【3月文獻(xiàn)戰(zhàn)報(bào)】Bioss抗體新增高分文獻(xiàn)精彩呈現(xiàn)

更新時(shí)間：2023-05-24 | 點(diǎn)擊率：1063

截止目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共24676篇，總影響因子115653.06分，發(fā)表在Nature, Science, Cell以及Immunity等頂級(jí)期刊的文獻(xiàn)共58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)等國際研究機(jī)構(gòu)上百所。

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近期收錄2023年2月引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共307篇（圖一，綠色柱），文章影響因子(IF) 總和高達(dá)2073.152，其中，10分以上文獻(xiàn)42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8篇 IF＞15 的文獻(xiàn)摘要，讓我們一起欣賞吧。

CELL [IF=66.85]

文獻(xiàn)引用抗體：bs-2735R

Anti-GSTP1 pAb

作者單位：北京大學(xué)化學(xué)與分子工程學(xué)院，北京分子科學(xué)國家實(shí)驗(yàn)室，合成與功能生物分子中心

摘要：A generalizable strategy with programmable site specificity for in situ profiling of histone modifications on unperturbed chromatin remains highly desirable but challenging. We herein developed a single-site-resolved multi-omics (SiTomics) strategy for systematic mapping of dynamic modifications and subsequent profiling of chromatinized proteome and genome defined by specific chromatin acylations in living cells. By leveraging the genetic code expansion strategy, our SiTomics toolkit revealed distinct crotonylation (e.g., H3K56cr) and β-hydroxybutyrylation (e.g., H3K56bhb) upon short chain fatty acids stimulation and established linkages for chromatin acylation mark-defined proteome, genome, and functions. This led to the identification of GLYR1 as a distinct interacting protein in modulating H3K56cr′s gene body localization as well as the discovery of an elevated super-enhancer repertoire underlying bhb-mediated chromatin modulations. SiTomics offers a platform technology for elucidating the “metabolites-modification-regulation" axis, which is widely applicable for multi-omics profiling and functional dissection of modifications beyond acylations and proteins beyond histones.

Signal Transduction and

Targeted Therapy [IF=38.104]

文獻(xiàn)引用抗體：bs-1570R

Anti-APOH pAb

作者單位：北京大學(xué)基礎(chǔ)醫(yī)學(xué)院生理學(xué)和病理生理學(xué)系，分子心血管科學(xué)教育部重點(diǎn)實(shí)驗(yàn)室

摘要：Hyperhomocysteinemia (HHcy) is a risk factor for chronic kidney diseases (CKDs) that affects about 85% CKD patients. HHcy stimulates B cells to secrete pathological antibodies, although it is unknown whether this pathway mediates kidney injury. In HHcy-treated 2-kidney, 1-clip (2K1C) hypertensive murine model, HHcy-activated B cells secreted anti-beta 2 glycoprotein I (β2GPI) antibodies that deposited in glomerular endothelial cells (GECs), exacerbating glomerulosclerosis and reducing renal function. Mechanistically, HHcy 2K1C mice increased phosphatidylethanolamine (PE) (18:0/20:4, 18:0/22:6, 16:0/20:4) in kidney tissue, as determined by lipidomics. GECs oxidative lipidomics validated the increase of oxidized phospholipids upon Hcy-activated B cells culture medium (Hcy-B CM) treatment, including PE (18:0/20:4?+?3[O], PE (18:0a/22:4?+?1[O], PE (18:0/22:4?+?2[O] and PE (18:0/22:4?+?3[O]). PE synthases ethanolamine kinase 2 (etnk2) and ethanolamine-phosphate cytidylyltransferase 2 (pcyt2) were increased in the kidney GECs of HHcy 2K1C mice and facilitated polyunsaturated PE synthesis to act as lipid peroxidation substrates. In HHcy 2K1C mice and Hcy-B CM-treated GECs, the oxidative environment induced by iron accumulation and the insufficient clearance of lipid peroxides caused by transferrin receptor (TFR) elevation and down-regulation of SLC7A11/glutathione peroxidase 4 (GPX4) contributed to GECs ferroptosis of the kidneys. In vivo, pharmacological depletion of B cells or inhibition of ferroptosis mitigated the HHcy-aggravated hypertensive renal injury. Consequently, our findings uncovered a novel mechanism by which B cell-derived pathogenic anti-β2GPI IgG generated by HHcy exacerbated hypertensive kidney damage by inducing GECs ferroptosis. Targeting B cells or ferroptosis may be viable therapeutic strategies for ameliorating lipid peroxidative renal injury in HHcy patients with hypertensive nephropathy.

