華盈生物2025 —— 繪生命全景,解空間奧秘:以多維蛋白組學(xué)技術(shù)引領(lǐng)創(chuàng)新研究新范式!-技術(shù)前沿-資訊-生物在線

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華盈生物2025 —— 繪生命全景,解空間奧秘:以多維蛋白組學(xué)技術(shù)引領(lǐng)創(chuàng)新研究新范式!

作者:上海華盈生物醫(yī)藥科技有限公司 暫無發(fā)布時(shí)間 (訪問量:11966)

<p><span style="color: #262626;">在生命科學(xué)研究范式發(fā)生深刻變革的今天,以蛋白組學(xué)及其前沿分支“空間蛋白組學(xué)”為代表的技術(shù)體系,已成為驅(qū)動源頭創(chuàng)新與重大發(fā)現(xiàn)的引擎。它們不僅能夠全景式解析生理病理過程中復(fù)雜的蛋白質(zhì)表達(dá)、互作與動態(tài)變化,更能將關(guān)鍵的分子事件精準(zhǔn)定位至特定的組織微區(qū)以及單個(gè)細(xì)胞,在空間維度上還原生命的真實(shí)架構(gòu)與功能網(wǎng)絡(luò),為理解發(fā)育、疾病、免疫等核心生命過程提供了前所未有的視角。</span></p> <p><span style="color: #262626;">作為這一科研范式變革的堅(jiān)定推動者,華盈生物始終致力于以前沿、完整、可定制的蛋白組學(xué)解決方案,賦能科學(xué)研究突破邊界。在過去的一年中,我們榮幸地見證了眾多合作伙伴在CNS及其子刊等國際頂級期刊上發(fā)表了一系列具有里程碑意義的高分研究成果。這些工作不僅解決了領(lǐng)域內(nèi)的重要科學(xué)問題,更生動展現(xiàn)了以整合性、單細(xì)胞分辨率空間蛋白組學(xué)為主導(dǎo)的新研究范式的巨大價(jià)值——它正在系統(tǒng)性地揭開生命復(fù)雜性的層層面紗,引領(lǐng)基礎(chǔ)研究與臨床轉(zhuǎn)化邁向更深刻、更精準(zhǔn)的新階段。我們期待繼續(xù)以堅(jiān)實(shí)的技術(shù)平臺和深度的服務(wù),與全國科研同仁攜手,共同繪制更加精細(xì)的生命圖譜,驅(qū)動更多源頭創(chuàng)新。我們甄選了若干合作伙伴的標(biāo)志性創(chuàng)新研究成果,以資交流與研討。</span></p> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="">1</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:復(fù)旦大學(xué)附屬中山醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #262626;"><strong><span style="color: #ff0000;">C</span></strong><strong><span style="color: #ff0000;">e</span></strong><strong><span style="color: #ff0000;">ll (IF:</span></strong><strong><span style="color: #ff0000;">42.5</span></strong><strong><span style="color: #ff0000;">)</span></strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:<strong>Cancer cells co-opt an inter-organ neuroimmune circuit to escape immune surveillance</strong></span></p> <p><span style="color: #262626;">該研究揭示了癌細(xì)胞通過ATF4-SLIT2-CGRP軸激活傷害感受神經(jīng)元,遠(yuǎn)程重塑腫瘤引流淋巴結(jié)(TDLN)的免疫狀態(tài),從而逃避免疫監(jiān)視的新機(jī)制,為聯(lián)合神經(jīng)調(diào)節(jié)和免疫治療提供了理論基礎(chǔ)。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>PCF空間單細(xì)胞蛋白組</strong></span><span style="color: #0987e0;">檢測服務(wù),助力研究者發(fā)現(xiàn)了眾多免疫細(xì)胞中,只有腫瘤相關(guān)巨噬細(xì)胞(TAM)和傷害感受神經(jīng)元具有顯著的共定位關(guān)系,為揭示“TAM激活傷害感受神經(jīng)元”的機(jī)制假說提供了直接的空間原位證據(jù)。</span></p> <section><img src="https://img.medsci.cn/e4345f172863f7232a9a7e6fb9bd7bc9493e3853d9fe894bbee0df89de3494ae.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section></section> </section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="">2</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:上海長征醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>C</strong><strong>e</strong><strong>ll (IF:</strong><strong>42.5</strong><strong>)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>An iPSC-derived CD19/BCMA CAR-NK therapy in a</strong><strong> </strong><strong>patient with systemic sclerosis</strong></span></p> <p><span style="color: #262626;">該研究設(shè)計(jì)并開發(fā)了iPSC來源的CD19/BCMA雙靶點(diǎn)的CAR-NK細(xì)胞產(chǎn)品QN-139b,并成功應(yīng)用在一例難治性硬皮病患者中,為重癥自身免疫病提供了變革性治療方案。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>LCM-MS</strong><strong>空間蛋白組</strong></span><span style="color: #0987e0;">檢測服務(wù)。LCM-MS空間蛋白組發(fā)現(xiàn)了CAR-NK灌輸后,在患者皮膚的基底層、汗腺層、上皮層和真皮膠原層中不同的生物學(xué)通路被激活,揭示了QN-139b通過雙靶點(diǎn)清除致病B細(xì)胞,可以重塑免疫穩(wěn)態(tài)和逆轉(zhuǎn)組織纖維化。