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    當前位置:首頁  >  新聞資訊  >  11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    更新時間:2025-01-21  |  點擊率:118

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    截止目前,引用Bioss產品發表的文獻共32473篇總影響因子159154.82分,發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共122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,請致電Bioss,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。

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現






    本文主要分享引用Bioss 產品發表文章至 Cell, SCIENCE, Immunity,  Advanced Materials, ACS Nano , Translational Medicine等期刊的 7篇 IF>15的文獻摘要,讓我們一起欣賞吧。



                                       

    Cell [IF=45.5]




















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品

    bs-0296P | Mouse IgG Other

    作者單位:中國科學院動物研究所

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:To systematically characterize the loss of tissue integrity and organ dysfunction resulting from aging, we produced an in-depth spatial transcriptomic profile of nine tissues in male mice during aging. We showed that senescence-sensitive spots(SSSs)colocalized with elevated entropy in organizational structure and that the aggregation of immunoglobulin-expressing cells is a characteristic feature of the microenvironment surrounding SSSs. Immunoglobulin G(IgG)accumulated across the aged tissues in both male and female mice, and a similar phenomenon was observed in human tissues, suggesting the potential of the abnormal elevation of immunoglobulins as an evolutionarily conserved feature in aging. Furthermore, we observed that IgG could induce a pro-senescent state in macrophages and microglia, thereby exacerbating tissue aging, and that targeted reduction of IgG mitigated aging across various tissues in male mice. This study provides a high-resolution spatial depiction of aging and indicates the pivotal role of immunoglobulin-associated senescence during the aging process.



                                                   

    Cell [IF=45.5]


























    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-41408P | Recombinant SARS-Cov-2 N protein, N-His | Other

    作者單位美國西奈山伊坎醫學院
    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要Pathogens constantly evolve and can develop mutations that evade host immunity and treatment. Addressing these escape mechanisms requires targeting evolutionarily conserved vulnerabilities, as mutations in these regions often impose fitness costs. We introduce adaptive multi-epitope targeting with enhanced avidity (AMETA), a modular and mult ivalent nanobody platform that conjugates potent bispecific nanobodies to a human immunoglobulin M(IgM)scaffold. AMETA can display 20+ nanobodies, enabling superior avidity binding to multiple conserved and neutralizing epitopes. By leveraging multi-epitope SARS-CoV-2 nanobodies and structure-guided design, AMETA constructs exponentially enhance antiviral potency, surpassing monomeric nanobodies by over a million-fold. These constructs demonstrate ultrapotent, broad, and durable efficacy against pathogenic sarbecoviruses, including Omicron sublineages, with robust preclinical results. Structural analysis through cryoelectron microscopy and modeling has uncovered multiple antiviral mechanisms within a single construct. At picomolar to nanomolar concentrations, AMETA efficiently induces inter-spike and inter-virus cross-linking, promoting spike post-fusion and striking viral disarmament. AMETA’s modularity enables rapid, cost-effective production and adaptation to evolving pathogens.






                                       

    Science [IF=44.7]




















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-0295G-Cy5 | Goat Anti-Rabbit IgG H&L, Cy5 conjugated | IF

    bs-0295G-Cy3 | Goat Anti-Rabbit IgG H&L, Cy3 conjugated | IF

    作者單位:南方科技大學

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:Living with water, cells are frequently challenged by osmotic perturbations. The imbalance between the osmotic pressures across the semipermeable plasma membrane forces water to move in or out of a cell(through a process known as osmosis), remolds its shape, and can have substantial effects on various cellular activities. To preserve appropriate water and to maintain a suitable size, cells must sense and adapt to osmotic changes within their surrounding environments. This is particularly true for most plant cells because they are directly exposed to the fluctuations of environmental osmolarity. For example, the root cells of land plants have to face osmotic stresses generated from dramatic changes of soil moisture, temperature, and salinity, which are major threats to agricultural production. Over the past decades, great efforts have been made to understand the adaptations of plants to such osmotic stresses, although how environmental osmotic changes are sensed by plant cells is far from fully understood.



                                       

    Advanced Materials [IF=27.4]




















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-23640R TLR9 Rabbit pAb IF, IHC

    作者單位:四川大學華西醫院

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:Orofacial muscles are particularly prone to refractory fibrosis after injury, leading to a negative effect on the patient's quality of life and limited therapeutic options. Gaining insights into innate inflammatory response-fibrogenesis homeostasis can aid in the development of new therapeutic strategies for muscle fibrosis. In this study, the crucial role of macrophages is identified in the regulation of orofacial muscle fibrogenesis after injury. Hypothesizing that orchestrating macrophage polarization and functions will be beneficial for fibrosis treatment, nanomaterials are engineered with polyethylenimine functionalization to regulate the macrophage phenotype by capturing negatively charged cell-free nucleic acids(cfNAs). This cationic nanomaterial reduces macrophage-related inflammation in vitr and demonstrates excellent efficacy in preventing orofacial muscle fibrosis in vivo. Single-cell RNA sequencing reveals that the cationic nanomaterial reduces the proportion of profibrotic Gal3+ macrophages through the cfNA-mediated TLR7/9-NF-κB signaling pathway, resulting in a shift in profibrotic fibro-adipogenic progenitors(FAPs) from the matrix-producing Fabp4+ subcluster to the matrix-degrading Igf1+ subcluster. The study highlights a strategy to target innate inflammatory response-fibrogenesis homeostasis and suggests that cationic nanomaterials can be exploited for treating refractory fibrosis.


