截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共24976篇，總影響因子117637.69分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻(xiàn)共59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2023年5月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共277篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)1876.807，其中，10分以上文獻(xiàn)39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Nature Nanotechnology, Immunity, Cancer Cell等期刊的7篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。
Signal Transduction and Targeted Therapy [IF=38.104]
文獻(xiàn)引用抗體：bs-4888R；Anti-Phospho-PPAR Gamma (ser273) pAb | WB
作者單位：清華大學(xué)生命科學(xué)學(xué)院
摘要：3-Hydroxybutyrate (3HB) is a small ketone body molecule produced endogenously by the body in the liver. Previous studies have shown that 3HB can reduce blood glucose level in type 2 diabetic (T2D) patients. However, there is no systematic study and clear mechanism to evaluate and explain the hypoglycemic effect of 3HB. Here we demonstrate that 3HB reduces fasting blood glucose level, improves glucose tolerance, and ameliorates insulin resistance in type 2 diabetic mice through hydroxycarboxylic acid receptor 2 (HCAR2). Mechanistically, 3HB increases intracellular calcium ion (Ca2+) levels by activating HCAR2, thereby stimulating adenylate cyclase (AC) to increase cyclic adenosine monophosphate (cAMP) concentration, and then activating protein kinase A (PKA). Activated PKA inhibits Raf1 proto-oncogene serine/threonine-protein kinase (Raf1) activity, resulting in a decrease in extracellular signal-regulated kinases 1/2 (ERK1/2) activity and ultimately inhibiting peroxisome proliferator-activated receptor γ (PPARγ) Ser273 phosphorylation in adipocytes. Inhibition of PPARγ Ser273 phosphorylation by 3HB altered the expression of PPARγ regulated genes and reduced insulin resistance. Collectively, 3HB ameliorates insulin resistance in type 2 diabetic mice through a pathway of HCAR2/Ca2+/cAMP/PKA/Raf1/ERK1/2/PPARγ.
ADVANCED FUNCTIONAL MATERIALS [IF=19.924]
文獻(xiàn)引用抗體：D-9101；DiI
作者單位：南方醫(yī)科大學(xué)基礎(chǔ)醫(yī)學(xué)院腫瘤研究所
摘要：The immunosuppressive tumor microenvironment (TME) severely limits the clinical applications of cancer immunotherapy. Herein, a hypoxia-responsive delivery system is constructed simply by coordinating ferric(Fe3+) with mitoxantrone (MTO), sulfasalazine (SAS), and hypoxia-sensitive dopamine derivative of polyethylene glycol (PEG) using “one-pot” reaction for the “closed-loop” synergistic enhancement of ferroptosis and immunotherapy. Hypoxia-sensitive PEG ensures the integrity of delivery system in circulation to prevent the premature leakage of drugs, and the detachment of PEG in the interior hypoxic TME can facilitate the deep penetration and the subsequent tumor uptake. The released iron and MTO induce the generation of reactive oxygen species (ROS), while SAS inhibits the elimination of lipid peroxides by inhibiting SLC7A11 subunit of glutamate-cystine antiporter, which synergistically induces immunogenic ferroptosis to promote dendritic cells maturation and T cells activation. The activated CD8+ T cells then release interferon γ (IFN-γ) and in turn enhance ferroptosis by downregulating the expression of SLC7A11. As a result, the “closed-loop” synergistic enhancement between ferroptosis and immunotherapy significantly prevents tumor growth and prolonged survival time of tumor-bearing mice with no obvious systemic toxicity. The excellent therapeutic effect together with the scalable synthesis and controllable quality will promise its translation to clinic as a novel immunotherapy.