</span></p> <section><img src="https://img.medsci.cn/77d64b54c3467374adbea43a55d16e4a35904189e606888767683089eef53307.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="">3</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:復(fù)旦大學(xué)附屬華山醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong><span class="">Cancer Cell</span> (IF:</strong><strong>44.5</strong><strong>)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Targeting tumor monocyte-intrinsic PD-L1 by rewiring STING signaling and enhancing STING agonist therapy</strong></span></p> <p><span style="color: #262626;">該項(xiàng)研究探討了STING信號通路在腫瘤免疫治療中的復(fù)雜作用,特別是其誘導(dǎo)的腫瘤單核細(xì)胞中PD-L1的高表達(dá)對抗STING激動劑療法產(chǎn)生耐藥性的影響。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>PEX100信號通路磷酸化<span class="">抗體芯片</span>檢測分析服務(wù)</strong></span><span style="color: #0987e0;">,系統(tǒng)解析了TLR2激活對STING下游JAK-STAT和NF-κB通路磷酸化水平的調(diào)控,為機(jī)制闡釋提供了關(guān)鍵證據(jù)。</span></p> <section><img src="https://img.medsci.cn/028ac4a857b5ddb97c50062985c518b046f723a892fa91b8bd14aeca614d5fa8.jpg" /></section> </section> </section> </section> </section> </section> </section> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="" data-num="2">4</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:中國醫(yī)學(xué)科學(xué)院腫瘤醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Signal Transduct Target Ther (IF: 52.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Characterization of the extrinsic and intrinsic signatures and therapeutic vulnerability of small cell lung cancers</strong></span></p> <p><span style="color: #262626;">這項(xiàng)研究全面描繪了小細(xì)胞肺癌(SCLC)的單細(xì)胞和空間圖譜,系統(tǒng)解析了SCLC的腫瘤微環(huán)境組成和癌細(xì)胞異質(zhì)性,并首次報(bào)道了FAK剪接變體可作為SCLC的預(yù)后標(biāo)志物和治療靶點(diǎn)。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>PCF空間單細(xì)胞蛋白組</strong></span><span style="color: #0987e0;">檢測服務(wù),助力研究者揭示了腫瘤組織和癌旁組織顯著差異的免疫微環(huán)境特征,并發(fā)現(xiàn)了對免疫治療反應(yīng)不同的患者中,腫瘤細(xì)胞上抗原呈遞分子<span class="">MHC</span>表達(dá)的顯著異質(zhì)性,為理解SCLC免疫逃逸機(jī)制提供了新視角。</span></p> <section><img src="https://img.medsci.cn/101926cb29d8f51d21361980c8e7f1483907dd5687c9554f11a18d78c19ce7be.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section></section> </section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="" data-num="3">5</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:上海長海醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Signal Transduct Target Ther (IF: 52.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:<strong>A novel long-acting C5a-blocking cyclic peptide prevents sepsis-induced organ dysfunction via effective blockade of the inflammatory cascade</strong></span></p> <p><span style="color: #262626;">這項(xiàng)研究開發(fā)和驗(yàn)證了一種新型長效 C5a 阻斷環(huán)肽(Cp1)在防治膿毒癥中作用效果。</span></p> <p><span style="color: #0987e0;">華盈生物提供的</span><span style="color: #ff0000;"><strong>Luminex</strong><strong>細(xì)胞因子</strong><strong>檢測服務(wù)</strong></span><span style="color: #0987e0;">協(xié)助研究團(tuán)隊(duì)全面評估了 Cp1 對炎癥級聯(lián)反應(yīng)的阻斷效果。通過對小鼠血漿及腹腔灌洗液中多種細(xì)胞因子與趨化因子的廣譜篩查,證實(shí)了 Cp1 能顯著抑制 IL-6、TNF-α 等關(guān)鍵因子的表達(dá),從而有效遏制“細(xì)胞因子風(fēng)暴”。