截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共31610篇，總影響因子154046.6分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻(xiàn)共108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)等國際知名研究機(jī)構(gòu)上百所。
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近期收錄2024年9月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共361篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)2253.2，其中，10分以上文獻(xiàn)52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Cancer Cell, Cell, Immunity, Nature Microbiology等期刊的 9篇 IF＞15的文獻(xiàn)摘要，讓我們一起欣賞吧。
Cancer Cell [IF=48.8]
文獻(xiàn)引用產(chǎn)品：
S0134 | Alcian Blue Stain Kit (pH 2.5) | Other
作者單位：中山大學(xué)附屬第一醫(yī)院
摘要：Microsatellite stable (MSS) colorectal cancers (CRCs) are often resistant to anti-programmed death-1 (PD-1) therapy. Here, we show that a CRC pathogen, Fusobacterium nucleatum (Fn), paradoxically sensitizes MSS CRC to anti-PD-1. Fecal microbiota transplantation (FMT) from patients with Fn-high MSS CRC to germ-free mice bearing MSS CRC confers sensitivity to anti-PD-1 compared to FMT from Fn-low counterparts. Single Fn administration also potentiates anti-PD-1 efficacy in murine allografts and CD34+-humanized mice bearing MSS CRC. Mechanistically, we demonstrate that intratumoral Fn generates abundant butyric acid, which inhibits histone deacetylase (HDAC) 3/8in CD8+ T cells, inducing Tbx21 promoter H3K27 acetylation and expression. TBX21 transcriptionally represses PD-1, alleviating CD8+ T cell exhaustion and promoting effector function. Supporting this notion, knockout of a butyric acid-producing gene in Fn abolishes its anti-PD-1 boosting effect. In patients with MSS CRC, high intratumoral Fn predicts favorable response to anti-PD-1 therapy, indicating Fn as a potential biomarker of immunotherapy response in MSS CRC.
CELL [IF=45.5]
文獻(xiàn)引用產(chǎn)品：
bs-2177R | Glypican 6 Rabbit pAb |IF
bs-11832R | Cux2 Rabbit pAb | IF
作者單位：美國加州大學(xué)
摘要：The development of successful therapeutics for dementias requires an understanding of their shared and distinct molecular features in the human brain. We performed single-nuclear RNA-seq and ATAC-seq in Alzheimer’s disease (AD), frontotemporal dementia (FTD), and progressive supranuclear palsy (PSP), analyzing 41 participants and ～1 million cells (RNA + ATAC) from three brain regions varying in vulnerability and pathological burden. We identify 32 shared, disease-associated cell types and 14 that are disease specific. Disease-specific cell states represent glial-immune mechanisms and selective neuronal vulnerability impacting layer 5 intratelencephalic neurons in AD, layer 2/3 intratelencephalic neurons in FTD, and layer 5/6 near-projection neurons in PSP. We identify disease-associated gene regulatory networks and cells impacted by causal genetic risk, which differ by disorder. These data illustrate the heterogeneous spectrum of glial and neuronal compositional and gene expression alterations in different dementias and identify therapeutic targets by revealing shared and disease-specific cell states.
CELL [IF=45.5]
文獻(xiàn)引用產(chǎn)品：
bs-1012R | BMP2 Rabbit pAb | WB, IHC
bs-5180R | AXL Rabbit pAb | WB, IHC
bsm-52179R | phospho-Nrf2 (Ser40) Recombinant Rabbit mAb | IHC
bs-8687R | p53 (FL-393) Rabbit pAb | WB
bs-1990R | MITF Rabbit pAb | IHC
作者單位：約翰霍普金斯大學(xué)
摘要：There is documented sex disparity in cutaneous melanoma incidence and mortality, increasing disproportionately with age and in the male sex. However, the underlying mechanisms remain unclear. While biological sex differences and inherent immune response variability have been assessed in tumor cells, the role of the tumor-surrounding microenvironment, contextually in aging, has been overlooked. Here, we show that skin fibroblasts undergo age-mediated, sex-dependent changes in their proliferation, senescence, ROS levels, and stress response. We find that aged male fibroblasts selectively drive an invasive, therapy-resistant phenotype in melanoma cells and promote metastasis in aged male mice by increasing AXL expression. Intrinsic aging in male fibroblasts mediated by EZH2 decline increases BMP2 secretion, which in turn drives the slower-cycling, highly invasive, and therapy-resistant melanoma cell phenotype, characteristic of the aged male TME. Inhibition of BMP2 activity blocks the emergence of invasive phenotypes and sensitizes melanoma cells to BRAF/MEK inhibition.
