【1月文獻戰報】Bioss抗體新增高分文獻精彩呈現

更新時間：2023-03-27 | 點擊率：1071

截止目前，引用Bioss產品發表的文獻共23452篇，總影響因子107756.664分，發表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共55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。

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近期收錄2023年1月引用Bioss產品發表的文獻共295篇（圖一，綠色柱），文章影響因子(IF) 總和高達2000.977，其中，10分以上文獻37篇（圖二）。

圖一

圖二

本文主要分享引用Bioss產品發表文章至Nature Nanotechnology, Immunity, Cancer Cell等期刊的5篇 IF＞15 的文獻摘要，讓我們一起欣賞吧。

NATURE [IF=69.504]

文獻引用抗體：bs-0634R-PE

Anti-Aquaporin 4 /PE pAb | FCM

作者單位：美國馬薩諸塞州波士頓哈佛大學醫學院布里格姆婦女醫院安·羅姆尼神經疾病中心

摘要：Multiple sclerosis is a chronic inflammatory disease of the central nervous system. Astrocytes are heterogeneous glial cells that are resident in the central nervous system and participate in the pathogenesis of multiple sclerosis and its model experimental autoimmune encephalomyelitis. However, few unique surface markers are available for the isolation of astrocyte subsets, preventing their analysis and the identification of candidate therapeutic targets; these limitations are further amplified by the rarity of pathogenic astrocytes. Here, to address these challenges, we developed focused interrogation of cells by nucleic acid detection and sequencing (FIND-seq), a high-throughput microfluidic cytometry method that combines encapsulation of cells in droplets, PCR-based detection of target nucleic acids and droplet sorting to enable in-depth transcriptomic analyses of cells of interest at single-cell resolution. We applied FIND-seq to study the regulation of astrocytes characterized by the splicing-driven activation of the transcription factor XBP1, which promotes disease pathology in multiple sclerosis and experimental autoimmune encephalomyelitis. Using FIND-seq in combination with conditional-knockout mice, in vivo CRISPR–Cas9-driven genetic perturbation studies and bulk and single-cell RNA sequencing analyses of samples from mouse experimental autoimmune encephalomyelitis and humans with multiple sclerosis, we identified a new role for the nuclear receptor NR3C2 and its corepressor NCOR2 in limiting XBP1-driven pathogenic astrocyte responses. In summary, we used FIND-seq to identify a therapeutically targetable mechanism that limits XBP1-driven pathogenic astrocyte responses. FIND-seq enables the investigation of previously inaccessible cells, including rare cell subsets defined by unique gene expression signatures or other nucleic acid markers.

ADVANCED MATERIALS

[IF=32.086]

文獻引用抗體：

bs-1563R; Anti-E.coli O157:H7 pAb

bs-2033R; Anti-E.coli DH-5 Alpha pAb

作者單位：CAS化學研究院分子科學研究所綠色印刷研究教育中心重點實驗室

摘要：Fast and accurate detection of microbial cells in clinical samples is highly valuable but remains a challenge. Here, a simple, culture-free diagnostic system is developed for direct detection of pathogenic bacteria in water, urine and serum samples using an optical colorimetric biosensor. It consists of printed nanoarrays chemically conjugated with specific antibodies that exhibits distinct color changes after capturing target pathogens. By utilizing the internal capillarity inside an evaporating droplet, target preconcentration is achieved within a few minutes to enable rapid identification and more efficient detection of bacterial pathogens. More importantly, the scattering signals of bacteria can be significantly amplified by the nanoarrays due to strong near-field localization, which supports a visualizable analysis of the growth, reproduction and cell activity of bacteria at the single-cell level. Finally, in addition to high selectivity, this nanoarray-based biosensor is also capable of accurate quantification and continuous monitoring of bacterial load on food over a broad linear range, with a detection limit of 10 CFU mL^?1. This work provides an accessible and user-friendly tool for point-of-care testing of pathogens in many clinical and environmental applications, and possibly enables a breakthrough in early prevention and treatment.

NATURE IMMUNOLOGY

[IF=31.25]