ACS Nano [IF=18.027]
文獻(xiàn)引用抗體：bs-5758R-AF647；Anti-FAPA/AF647 pAb | FCM
作者單位：韓國高等科學(xué)技術(shù)研究所(KAIST)KAIST生物科學(xué)系
摘要：Cancer-associated fibroblasts (CAFs), which are dominant cell types in the tumor microenvironment (TME), support tumor growth by secreting cytokines and forming an extracellular matrix (ECM) that hampers the penetration of chemical and biological therapeutics within the tumor and thereby limits their therapeutic efficacy. Here, we report a cancer nanovaccine targeting fibroblast activation protein α (FAP)-expressing CAFs as a potential pan-tumor vaccine. We predicted immunodominant FAP-specific epitope peptides in silico and selected two candidate peptides after in vitro and in vivo screening for immunogenicity and antitumor efficacy. Next, we developed a nanoparticle-based vaccine that displays the two selected epitope peptides on the surface of lipid nanoparticles encapsulating CpG adjuvant (FAPPEP-SLNPs). Immunization with one of two FAPPEP-SLNP nanovaccines led to considerable growth inhibition of various tumors, including desmoplastic tumors, by depletingFAP+ CAFs and thereby reducing ECM production in the TME while causing little appreciable adverse effects. Furthermore, when combined with a chemotherapeutic drug, the FAPPEP-SLNP nanovaccine increased drug accumulation and resulted in a synergistic antitumor efficacy far better than that of each corresponding monotherapy. These findings suggest that our FAPPEP-SLNP nanovaccine has potential for use as an “off-the-shelf” pan-tumor vaccine applicable to a variety of tumors and may be a suitable platform for use in various combination therapies.
ACS Nano [IF=18.027]
文獻(xiàn)引用抗體：bs-0283P-FITC；OVA / FITC
作者單位：中國科學(xué)院理化技術(shù)研究所低溫生物醫(yī)學(xué)工程北京重點(diǎn)實(shí)驗(yàn)室和低溫學(xué)重點(diǎn)實(shí)驗(yàn)室液態(tài)金屬與低溫生物醫(yī)學(xué)研究中心
摘要：Therapeutic cancer vaccines have been vigorously sought to bolster host adaptive immunity against metastatic cancers, but tumor heterogeneity, ineffective antigen utilization, and immunosuppressive tumor microenvironment hinder their clinical applications. Autologous antigen adsorbability and stimulus-release carrier coupling with immunoadjuvant capacity are urgent for personalized cancer vaccines. Here, we propose a perspective strategy of using a multipotent gallium-based liquid metal (LM) nanoplatform for personalized in situ cancer vaccines (ISCVs). The antigen-capturing and immunostimulatory LM nanoplatform can not only effectively destroy orthotopic tumors to generate multifarious autologous antigens upon external energy stimulation (photothermal/photodynamic effect) but also capture and transport antigens into dendritic cells (DCs) to enhance antigen utilization (adequate DCs uptake, antigen-endo/lysosomal escape) and facilitate DCs activation (mimic alum immunoadjuvant capacity), which ultimately awaken systemic antitumor immunity (expand cytotoxic T lymphocytes and modulate tumor microenvironment). With immune checkpoint blockade (anti-PD-L1) to further relieve the immunosuppressive tumor microenvironment, the positive tumoricidal immunity feedback loop was established to effectively eliminate orthotopic tumors, inhibit abscopal tumor growth, relapse, and metastasis as well as tumor-specific prevention. Collectively, this study demonstrates the potential of a multipotent LM nanoplatform for personalized ISCVs, which will open frontier exploration of LM-based immunostimulatory biomaterials and may encourage further investigation of precise individualized immunotherapy.