Immunity [IF=25.5]
文獻(xiàn)引用產(chǎn)品：
bs-15186R-A647 | C4a+C4b Rabbit pAb | WB, IF
bs-10750R-A647 | C1QA Rabbit pAb | WB, IF (產(chǎn)品已升級為貨號bs-11336R）
bs-10750R-A488 | C1QA Rabbit pAb | WB, IF (產(chǎn)品已升級為貨號bs-11336R）
bs-0367G-A647 | Complement C3 Goat pAb | WB, IF
bs-7527R | FAIM3 Rabbit pAb | WB, IF
作者單位：德國慕尼黑大學(xué)醫(yī)院
摘要：Venous thromboembolism (VTE) is a common, deadly disease with an increasing incidence despite preventive efforts. Clinical observations have associated elevated antibody concentrations or antibody-based therapies with thrombotic events. However, how antibodies contribute to thrombosis is unknown. Here, we show that reduced blood flow enabled immunoglobulin M (IgM) to bind to FcμR and the polymeric immunoglobulin receptor (pIgR), initiating endothelial activation and platelet recruitment. Subsequently, the procoagulant surface of activated platelets accommodated antigen- and FcγR-independent IgG deposition. This leads to classical complement activation, setting in motion a prothrombotic vicious circle. Key elements of this mechanism were present in humans in the setting of venous stasis as well as in the dysregulated immunothrombosis of COVID-19. This antibody-driven thrombosis can be prevented by pharmacologically targeting complement. Hence, our results uncover antibodies as previously unrecognized central regulators of thrombosis. These findings carry relevance for therapeutic application of antibodies and open innovative avenues to target thrombosis without compromising hemostasis.
Nature Microbiology [IF=20.5]
文獻(xiàn)引用產(chǎn)品：
bs-0403R | Rabbit Anti-MG IgG H&L | WB
作者單位：英國斯特拉斯克萊德大學(xué)
摘要：Parasitic nematodes have an intimate, chronic and lifelong exposure to vertebrate tissues. Here we mined 41 published parasitic nematode transcriptomes from vertebrate hosts and identified 91 RNA viruses across 13 virus orders from 24 families in ~70% (28 out of 41) of parasitic nematode species, which include only 5 previously reported viruses. We observe widespread distribution of virus–nematode associations across multiple continents, suggesting an ancestral acquisition event and host–virus co-evolution. Characterization of viruses of Brugia malayi (BMRV1) and Onchocerca volvulus (OVRV1) shows that these viruses are abundant in reproductive tissues of adult parasites. Importantly, the presence of BMRV1 RNA in B. malayi parasites mounts an RNA interference response against BMRV1 suggesting active viral replication. Finally, BMRV1 and OVRV1 were found to elicit antibody responses in serum samples from infected jirds and infected or exposed humans, indicating direct exposure to the immune system.
Nature Microbilogy [IF=20.5]
文獻(xiàn)引用產(chǎn)品：
bs-0812R | IL-1 Beta Rabbit pAb | IHC
作者單位：香港理工大學(xué)
摘要：Joint pain and osteoarthritis can occur as coronavirus disease 2019 (COVID-19) sequelae after infection. However, little is known about the damage to articular cartilage. Here we illustrate knee joint damage after wild-type, Delta and Omicron variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in vivo. Rapid joint injury with cystic lesions at the osteochondral junction was observed in two patients with post-COVID osteoarthritis and recapitulated in a golden Syrian hamster model. SARS-CoV-2-activated endothelin-1 signalling increased vascular permeability and caused viral spike proteins leakage into the subchondral bone. Osteoclast activation, chondrocyte dropout and cyst formation were confirmed histologically. The US Food and Drug Administration-approved endothelin receptor antagonist, macitentan, mitigated cystic lesions and preserved chondrocyte number in the acute phase of viral infection in hamsters. Delayed macitentan treatment at post-acute infection phase alleviated chondrocyte senescence and restored subchondral bone loss. It is worth noting that it could also attenuate viral spike-induced joint pain. Our work suggests endothelin receptor blockade as a novel therapeutic strategy for post-COVID arthritis.
