截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共29993篇，總影響因子146235.33分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻(xiàn)共68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。
我們每月收集引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)。若您在當(dāng)月已發(fā)表SCI文章，但未被我公司收集，請致電Bioss，我們將贈予現(xiàn)金鼓勵，金額標(biāo)準(zhǔn)請參考“發(fā)文章 領(lǐng)獎金”活動頁面。
近期收錄2024年3月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共382篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)2545.8，其中，10分以上文獻(xiàn)57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, Immunity, Cancer Cell等期刊的9篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。
Science [IF=56.9]
文獻(xiàn)引用抗體：bsm-33034M
Beta tubulin Mouse mAb | WB
作者單位：哈佛大學(xué)、麻省理工學(xué)院
摘要：Conditional protein degradation tags (degrons) are usually >100 amino acids long or are triggered by small molecules with substantial off-target effects, thwarting their use as specific modulators of endogenous protein levels. We developed a phage-assisted continuous evolution platform for molecular glue complexes (MG-PACE) and evolved a 36–amino acid zinc finger (ZF) degron (SD40) that binds the ubiquitin ligase substrate receptor cereblon in complex with PT-179, an orthogonal thalidomide derivative. Endogenous proteins tagged in-frame with SD40 using prime editing are degraded by otherwise inert PT-179. Cryo–electron microscopy structures of SD40 in complex with ligand-bound cereblon revealed mechanistic insights into the molecular basis of SD40’s activity and specificity. Our efforts establish a system for continuous evolution of molecular glue complexes and provide ZF tags that overcome shortcomings associated with existing degrons.
Military Medical Research [IF=21.1]
文獻(xiàn)引用抗體：
bs-19952R；TMEM120A Rabbit pAb | WB、CoIP
bs-4915R；ACCN1 Rabbit pAb | WB、CoIP
bs-3527R；KIF17 Rabbit pAb | WB、CoIP
bs-23166R；Myc tag Rabbit pAb | WB、CoIP
bs-17085R；KIF3B Rabbit pAb | CoIP
作者單位：中山大學(xué)附屬腫瘤醫(yī)院
摘要：The results showed that EndoA2 was primarily distributed in neurofilament-200-positive (NF200+) medium-to-large diameter dorsal root ganglion (DRG) neurons of mice and humans. Loss of EndoA2 in mouse NF200+ DRG neurons selectively impaired the tactile and mechanical allodynia. Furthermore, EndoA2 interacted with the mechanically sensitive ion channel Piezo2 and promoted the membrane trafficking of Piezo2 in DRG neurons. Moreover, as an adaptor protein, EndoA2 also bound to kinesin family member 5B (KIF5B), which was involved in the EndoA2-mediated membrane trafficking process of Piezo2. Loss of EndoA2 in mouse DRG neurons damaged Piezo2-mediated rapidly adapting mechanically activated currents, and re-expression of EndoA2 rescued the MA currents. In addition, interference with EndoA2 also suppressed touch sensitivity and mechanical hypersensitivity in nonhuman primates.
ADVANCED FUNCTIONAL MATERIALS [IF=19.0]
文獻(xiàn)引用抗體：bs-0195R
CD31 Rabbit pAb | IF
作者單位：四川大學(xué)
摘要：Hydrogel coatings, with natural tissue-like mechanical and biological compatibility, demonstrate promise for bulk material applications. However, existing coating methods lack efficiency and control, especially when dealing with complex geometries, diverse substrate materials, and varying sizes. In this study, an enzyme-immobilized surface-catalyzed cross-link approach is proposed for the growth of hydrogel coatings on multiple substrates, accommodating various materials and shapes. The hydrogel coating is formed through the catalytic action of interface-immobilized enzymes, which induce the crosslinking of hyaluronic acid, and its mechanical properties are further enhanced by introducing a secondary polyacrylamide network. This approach enables the controlled growth of conformal double network hydrogel coatings with a desired thickness on a wide range of substrate surfaces and devices. Notably, the hydrogel coating exhibits remarkable lubricity and anti-thrombotic properties, especially desire for medical intervention devices. This advancement offers a universal route to impart biocompatible soft interfaces to bulk materials or devices.
Bioactive Materials [IF=18.9]
文獻(xiàn)引用產(chǎn)品：D50415
Staurosporine | IF
作者單位：中山大學(xué)附屬腫瘤醫(yī)院
摘要：Apoptosis has long been recognized as a significant mechanism for inhibiting tumor formation, and a plethora of stimuli can induce apoptosis during the progression and treatment of tumors. Moreover, tumor-derived apoptotic extracellular vesicles (apoEVs) are inevitably phagocytosed by live tumor cells, promoting tumor heterogeneity. Understanding the mechanism by which apoEVs regulate tumor cells is imperative for enhancing our knowledge of tumor metastasis and recurrence. Herein, we conducted a series of in vivo and in vitro experiments, and we report that tumor-derived apoEVs promoted lung adenocarcinoma (LUAD) metastasis, self-renewal and chemoresistance. Mechanistically, we demonstrated that apoEVs facilitated tumor metastasis and stemness by initiating the epithelial-mesenchymal transition program and upregulating the transcription of the stem cell factor SOX2. In addition, we found that ALDH1A1, which was transported by apoEVs, activated the NF-κB signaling pathway by increasing aldehyde dehydrogenase enzyme activity in recipient tumor cells. Furthermore, targeting apoEVs-ALDH1A1 significantly abrogated these effects. Collectively, our findings elucidate a novel mechanism of apoEV-dependent intercellular communication between apoptotic tumor cells and live tumor cells that promotes the formation of cancer stem cell-like populations, and these findings reveal that apoEVs-ALDH1A1 may be a potential therapeutic target and biomarker for LUAD metastasis and recurrence.