文獻引用抗體：bs-6480R

Anti-CH25H pAb | WB

作者單位：美國馬薩諸塞州伍斯特市馬薩諸塞大學陳醫學院病理科

摘要：Immunoglobulin A (IgA) secretion by plasma cells, terminally differentiated B cells residing in the intestinal lamina propria, assures microbiome homeostasis and protects the host against enteric infections. Exposure to diet-derived and commensal-derived signals provides immune cells with organizing cues that instruct their effector function and dynamically shape intestinal immune responses at the mucosal barrier. Recent data have described metabolic and microbial inputs controlling T cell and innate lymphoid cell activation in the gut; however, whether IgA-secreting lamina propria plasma cells are tuned by local stimuli is completely unknown. Although antibody secretion is considered to be imprinted during B cell differentiation and therefore largely unaffected by environmental changes, a rapid modulation of IgA levels in response to intestinal fluctuations might be beneficial to the host. In the present study, we showed that dietary cholesterol absorption and commensal recognition by duodenal intestinal epithelial cells lead to the production of oxysterols, evolutionarily conserved lipids with immunomodulatory functions. Using conditional cholesterol 25-hydroxylase deleter mouse line we demonstrated that 7α,25-dihydroxycholesterol from epithelial cells is critical to restrain IgA secretion against commensal- and pathogen-derived antigens in the gut. Intestinal plasma cells sense oxysterols via the chemoattractant receptor GPR183 and couple their tissue positioning with IgA secretion. Our findings revealed a new mechanism linking dietary cholesterol and humoral immune responses centered around plasma cell localization for efficient mucosal protection.

NATURE CELL BIOLOGY

[IF=28.213]

文獻引用抗體：

bs-0832R;Anti-MICA pAb | FCM

作者單位：中國廣州中山大學中山醫學院中山紀念醫院RNA生物醫學研究所

摘要：T?cell acute lymphoblastic leukaemia (T-ALL) is an aggressive malignancy with poor prognosis, but a decisive marker and effective treatment for leukaemia stem cells (LSCs) remain unclear. Here, using lineage tracing, limiting dilution assays and in vivo live imaging approaches, we identify rare inhibitory receptor programmed cell death?1 (PD-1)-expressing cells that reside at the apex of leukaemia hierarchy for initiation and relapse in T-ALL. Ablation of PD-1-expressing cells, deletion of PD-1 in T-ALL cells or blockade of PD-1 or PD-1 ligand?1 significantly eradicated LSCs and suppressed disease progression. Combination therapy using PD-1 blockade and chemotherapy substantially extended the survival of mice engrafted with mouse or human T-ALL cells. Mechanistically, PD-1⁺ LSCs had high NOTCH1–MYC activity for disease initiation. Furthermore, PD-1 signalling maintained quiescence and protected LSCs against T?cell receptor-signal-induced apoptosis. Overall, our data highlight the hierarchy of leukaemia by identifying PD-1⁺ LSCs and provide a therapeutic approach for the elimination of LSCs through PD-1 blockade in T-ALL.

BRAIN BEHAVIOR AND IMMUNITY

[IF=19.227]

文獻引用抗體：

bs-2455R;Anti-CLEC7A pAb | WB

bs-3393R;Anti-Phospho-SIRT1 (Ser47) pAb | WB

作者單位：西班牙巴塞羅那大學神經科學研究所醫學院生物醫學系

摘要：In the last two decades, microglia have emerged as key contributors to disease progression in many neurological disorders, not only by exerting their classical immunological functions but also as extremely dynamic cells with the ability to modulate synaptic and neural activity. This dynamic behavior, together with their heterogeneous roles and response to diverse perturbations in the brain parenchyma has raised the idea that microglia activation is more diverse than anticipated and that understanding the molecular mechanisms underlying microglial states is essential to unravel their role in health and disease from development to aging. The Ikzf1 (a.k.a. Ikaros) gene plays crucial roles in modulating the function and maturation of circulating monocytes and lymphocytes, but whether it regulates microglial functions and states is unknown. Using genetic tools, here we describe that Ikzf1 is specifically expressed in the adult microglia in brain regions such as cortex and hippocampus. By characterizing the Ikzf1 deficient mice, we observed that these mice displayed spatial learning deficits, impaired hippocampal CA3-CA1 long-term potentiation, and decreased spine density in pyramidal neurons of the CA1, which correlates with an increased expression of synaptic markers within microglia. Additionally, these Ikzf1 deficient microglia exhibited a severe abnormal morphology in the hippocampus, which is accompanied by astrogliosis, an aberrant composition of the inflammasome, and an altered expression of disease-associated microglia molecules. Interestingly, the lack of Ikzf1 induced changes on histone 3 acetylation and methylation levels in the hippocampus. Since the lack of Ikzf1 in mice appears to induce the internalization of synaptic markers within microglia, and severe gliosis we then analyzed hippocampal Ikzf1 levels in several models of neurological disorders. Ikzf1 levels were increased in the hippocampus of these neurological models, as well as in postmortem hippocampal samples from Alzheimer’s disease patients. Finally, over-expressing Ikzf1 in cultured microglia made these cells hyporeactive upon treatment with lipopolysaccharide, and less phagocytic compared to control microglia. Altogether, these results suggest that altered Ikzf1 levels in the adult hippocampus are sufficient to induce synaptic plasticity and memory deficits via altering microglial state and function.

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