</span></p> <section><img src="https://img.medsci.cn/fe5dd7213d7fb50b3c2c281336296a5bd6ecd34a799693b7e2027ee40c03f04e.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="" data-num="4">6</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:清華大學(xué)</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Signal Transduct Target Ther (IF: 52.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Clinical investigation on nebulized human umbilical cord</strong><strong> </strong><strong>MSC-derived extracellular vesicles for pulmonary</strong><strong>fi</strong><strong>brosis</strong><strong> </strong><strong>treatment</strong></span></p> <p><span style="color: #262626;">該研究開發(fā)了一種安全、有效且臨床可行的霧化人臍帶間充質(zhì)干細(xì)胞外泌體(hUCMSC-EVs)療法,為肺纖維化提供了一種新型無細(xì)胞治療策略。</span></p> <p><span style="color: #262626;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>外泌體</strong><strong>蛋白組學(xué)</strong><strong>檢測服務(wù)</strong></span><span style="color: #262626;">,揭示了hUCMSC-EVs蛋白富集到很多組織重構(gòu)的生物學(xué)通路中。很多蛋白參與超高分子纖維組成,及細(xì)胞骨架組成,這些都與纖維化直接相關(guān),為解釋hUCMSC-EVs參與肺組織的纖維化重建提供了分子層面的證據(jù)。</span></p> <section><img src="https://img.medsci.cn/c9c2b4de33e5ea1028496e3332d34819e1043d9e9bf5f214a82c10d6e8e139ac.jpg" /></section> </section> </section> </section> </section> </section> </section> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="" data-num="3">7</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬同濟(jì)醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>J Hepatol (IF: 33)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>TGM2-mediated histone serotonylation promotes HCC progression via MYC signalling pathway</strong></span></p> <p><span style="color: #262626;">該研究發(fā)現(xiàn)了核定位的谷氨酰胺轉(zhuǎn)移酶2(TGM2)介導(dǎo)的H3Q5ser 修飾通過MYC 信號通路促進(jìn)肝細(xì)胞癌進(jìn)展。TGM2可作為HCC的預(yù)后生物標(biāo)志物,靶向其谷氨酰胺轉(zhuǎn)移酶活性可能是抑制HCC進(jìn)展的有效策略。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>20K人類蛋白組芯片</strong><strong>檢測</strong><strong>服務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了轉(zhuǎn)錄中介因子TRIM28可以直接和TGM2結(jié)合。TRIM28可以介導(dǎo)TGM2向MYC募集,促進(jìn) H3Q5ser 修飾 MYC 靶基因。</span></p> <section><img src="https://img.medsci.cn/1f2f2a7fecbff14f48e68eb7681b6b744c26d140053635419b5e3866eae8ad5f.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section></section> </section> <section> <section style="color: #0987e0;"><strong>08</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:南方醫(yī)科大學(xué)珠江醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Gut</strong><strong> (IF:</strong><strong>26.2</strong><strong>)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Gut microbial-derived N-acetylmuramic acid alleviates colorectal cancer via the AKT1 pathway</strong></span></p> <p><span style="color: #262626;">該研究揭示了一種特定的肽聚糖片段<span class="">N-乙酰胞壁酸</span>(NAM)通過靶向并阻斷AKT1磷酸化的方式調(diào)控下游信號通路,發(fā)揮治療結(jié)直腸癌的創(chuàng)新機(jī)制。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>20K人類蛋白組芯片靶</strong><strong>點(diǎn)篩選</strong><strong>和SPR驗(yàn)證</strong><strong>靶點(diǎn)結(jié)合的檢測服</strong><strong>務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了AKT1是NAM的直接結(jié)合靶點(diǎn)蛋白。</span></p> <section><img src="https://img.medsci.cn/2fc19f5da74b002de61efe27ae7635f37e2f425a51600859f1d3a2a3c03ef5a1.