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    【4月文獻戰報】Bioss抗體新增高分文獻精彩呈現-北京博奧森生物技術有限公司
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    【4月文獻戰報】Bioss抗體新增高分文獻精彩呈現
    發表者:北京博奧森生物      發表時間:2022-5-20

    截止目前,引用Bioss產品發表的文獻共18150,總影響因子78229.601分,發表在Nature/Science/Cell/Immunity等頂級期刊的文獻共52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。

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    近期收錄2022年4月引用 Bioss 產品發表的文獻200篇(圖一),文章影響因子總和高達1110.664分,其中10分以上文獻有13篇,20分以上文獻有2篇(圖二)。

    圖一


    圖二

    Bioss 小編與您一起分享來自 Nature Nanotechnology/Immunity/Cancer Cell 等期刊的6篇 IF>10的文獻摘要,讓我們欣賞吧。


    Cell Metabolism [IF=27.287]

    文獻引用抗體

    bsm-0978M (Anti-GAPDH mAb; WB)

    作者單位:韓國首爾國立大學生物科學學院,分子生物學與遺傳學研究所,脂肪細胞結構與功能中心

    摘要:Emerging evidence indicates that the accretion of senescent cells is linked to metabolic disorders. However, the underlying mechanisms and metabolic consequences of cellular senescence in obesity remain obscure. In this study, we found that obese adipocytes are senescence-susceptible cells accompanied with genome instability. Additionally, we discovered that SREBP1c may play a key role in genome stability and senescence in adipocytes by modulating DNA-damage responses. Unexpectedly, SREBP1c interacted with PARP1 and potentiated PARP1 activity during DNA repair, independent of its canonical lipogenic function. The genetic depletion of SREBP1c accelerated adipocyte senescence, leading to immune cell recruitment into obese adipose tissue. These deleterious effects provoked unhealthy adipose tissue remodeling and insulin resistance in obesity. In contrast, the elimination of senescent adipocytes alleviated adipose tissue inflammation and improved insulin resistance. These findings revealed distinctive roles of SREBP1c-PARP1 axis in the regulation of adipocyte senescence and will help decipher the metabolic significance of senescence in obesity.



    Autophagy [IF=16.016]

    文獻引用抗體

    bs-1353R (Anti-BECN1 pAb; IF)

    bs-0295D-AF555 (Donkey Anti-rabbit IgG H&L/AF555; IF)

    bs-0296R-AF488 (Rabbit Anti-Mouse IgG H&L/AF488; IF)

    作者單位:華中農業大學動物科學與獸醫學院干細胞與再生生物學研究所

    摘要:Macroautophagy/autophagy is a cellular and energy homeostatic mechanism that contributes to maintain the number of primordial follicles, germ cell survival, and anti-ovarian aging. However, it remains unknown whether autophagy in granulosa cells affects oocyte maturation. Here, we show a clear tendency of reduced autophagy level in human granulosa cells from women of advanced maternal age, implying a potential negative correlation between autophagy levels and oocyte quality. We therefore established a co-culture system and show that either pharmacological inhibition or genetic ablation of autophagy in granulosa cells negatively affect oocyte quality and fertilization ability. Moreover, our metabolomics analysis indicates that the adverse impact of autophagy impairment on oocyte quality is mediated by downregulated citrate levels, while exogenous supplementation of citrate can significantly restore the oocyte maturation. Mechanistically, we found that ACLY (ATP citrate lyase), which is a crucial enzyme catalyzing the cleavage of citrate, was preferentially associated with K63-linked ubiquitin chains and recognized by the autophagy receptor protein SQSTM1/p62 for selective autophagic degradation. In human follicles, the autophagy level in granulosa cells was downregulated with maternal aging, accompanied by decreased citrate in the follicular fluid, implying a potential correlation between citrate metabolism and oocyte quality. We also show that elevated citrate levels in porcine follicular fluid promote oocyte maturation. Collectively, our data reveal that autophagy in granulosa cells is a beneficial mechanism to maintain a certain degree of citrate by selectively targeting ACLY during oocyte maturation.



    JCI【IF=14.808】

    文獻引用抗體

    bs-5758R (Anti-FAP pAb; IF)

    作者單位:日本愛媛大學高級研究支持中心實驗動物研究部

    摘要:Rheumatoid arthritis (RA) is characterized by chronic synovial inflammation with aberrant epigenetic alterations, eventually leading to joint destruction. However, the epigenetic regulatory mechanisms underlying RA pathogenesis remain largely unknown. Here we showed that Ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) is a central epigenetic regulator that suppressively orchestrates multiple pathogeneses in RA. UHRF1 expression was remarkably up-regulated in synovial fibroblasts (SF) from arthritis model mice and RA patients. Mice with SF-specific Uhrf1 conditional knockout showed more severe arthritic phenotypes than littermate control. Uhrf1-deficient SF also exhibited enhanced apoptosis resistance and up-regulated expression of several cytokines including Ccl20. In RA patients, DAS28, CRP, and Th17 accumulation as well as apoptosis resistance were negatively correlated with UHRF1 expression in synovium. Finally, Ryuvidine administration that stabilizes UHRF1 ameliorated arthritis pathogeneses in a mouse model of RA. This study demonstrated that UHRF1 expressed in RA SF can contribute to negative feedback mechanisms that suppress multiple pathogenic events in arthritis, suggesting that targeting UHRF1 could be one of the therapeutic strategies for RA.