ACS Nano [IF=18.027]

文獻(xiàn)引用抗體：

bs-3884R; Anti-GPX4 pAb | WB

bs-0732R; Anti-Cyclooxygenase 2 pAb | WB

作者單位：重慶大學(xué)生物工程學(xué)院生物流變科學(xué)與技術(shù)教育部重點(diǎn)實(shí)驗(yàn)室

摘要：The hypoxia microenvironment of solid tumors poses a technological bottleneck for ferroptosis and immunotherapy in clinical oncology. Nanoreactors based on special physiological signals in tumor cells are able to avoid various tumor tolerance mechanisms by alleviating the intracellular hypoxia environment. Herein we reported a nanoreactor Cu_2-xSe that enabled the conversion of Cu elements between Cu⁺ and Cu²⁺ for the generation of O₂ and the consumption of intracellular GSH content. Furthermore, to enhance the catalytic and ferroptosis-inducing activities of the nanoreactors, the ferroptosis agonist Erastin was loaded on the ZIF-8 coating on the surface of Cu_2-xSe to up-regulate the expression of NOX4 protein, increase the intracellular H₂O₂ content, catalyze the Cu⁺ to produce O₂ and activate ferroptosis. In addition, the nanoreactors were simultaneously surface functionalized with PEG polymer and folic acid molecules, which ensured the in vivo blood circulation and tumor-specific uptake. In vitro and in vivo experiments demonstrated that the functionalized self-supplying nanoreactors can amplify the ability to generate O₂ and consume intracellular GSH via the interconversion of Cu elements Cu⁺ and Cu²⁺, and impair the GPX4/GSH pathway and HIF-1α protein expression. At the same time, by alleviating the intracellular hypoxia environment, the expression of miR301, a gene in the secreted exosomes was decreased, which ultimately affected the phenotype polarization of TAMs and increased the content of IFN γ secreted by CD8⁺ T cells, which further promoted the ferroptosis induced by Erastin-loaded nanoreactors. This combined therapeutic strategy of activating the tumor immune response and ferroptosis via self-supplying nanoreactors provides a potential strategy for clinical application..

Nature Communications

[IF=17.694]

文獻(xiàn)引用抗體：bs-0842R

Anti-Myc tag pAb

作者單位：中國科學(xué)院納米材料生物醫(yī)學(xué)效應(yīng)與納米安全重點(diǎn)實(shí)驗(yàn)室&中國科學(xué)院納米科學(xué)中心

摘要：Micro-nano biorobots based on bacteria have demonstrated great potential for tumor diagnosis and treatment. The bacterial gene expression and drug release should be spatiotemporally controlled to avoid drug release in healthy tissues and undesired toxicity. Herein, we describe an alternating magnetic field-manipulated tumor-homing bacteria developed by genetically modifying engineered Escherichia coli with Fe₃O₄@lipid nanocomposites. After accumulating in orthotopic colon tumors in female mice, the paramagneticFe₃O₄ nanoparticles enable the engineered bacteria to receive and convert magnetic signals into heat, thereby initiating expression of lysis proteins under the control of a heat-sensitive promoter. The engineered bacteria then lyse, releasing its anti-CD47 nanobody cargo, that is pre-expressed and within the bacteria. The robust immunogenicity of bacterial lysate cooperates with anti-CD47 nanobody to activate both innate and adaptive immune responses, generating robust antitumor effects against not only orthotopic colon tumors but also distal tumors in female mice. The magnetically engineered bacteria also enable the constant magnetic field-controlled motion for enhanced tumor targeting and increased therapeutic efficacy. Thus, the gene expression and drug release behavior of tumor-homing bacteria can be spatiotemporally manipulated in vivo by a magnetic field, achieving tumor-specific CD47 blockage and precision tumor immunotherapy.

Nature Communications

[IF=17.694]

文獻(xiàn)引用抗體：

bs-5180R; Anti-AXL pAb | WB

bs-5181R; Anti-phospho-AXL(Tyr698+Tyr702+Tyr703) pAb | WB

bs-18791R; Anti-phospho-MERTK(Tyr749 + Tyr753 + Tyr754) pAb | WB

bs-0283P; OVA

bs-0283P-PE; OVA / PE

bs-0283P-Cy5; OVA / Cy5

作者單位：北京理工大學(xué)生命科學(xué)學(xué)院

摘要：Efferocytosis inhibition is emerging as an attractive strategy for antitumor immune therapy because of the subsequent leak of abundant immunogenic contents. However, the practical efficacy is seriously impeded by the immunosuppressive tumor microenvironments. Here, we construct a versatile nanosystem that can not only inhibit the efferocytosis but also boost the following antitumor immunity. MerTK inhibitor UNC2025 is loaded into the bacterial outer membrane vesicles (OMVs), which are then modified with maleimide (mU@OMVs). The prepared mU@OMVs effectively inhibits the efferocytosis by promoting the uptake while preventing the MerTK phosphorylation of tumor associated macrophages, and then captures the released antigens through forming universal thioether bonds. The obtained in situ vaccine effectively transfers to lymph nodes by virtue of the intrinsic features of OMVs, and then provokes intense immune responses that can efficiently prevent the growth, metastasis and recurrence of tumors in mice, providing a generalizable strategy for cancer immunotherapy.