                                        

    Science Translational

    Medicine [IF=15.8]




















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-8621R | PDE3B Rabbit pAb | WB

    作者單位:中山大學附屬第一醫院

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:In liver transplantation, donor livers are typically stored in a preservation solution at 4°C for up to 12 hours. However, this short preservation duration can lead to various issues, such as suboptimal donor-recipient matching and limited opportunities for organ sharing. Previous studies have developed a long-term preservation method called supercooling liver preservation(SLP) to address these issues. However, in this study using a rat model, we observed that long-term SLP led to more severe liver damage compared with clinically prevalent traditional static cold storage(SCS) for durations less than 8 hours. To understand the potential mechanism of SLP-induced liver injury, we conducted an integrative metabolomic, transcriptomic, and proteomic analysis. We identified the PDE3B-cAMP-autophagy pathway as a key determinant of SLP-induced liver injury. Specifically, we found that PDE3B was elevated during SLP, which promoted a reduction of cAMP metabolites, triggering an AMPK-dependent autophagy process that led to liver injury in rats. We found that blocking the reduction in cAMP using the PDE3B inhibitor cilostamide inhibited autophagy and substantially ameliorated liver injury during 48-hour SLP in rat livers. Furthermore, we validated the effectiveness of cilostamide treatment in preventing liver injury in pig and human liver 48-hour SLP models. In summary, our results reveal that metabolic reprogramming involving the PDE3B-cAMP-autophagy axis is the key determinant of liver injury in long-term SLP and provide an early therapeutic strategy to prevent liver injury in this setting.



                                       
    ACS Nano [IF=15.8]



















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-16644R | H9N2 Hemagglutinin HA1 Rabbit pAb | WB
    bs-2001R | H1N1 Hemagglutinin 1 Rabbit pAb | WB

    作者單位:北京大學

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:The coronavirus disease 2019(COVID 19)pandemic has driven major advances in virus research. The role of glycans in viral infection has been revealed, with research demonstrating that terminal sialic acids are key receptors during viral attachment and infection into host cells. However, there is an urgent demand for universal tools to study the mechanism of sialic acids in viral infections, as well as to develop therapeutic agents against epidemic viruses through the downregulation of terminal sialic acid residues on glycans acting as a glyco-virus checkpoint to accelerate virus clearance. In this study, we developed a robust sialic acids blockade tool termed local and noninvasive glyco-virus checkpoint nanoblockades(LONG NBs), which blocked cell surface sialic acids by endogenously and continuously inhibiting the de novo sialic acids biosynthesis pathway. Furthermore, LONG NBs could accurately characterize the sialic acid-dependent profiles of multiple virus variants and protected the host against partial SARS-CoV-2, rotavirus, and influenza A virus infections after local and noninvasive administration. Our results suggest that LONG NBs represent a promising tool to facilitate in-depth research on the mechanism of viral infection, and serve as a broad-spectrum protectant against existing and emerging viral variants via glyco-virus checkpoint blockade.



                                         

    ACS Nano [IF=15.8]




















    11月文獻戰報Bioss抗體新增高分文獻精彩呈現


    文獻引用產品:

    bs-6313R | 4 Hydroxynonenal Rabbit pAb | IHC
    作者單位:蘇州大學

    11月文獻戰報Bioss抗體新增高分文獻精彩呈現

    摘要:Recent research has highlighted the pivotal role of lipoxygenases in modulating ferroptosis and immune responses by catalyzing the generation of lipid peroxides. However, the limitations associated with protein enzymes, such as poor stability, low bioavailability, and high production costs, have motivated researchers to explore biomimetic materials with lipoxygenase-like activity. Here, we report the discovery of lipoxygenase-like two-dimensional (2D) MoSnanosheets capable of catalyzing lipid peroxidation and inducing ferroptosis. The resulting catalytic products were successfully identified using mass spectrometry and a luminescent substrate. Unlike native lipoxygenases, MoSnanosheets exhibited exceptional catalytic activity at extreme pH, high temperature, high ionic strength, and organic solvent conditions. Structure–activity relationship analysis indicates that sulfur atomic vacancy sites on MoSnanosheets are responsible for their catalytic activity. Furthermore, the lipoxygenase-like activity of MoS2 nanosheets was demonstrated within mammalian cells and animal tissues, inducing distinctive ferroptotic cell death. In summary, this research introduces an alternative to lipoxygenase to regulate lipid peroxidation in cells, offering a promising avenue for ferroptosis induction.





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