Advanced Functional Materials [IF=19.0]
文獻(xiàn)引用產(chǎn)品：
bs-4727R | MRC1 Rabbit pAb | FC
作者單位：藥物化學(xué)生物學(xué)國家重點(diǎn)實(shí)驗(yàn)室
摘要：Modulating inflammation is crucial for repairing vascular injury. Phagocytosis of apoptotic cells represents an effective mechanism for attenuating inflammation and improving regeneration during natural healing. However, strategies for repairing vascular injuries using biomaterials derived from apoptotic cells are still undeveloped. Herein, apoptotic body-mimetic nanovesicles (ApoNVs) derived from rat adipose-derived mesenchymal stem cells (rASCs) are prepared using a one-step extrusion method. ApoNVs inherit the unique anti-inflammatory and pro-regenerative properties of the parental apoptotic rASCs, as evidenced by enhanced M2 polarization of macrophages and promoted endothelial cell proliferation and migration following treatment with ApoNVs. Moreover, ApoNVs enhance the contractile phenotype of vascular smooth muscle cells through the mediation of ApoNVs-induced repolarized macrophages. After engineering ApoNVs with P-selectin binding peptide (ApoNVs-PBP), their ability to target injured artery increased nearly sevenfold compared to unmodified ApoNVs. In a rat wire-mediated femoral artery injury model, ApoNVs-PBP effectively suppress inflammation and significantly reduce blood flow velocity and neointimal hyperplasia at the injury site. ApoNVs exhibit similar therapeutic effects, though to a lesser extent. This study provides strong evidence validating the targeted delivery of ApoNVs as an innovative approach for repairing vascular injury and highlights their potential in treating other inflammatory diseases.
Advanced Fiber Materials [IF=17.2]
文獻(xiàn)引用產(chǎn)品：
bs-1134R | RUNX2 Rabbit pAb | IHC
bs-4917R | Osteocalcin Rabbit pAb | IHC
作者單位：青島大學(xué)附屬醫(yī)院
摘要：The development of biomimetic scaffolds that can promote osteogenic induction and vascularization is of great importance for the repair of large bone defects. In the present study, inorganic bioactive glass (BG) and organic polycaprolactone (PCL) are effectively combined by electrospinning and electrospray techniques to construct three-dimensional (3D) BG/PCL microfibrous spheres for the repair of bulk bone defects. The hybrid fibers, as well as the as-obtained 3D structure, can mimic the composition and architecture of native bone tissues. Furthermore, the BG/PCL microfibrous spheres show excellent biocompatibility and provide sufficient space and attachment sites for cell growth. The osteogenic differentiation of bone mesenchymal stem cells is also effectively facilitated when cultured on such hybrid microfibrous spheres. In vivo investigation utilizing rat femoral condyle bone defect models demonstrates that the BG/PCL microfibrous spheres loaded with bone mesenchymal stem cells can induce angiogenesis and promote the upregulation of bone-related protein expression, thus effectively facilitating bone regeneration at the defect site. The collective findings indicate that such BG/PCL hybrid microfibrous spheres have the potential to be effective carriers of stem cells. The microfibrous spheres loaded with stem cells have promising potential to be utilized as implantable biomaterials for the repair of bone defects.
ACS Nano [IF=15.8]
文獻(xiàn)引用產(chǎn)品：
bs-5913R-FITC | Calreticulin Rabbit pAb, FITC conjugated | IF, FC
bs-5913R-BF488 | Calreticulin Rabbit pAb, BF488 conjugated | IF, FC
作者單位：中國科學(xué)院上海藥物研究所
摘要：The refractory luminal androgen receptor (LAR) subtype of triple-negative breast cancer (TNBC) patients is challenged by significant resistance to neoadjuvant chemotherapy and increased immunosuppression. Regarding the distinct upregulation of glutathione (GSH) and glutathione peroxidase 4 (GPX4) in LAR TNBC tumors, we herein designed a GSH-depleting phospholipid derivative (BPP) and propose a BPP-based nanotherapeutics of RSL-3 (GDNS), aiming to deplete intracellular GSH and repress GPX4 activity, thereby potentiating ferroptosis for treating LAR-subtype TNBC. GDNS treatment drastically downregulated the expression of GSH and GPX4, resulting in a 33.88-fold enhancement of lipid peroxidation and significant relief of immunosuppression in the 4T1 TNBC model. Moreover, GDNS and its combination with antibody against programed cell death protein 1 (antiPD-1) retarded tumor growth and produced 2.83-fold prolongation of survival in the LAR-positive TNBC model. Therefore, the GSH-disrupting GDNS represents an encouraging strategy to potentiate ferroptosis for treating refractory LAR-subtype TNBC.