Nature Communications

[IF=17.694]

文獻(xiàn)引用抗體：bs-11966R

SPOCK2 | IF

作者單位：美國休斯頓德克薩斯大學(xué)健康科學(xué)中心麥戈文醫(yī)學(xué)院綜合生物學(xué)和藥理學(xué)系

摘要：N6-methyladenosine (m⁶A), one of the most prevalent mRNA modifications in eukaryotes, plays a critical role in modulating both biological and pathological processes. However, it is unknown whether mutant p53 neomorphic oncogenic functions exploit dysregulation of m⁶A epitranscriptomic networks. Here, we investigate Li-Fraumeni syndrome (LFS)-associated neoplastic transformation driven by mutant p53 in iPSC-derived astrocytes, the cell-of-origin of gliomas. We find that mutant p53 but not wild-type (WT) p53 physically interacts with SVIL to recruit the H3K4me3 methyltransferase MLL1 to activate the expression of m⁶A reader YTHDF2, culminating in an oncogenic phenotype. Aberrant YTHDF2 upregulation markedly hampers expression of multiple m⁶A-marked tumor-suppressing transcripts, including CDKN2B and SPOCK2, and induces oncogenic reprogramming. Mutant p53 neoplastic behaviors are significantly impaired by genetic depletion of YTHDF2 or by pharmacological inhibition using MLL1 complex inhibitors. Our study reveals how mutant p53 hijacks epigenetic and epitranscriptomic machinery to initiate gliomagenesis and suggests potential treatment strategies for LFS gliomas.

Nature Communications

[IF=17.694]

文獻(xiàn)引用抗體：bs-1759R

Anti-Met Enkephalin pAb | FCM

作者單位：香港大學(xué)藥物生物技術(shù)國家重點(diǎn)實(shí)驗(yàn)室

摘要：Lymph nodes (LNs) are always embedded in the metabolically-active white adipose tissue (WAT), whereas their functional relationship remains obscure. Here, we identify fibroblastic reticular cells (FRCs) in inguinal LNs (iLNs) as a major source of IL-33 in mediating cold-induced beiging and thermogenesis of subcutaneous WAT (scWAT). Depletion of iLNs in male mice results in defective cold-induced beiging of scWAT. Mechanistically, cold-enhanced sympathetic outflow to iLNs activates β1- and β2-adrenergic receptor (AR) signaling in FRCs to facilitate IL-33 release into iLN-surrounding scWAT, where IL-33 activates type 2 immune response to potentiate biogenesis of beige adipocytes. Cold-induced beiging of scWAT is abrogated by selective ablation of IL-33 or β1- and β2-AR in FRCs, or sympathetic denervation of iLNs, whereas replenishment of IL-33 reverses the impaired cold-induced beiging in iLN-deficient mice. Taken together, our study uncovers an unexpected role of FRCs in iLNs in mediating neuro-immune interaction to maintain energy homeostasis.

Nature Communications

[IF=17.694]

文獻(xiàn)引用抗體：

bs-1092R; Anti-MRP2/ABCC2 pAb | IHC

bs-14165R; Anti-CYP8B1 pAb | IHC

作者單位：中國重慶軍醫(yī)大學(xué)新橋醫(yī)院消化內(nèi)科

摘要：Intrahepatic cholestasis of pregnancy (ICP) is a female pregnancy-specific disorder that is characterized by increased serum bile acid and adverse fetal outcomes. The aetiology and mechanism of ICP are poorly understood; thus, existing therapies have been largely empiric. Here we show that the gut microbiome differed significantly between individuals with ICP and healthy pregnant women, and that colonization with gut microbiome from ICP patients was sufficient to induce cholestasis in mice. The gut microbiomes of ICP patients were primarily characterized by Bacteroides fragilis (B. fragilis), and B. fragilis was able to promote ICP by inhibiting FXR signaling via its BSH activity to modulate bile acid metabolism. B. fragilis-mediated FXR signaling inhibition was responsible for excessive bile acid synthesis and interrupted hepatic bile excretion to ultimately promote the initiation of ICP. We propose that modulation of the gut microbiota-bile acid-FXR axis may be of value for ICP treatment.

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