    CEJ【IF=13.273】

    文獻引用抗體

    bs-6194R (Anti-Sclerostin pAb; Other)

    作者單位:云南昆明醫科大學干細胞與再生醫學重點實驗室,科技成果孵化中心

    摘要:Biomaterial-based tissue engineering has emerged as a hotspot in the field of osteanagenesis. Due to invasive operation in the transplantation process always bring irreparable damage to patients, approaches that enable innate repair mechanisms hold considerable promise for bone repair. To this end, a rational design based on in situ recruitment of stem cells is proposed to circumvent the troublesome problem. In this study, an interpenetration network hydrogel is developed utilizing chitosan (CS), in which the enriched bone marrow mesenchymal stem cells (BMSCs) can undergo a tridimensional and freely proliferation. Moreover, the encapsulation of biological growth factor Wnt3a promotes the differentiation of osteoprogenitor cells with an asymmetric cell divisions (ACD) manner, thereby accelerating bone formation. With this “smart biomaterials”, a robust instant stem cell ingrowth within the deformable hydrogel and a high efficiency of bone regeneration on a murine skull are observed, both of which are vital for clinical applications. Such an osteoinductive system represents the advanced design concept to repair bone defects effectively, and offers a promising strategy for the development of future bone tissue engineering.



    JPR【IF=13.007】

    文獻引用抗體

    bs-0027R (Anti-MT1 pAb; WB, IHC)

    bs-0963R (Anti-MT2 pAb; WB, IHC)

    作者單位:中山大學中山眼科中心眼科國家重點實驗室,廣東省眼科與視覺科學重點實驗

    摘要:Central serous chorioretinopathy (CSC) is a vision-threatening disease with no validated treatment and unclear pathogenesis. It is characterized by dilation and leakage of choroidal vasculature, resulting in the accumulation of subretinal fluid, and serous detachment of the neurosensory retina. Numerous studies have demonstrated that melatonin had multiple protective effects against endothelial dysfunction, vascular inflammation, and blood–retinal barrier (BRB) breakdown. However, the effect of melatonin on CSC, and its exact pathogenesis, is not well understood thus far. In this study, an experimental model was established by intravitreal injection of aldosterone in rats, which mimicked the features of CSC. Our results found that melatonin administration in advance significantly inhibited aldosterone-induced choroidal thickening and vasodilation by reducing the expression of calcium-activated potassium channel KCa2.3, and attenuated tortuosity of choroid vessels. Moreover, melatonin protected the BRB integrity and prevented the decrease in tight junction protein (ZO-1, occludin, and claudin-1) levels in the rat model induced by aldosterone. Additionally, the data also showed that intraperitoneal injection of melatonin in advance inhibited aldosterone-induced macrophage/microglia infiltration, and remarkably diminished the levels of inflammatory cytokines (interleukin-6 [IL-6], IL-1β, and cyclooxygenase-2), chemokines (chemokine C–C motif ligand 3, and C–X–C motif ligand 1), and matrix metalloproteinases (MMP-2 and MMP-9). Luzindole, as the nonselective MT1 and MT2 antagonist, and 4-phenyl-2-propionamidotetraline, as the selective MT2 antagonist, neutralized the melatonin-induced inhibition of choroidal thickening and choroidal vasodilation, indicating that melatonin might exert the effects via binding to its receptors. Furthermore, the IL-17A/nuclear factor-κB signaling pathway was activated by intravitreal administration of aldosterone, while it was suppressed in melatonin-treated in advance rat eyes. This study indicates that melatonin could serve as a promising safe therapeutic strategy for CSC patients.



    APSB【IF=11.413】


    文獻引用抗體

    bs-0296G-PE (Goat Anti-Mouse IgG H&L/PE; FCM)

    作者單位:武漢大學基礎醫學學院藥理學系

    摘要:Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide and macrophage polarization plays an important role in its pathogenesis. However, which molecule regulates macrophage polarization in NAFLD remains unclear. Herein, we showed NAFLD mice exhibited increased 17β-hydroxysteroid dehydrogenase type 7 (17β-HSD7) expression in hepatic macrophages concomitantly with elevated M1 polarization. Single-cell RNA sequencing on hepatic non-parenchymal cells isolated from wild-type littermates and macrophage-17β-HSD7 knockout mice fed with high fat diet (HFD) for 6 weeks revealed that lipid metabolism pathways were notably changed. Furthermore, 17β-HSD7 deficiency in macrophages attenuated HFD-induced hepatic steatosis, insulin resistance and liver injury. Mechanistically, 17β-HSD7 triggered NLRP3 inflammasome activation by increasing free cholesterol content, thereby promoting M1 polarization of macrophages and the secretion of pro-inflammatory cytokines. In addition, to help demonstrate that 17β-HSD7 is a potential drug target for NAFLD, fenretinide was screened out from an FDA-approved drug library based on its 17β-HSD7 dehydrogenase inhibitory activity. Fenretinide dose-dependently abrogated macrophage polarization and pro-inflammatory cytokines production, and subsequently inhibited fat deposition in hepatocytes co-cultured with macrophages. In conclusion, our findings suggest that blockade of 17β-HSD7 signaling by fenretinide would be a drug repurposing strategy for NAFLD treatment.

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