Bioactive Materials [IF=18.9]
文獻(xiàn)引用產(chǎn)品：bs-1183R
IL17A Rabbit pAb | WB
作者單位：中南大學(xué)湘雅醫(yī)院
摘要：Intervertebral disc degeneration (IVDD) can be caused by aging, injury, and genetic factors. The pathological changes associated with IVDD include the excessive accumulation of reactive oxygen species (ROS), cellular pyroptosis, and extracellular matrix (ECM) degradation. There are currently no approved specific molecular therapies for IVDD. In this study, we developed a multifunctional and microenvironment-responsive metal-phenolic network release platform, termed TMP@Alg-PBA/PVA, which could treat (IL-1β)-induced IVDD. The metal-phenolic network (TA-Mn-PVP, TMP) released from this platform targeted mitochondria to efficiently scavenge ROS and reduce ECM degradation. Pyroptosis was suppressed through the inhibition of the IL-17/ERK signaling pathway. These findings demonstrate the versatility of the platform. And in a rat model of IVDD, TMP@Alg-PBA/PVA exhibited excellent therapeutic effects by reducing the progression of the disease. TMP@Alg-PBA/PVA, therefore, presents clinical potential for the treatment of IVDD.
Nano Today [IF=17.4]
文獻(xiàn)引用抗體：
bs-1439R；JAK1 Rabbit pAb | WB
bs-2808R；JAK3 Rabbit pAb | WB
bs-55208R；STAT3 Rabbit pAb | WB
bs-22386R；phospho-STAT3 (Tyr705) Rabbit pAb | WB
bs-4599R；MMP-2 Rabbit pAb | WB
bs-20619R；MMP9 Rabbit pAb | WB
作者單位：沈陽藥科大學(xué)
摘要：Darutigenol (DL) is an active diterpenoid extracted from the traditional Chinese medicine Sigesbeckia glabrescens (Makino) Makino, widely employed in the treatment of rheumatoid arthritis (RA) for centuries in China. However, the anti-inflammatory mechanism of DL requires further exploration. In this study, we discovered that DL could scavenge reactive oxygen species (ROS) and nitric oxide (NO), and reduce the secretion of proinflammatory cytokines, inducing the M1-to-M2 polarization of macrophages in vitro. In vivo, DL was demonstrated to exert an anti-inflammatory effect via the JAK1, 3/STAT3 and MAPK pathways. It also showed efficacy in repairing cartilage damage via downregulating the proteins MMP2/MMP9 and inhibiting angiogenesis through the CXCL12/CXCR7 system in synovial tissues. However, the application and therapeutic effect of DL was constrained by its poor water solubility and low bioavailability. To address these limitations, ROS-responsive prodrug nanoassemblies were employed, which could be passively transported to the joint inflammation site and decomposed in the inflammatory environment to release DL. The therapeutic effect of prodrug nanoassemblies was superior to that of DL, with negligible toxicity to organs. In summary, we clarified the anti-RA mechanism of DL and constructed an efficient and safe drug delivery system, which provided a strategy for the further application and development of active compounds in traditional Chinese medicine.
ACS Nano [IF=17.1]
文獻(xiàn)引用抗體：bs-0295G-HRP
Goat Anti-Rabbit IgG H&L / HRP | WB
作者單位：天然藥物及仿生藥物國家重點(diǎn)實(shí)驗(yàn)室
摘要：Osteoarthritis (OA) is a degenerative joint disease characterized by progressive erosion of the articular cartilage and inflammation. Mesenchymal stem cells’ (MSCs) transplantation in OA treatment is emerging, but its clinical application is still limited by the low efficiency in oriented differentiation. In our study, to improve the therapeutic efficiencies of MSCs in OA treatment by carbonic anhydrase IX (CA9) siRNA (siCA9)-based inflammation regulation and Kartogenin (KGN)-based chondrogenic differentiation, the combination strategy of MSCs and the nanomedicine codelivering KGN and siCA9 (AHK-CaP/siCA9 NPs) was used. In vitro results demonstrated that these NPs could improve the inflammatory microenvironment through repolarization of M1 macrophages to the M2 phenotype by downregulating the expression levels of CA9 mRNA. Meanwhile, these NPs could also enhance the chondrogenesis of bone marrow-derived mesenchymal stem cells (BMSCs) by upregulating the pro-chondrogenic TGF-β1, ACAN, and Col2α1 mRNA levels. Moreover, in an advanced OA mouse model, compared with BMSCs alone group, the lower synovitis score and OARSI score were found in the group of BMSCs plus AHK-CaP/siCA9 NPs, suggesting that this combination approach could effectively inhibit synovitis and promote cartilage regeneration in OA progression. Therefore, the synchronization of regulating the inflammatory microenvironment through macrophage reprogramming (CA9 gene silencing) and promoting MSCs oriented differentiation through a chondrogenic agent (KGN) may be a potential strategy to maximize the therapeutic efficiency of MSCs for OA treatment.