Nature Communications [IF=17.694]
文獻(xiàn)引用抗體：bs-10947R；Anti-Bradykinin pAb / HRP
作者單位：復(fù)旦大學(xué)中山醫(yī)院轉(zhuǎn)化腦研究所醫(yī)學(xué)神經(jīng)生物學(xué)國家重點(diǎn)實(shí)驗(yàn)室，教育部腦科學(xué)前沿中心
摘要：An important role for liver in the regulation of adipose tissue thermogenesis upon cold exposure has been suggested; however, the underlying mechanisms remain incompletely defined. Here, we identify elevated serum bradykinin levels in response to acute cold exposure in male mice. A bolus of anti-bradykinin antibodies reduces body temperature during acute cold exposure, whereas bradykinin has the opposite effect. We demonstrate that bradykinin induces brown adipose tissue thermogenesis and white adipose tissue browning, and bradykinin increases uncoupling protein 1 (UCP1) expression in adipose tissue. The bradykinin B2 receptor (B2R), adrenergic signaling and nitric oxide signaling are involved in regulating bradykinin-increased UCP1 expression. Moreover, acute cold exposure inhibits hepatic prolyl endopeptidase (PREP) activity, causing reduced liver bradykinin degradation and increased serum bradykinin levels. Finally, by blocking the breakdown of bradykinin, angiotensin-converting enzyme inhibitors (ACEIs) increase serum bradykinin levels and induce brown adipose tissue thermogenesis and white adipose tissue browning via B2R. Collectively, our data provide new insights into the mechanisms underlying organ crosstalk in whole-body physiology control during cold exposure and also suggest bradykinin as a possible anti-obesity target.
Nature Communications [IF=17.694]
文獻(xiàn)引用抗體：bs-20694R；Anti-Beta tubulin pAb / HRP
作者單位：沈陽藥科大學(xué)無涯創(chuàng)新學(xué)院藥劑學(xué)系
摘要：The immunologically “cold” microenvironment of triple negative breast cancer results in resistance to current immunotherapy. Here, we reveal the immunoadjuvant property of gas therapy with cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation to augment aggregation-induced emission (AIE)-active luminogen (AIEgen)-based photoimmunotherapy. A virus-mimicking hollow mesoporous tetrasulfide-doped organosilica is developed for co-encapsulation of AIEgen and manganese carbonyl to fabricate gas nanoadjuvant. As tetra-sulfide bonds are responsive to intratumoral glutathione, the gas nanoadjuvant achieves tumor-specific drug release, promotes photodynamic therapy, and produces hydrogen sulfide (H2S). Upon near-infrared laser irradiation, the AIEgen-mediated phototherapy triggers the burst of carbon monoxide (CO)/Mn2+. Both H2S and CO can destroy mitochondrial integrity to induce leakage of mitochondrial DNA into the cytoplasm, serving as gas immunoadjuvants to activate cGAS-STING pathway. Meanwhile, Mn2+ can sensitize cGAS to augment STING-mediated type I interferon production. Consequently, the gas nanoadjuvant potentiates photoimmunotherapy of poorly immunogenic breast tumors in female mice.
Nature Communications [IF=17.694]
文獻(xiàn)引用抗體：bs-3573R；Anti-ADAMTS5 pAb | IHC
作者單位：北京大學(xué)深圳醫(yī)院骨與關(guān)節(jié)外科
摘要：Intra-articular injection of therapeutics is an effective strategy for treating osteoarthritis (OA), but it is hindered by rapid drug diffusion, thereby necessitating high-frequency injections. Hence, the development of a biofunctional hydrogel for improved delivery is required. In this study, we introduce a liposome-anchored teriparatide (PTH (1–34)) incorporated into a gallic acid-grafted gelatin injectable hydrogel (GLP hydrogel). We show that the GLP hydrogel can form in situ and without affecting knee motion after intra-articular injection in mice. We demonstrate controlled, sustained release of PTH (1–34) from the GLP hydrogel. We find that the GLP hydrogel promotes ATDC5 cell proliferation and protects the IL-1β-induced ATDC5 cells from further OA progression by regulating the PI3K/AKT signaling pathway. Further, we show that intra-articular injection of hydrogels into an OA-induced mouse model promotes glycosaminoglycans synthesis and protects the cartilage from degradation, supporting the potential of this biomaterial for OA treatment.
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