preparatory nesting by modulating a broad network of downstream targets. Our study deciphers the role of midbrain CART+ neurons in behavioral adaptations during pregnancy vital for reproductive fitness.






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文獻 3

[IF=16.806] Advanced Science
DOI: 10.1002/advs.202104888
文獻引用抗體bs-1806R | Anti-UTS2R pAb | ICC,IF
Institution : 中國科學院大學,上海生物化學與細胞生物學研究所,分子細胞科學卓越中心,細胞生物學國家重點實驗室
Abstract : ntervertebral disc degeneration (IDD) results from the dysfunction of nucleus pulposus (NP) cells and the exhaustion of NP progenitors (ProNPs). The cellular applications of NP cells during IDD are currently limited due to the lack of in vivo studies showing whether NP cells are heterogeneous and contain ProNPs throughout postnatal stages. In this study, single-cell RNA sequencing of purified NP cells is used to map four molecularly defined populations and urotensin II receptor (UTS2R)-expressing postnatal ProNPs is identified, which are markedly exhausted during IDD, in mouse and human specimens. The lineage tracing shows that UTS2R+ProNPs preferentially resides in the NP periphery with its niche factor tenascin-C and give rise to functional NP cells. It is also demonstrated that transplanting UTS2R+ProNPs with tenascin-C into injured intervertebral discs attenuate the progression of IDD. The study provides a novel NP cell atlas, identified resident ProNPs with regenerative potential, and revealed promising diagnostic and therapeutic targets for IDD.






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文獻 4

[IF=16.806] Advanced Science
DOI: 10.1002/advs.202104469
文獻引用抗體bs-5791R-Bio | Anti-Integrin Alpha V + Beta 6/Biotin pAb | IHC,IF

Institution : 美國約翰霍普金斯大學醫學院骨外科

Abstract : Tendinopathy is a common tendon disorder that causes pain and impairs function. It is the most common reason for consultation with musculoskeletal specialists. The available therapies for tendinopathy are limited in number and efficacy and have unclear cellular and molecular mechanisms. Here it is shown that transforming growth factor-beta (TGF-β) activated by integrin αvβ6 promotes tendinopathy in mice. Excessive active TGF-β is found during tendinopathy progression, which led to tenocytes’ phenotype transition to chondrocytes. Transgenic expression of active TGF-β in tendons induced spontaneous tendinopathy, whereas systemic injection of a TGF-β neutralizing antibody attenuated tendinopathy. Inducible knockout of the TGF-β type 2 receptor gene (Tgfbr2) in tenocytes inhibited tendinopathy progression in mice. Moreover, it is found that integrin αvβ6 induces TGF-β activation in response to mechanical load in tendons. Conditional knockout of the integrin αv gene in tendons prevented tendinopathy in mice. The study suggests that integrin αvβ6 activation of TGF-β is the mechanism of tendinopathy, and that integrin αvβ6 may be a therapeutic target in tendinopathy.






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文獻 5

[IF=15.881] ACS Nano
DOI: 10.1021/acsnano.1c08913
文獻引用抗體
bs-1278R | Anti-8-OHdG/DNA/RNA damage pAb | Other
bs-8551R | Anti-3-nitrotyrosine pAb | Other
Institution : 中南大學湘雅藥學院
Abstract : Sepsis, a life-threating illness caused by deregulated host immune responses to infections, is characterized by overproduction of multiple reactive oxygen and nitrogen species (RONS) and excessive pyroptosis, leading to high mortality. However, there is still no approved specific molecular therapy to treat sepsis. Here we reported drug-free tea polyphenols nanoparticles (TPNs) with intrinsic broad-spectrum RONS scavenging and pyroptosis-blocking activities to treat endotoxin (LPS)-induced sepsis in mice. The RONS scavenging activities originated from the polyphenols-derived structure, while the pyroptosis blockage was achieved by inhibiting gasdermin D (GSDMD) mediating the pore formation and membrane rupture, showing multifunctionalities for sepsis therapy. Notably, TPNs suppress GSDMD by inhibiting the oligomerization of GSDMD rather than the cleavage of GSDMD, thus displaying high pyroptosis-inhibition efficiency. As a result, TPNs showed an excellent therapeutic efficacy in sepsis mice model, as evidenced by survival rate improvement, hypothermia amelioration, and the organ damage protection. Collectively, TPNs present biocompatible candidates for the treatment of sepsis.






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文獻 6

[IF=14.919] Nature Communications
DOI: 10.1038/s41467-022-28533-z
文獻引用抗體bs-1629R | Anti-CXCR2 pAb | Other
Institution : 新加坡國立大學楊潞齡醫學院生理學系
Abstract : Hand, foot and mouth disease (HFMD) caused by Human Enterovirus A71 (HEVA71) infection is typically a benign infection. However, in minority of cases, children can develop severe neuropathology that culminate in fatality. Approximately 36.9% of HEVA71-related hospitalizations develop neurological complications, of which 10.5% are fatal. Yet, the mechanism by which HEVA71 induces these neurological deficits remain unclear. Here, we show that HEVA71-infected astrocytes release CXCL1 which supports viral replication in neurons by activating the CXCR2 receptor-associated ERK1/2 signaling pathway. El
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