ACS Nano [IF=17.1]
文獻(xiàn)引用抗體：
bs-10196R；alpha smooth muscle Actin Rabbit pAb | IHC
bs-0195R；CD31 Rabbit pAb | IHC
bs-12364R；SCXA Rabbit pAb | IHC
bs-7525R；TNMD Rabbit pAb | IHC
bs-4917R；Osteocalcin Rabbit pAb | IHC
bs-1134R；RUNX2 Rabbit pAb | IHC
作者單位：重慶大學(xué)
摘要：Supramolecular hydrogels emerge as a promising paradigm for sutureless wound management. However, their translation is still challenged by the insufficient mechanical robustness in the context of complex wounds in dynamic tissues. Herein, we report a tissue-adhesive supramolecular hydrogel membrane based on biocompatible precursors for dressing wounds in highly dynamic tissues, featuring robust mechanical resilience through programmable strain-adaptive entanglement among microdomains. Specifically, the hydrogels are synthesized by incorporating a long-chain polyurethane segment into a Schiff base-ligated short-chain oxidized cellulose/quaternized chitosan network via acylhydrazone bonding, which readily establishes interpenetrating entangled microdomains in dynamic cross-linked hydrogel matrices to enhance their tear and fatigue resistance against extreme mechanical stresses. After being placed onto dynamic tissues, the hydrogel dressing could efficiently absorb blood to achieve rapid hemostasis. Moreover, metal ions released from ruptured erythrocytes could be scavenged by the Schiff base linkers to form additional ionic bonds, which would trigger the cross-linking of the short-chain components and establish abundant crystalline microdomains, eventually leading to the in situ stiffening of the hydrogels to endure heavy mechanical loads. Benefiting from its hemostatic capacity and strain adaptable mechanical performance, this hydrogel wound dressing shows promise for the clinical management of various traumatic wounds.
ACS Nano [IF=17.1]
文獻(xiàn)引用抗體：
bs-28034R；Bax Rabbit pAb | WB
bsm-33199M；Active Caspase 3 Mouse mAb | WB、IF
bs-1074R；Nrf2 Rabbit pAb | WB
bs-2075R；Heme Oxygenase 1 Rabbit pAb | WB
bs-4900R；KEAP1 Rabbit pAb | WB
bs-23407R；NQO1 Rabbit pAb | WB
bs-34023R；ZO-1 Rabbit pAb | WB
bs-10011R；Occludin Rabbit pAb | WB
bsm-33117M；NFKB p65 Mouse mAb | WB
bs-3485R；Phospho-NFKB p65 (Ser468) Rabbit pAb | WB
bs-1287R；IKB alpha Rabbit pAb | WB
bs-18129R；phospho-IKB alpha (Ser36) Rabbit pAb | WB
bs-1128R；SLC5A1 Rabbit pAb | WB
bsm-52793R；TFRC Recombinant Rabbit mAb | WB
bsm-52290R；beta Tubulin Recombinant Rabbit mAb | WB
bsm-33036M；beta-Actin (Loading Control) Mouse mAb | WB
作者單位：中國科學(xué)院長春應(yīng)用化學(xué)研究所
摘要：Restoration of blood-brain barrier (BBB) dysfunction, which drives worse outcomes of ischemic stroke, is a potential target for therapeutic opportunities, whereas a sealed BBB blocks the therapeutics entrance into the brain, making the BBB protection strategy paradoxical. Post ischemic stroke, hypoxia/hypoglycemia provokes the up-regulation of transmembrane glucose transporters and iron transporters due to multiple metabolic disorders, especially in brain endothelial cells. Herein, we develop a myricetin oligomer-derived nanostructure doped with Ce to bypass the BBB which is cointermediated by glucose transporters and iron transporters such as glucose transporters 1 (GLUT1), sodium/glucose cotransporters 1 (SGLT1), and transferrin(Tf) reporter (TfR). Moreover, it exhibits BBB restoration capacity by regulating the expression of tight junctions (TJs) through the activation of protective autophagy. The myricetin oligomers scaffold not only acts as targeting moiety but is the prominent active entity that inherits all diverse pharmacological activities of myricetin. The suppression of oxidative damage, M1 microglia activation, and inflammatory factors makes it a multitasking nanoagent with a single component as the scaffold, targeting domain and curative components.