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>0</strong><strong title="" data-original-title="" data-num="5">9</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:華中科技大學(xué)同濟(jì)醫(yī)學(xué)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Nat Commun (IF: 15.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>High-content screening identifies ganoderic acid A as a senotherapeutic to prevent cellular senescence and extend healthspan in preclinical models</strong></span></p> <p><span style="color: #262626;">這項(xiàng)研究通過高內(nèi)涵篩選發(fā)現(xiàn)了一種低毒性的抗衰老天然產(chǎn)物靈芝酸A,并證實(shí)了靈芝酸A能夠預(yù)防多個(gè)物種的衰老,為開發(fā)新型抗衰老藥物提供了新思路。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>20K人類蛋白組芯片</strong><strong>檢測服務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了靈芝酸A可以直接與TCOF1結(jié)合以維持核糖體穩(wěn)態(tài),從而減輕多種細(xì)胞衰老表型。</span></p> <section><img src="https://img.medsci.cn/2730a9cc80fa9ba363736eeaf174e93a345cc98c428a34d13c68ee3b3a196268.jpg" /></section> </section> </section> </section> </section> </section> </section> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>10</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:首都兒科研究所</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Nat Commun (IF: 15.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Parallel comparison of T cell and B cell subpopulations of adenoid hypertrophy and tonsil hypertrophy of children</strong></span></p> <p><span style="color: #262626;">該研究首次在單細(xì)胞水平揭示了兒童腺樣體肥大與扁桃體肥大的免疫微環(huán)境差異,闡明了腺樣體以免疫抑制為主導(dǎo)、扁桃體以適應(yīng)性免疫應(yīng)答為主的機(jī)制。</span></p> <p><span style="color: #0987e0;">華盈生物提供的</span><span style="color: #ff0000;"><strong>Luminex 細(xì)胞因子檢測服務(wù)</strong></span><span style="color: #0987e0;">協(xié)助團(tuán)隊(duì)對分選的 B 細(xì)胞與T 細(xì)胞分泌的關(guān)鍵細(xì)胞因子進(jìn)行了深度分析,揭示了腺樣體肥大組織具有更強(qiáng)的免疫抑制特性及較弱的免疫反應(yīng)能力。</span></p> <section><img src="https://img.medsci.cn/80da1cf2f923ed74468c394c12cefce6f8a5f14e47c8369181091e186238f561.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section><strong style="color: #0987e0;">11</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:北京大學(xué)腫瘤醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Nat Commun (IF: 15.7)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Harnessing the FGFR2/NF2/YAP signaling-dependent necroptosis to develop an FGFR2/IL-8 dual blockade therapeutic strategy</strong></span></p> <p><span style="color: #262626;">該研究系統(tǒng)闡明了FGFR2抑制劑通過NF2-YAP-MST1軸誘導(dǎo)壞死性凋亡的機(jī)制,并揭示了IL-8/PD-L1介導(dǎo)的免疫逃逸。聯(lián)合FGFR2抑制劑與免疫檢查點(diǎn)阻斷劑的策略為ESCC治療提供了新方向,具有重要臨床轉(zhuǎn)化價(jià)值。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>細(xì)胞因子檢測服務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了壞死性凋亡通過IL-8上調(diào)PD-L1的表達(dá),介導(dǎo)免疫逃逸。</span></p> <section><img src="https://img.medsci.cn/4a58b4b2e62ccbfdb204a39430a48ae8f41c7875f81dd4c86b4f701d05e1a909.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>12</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:南方醫(yī)科大學(xué)南方醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Cancer Commun (IF: 24.9)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Targeting SPHK1 in macrophages remodels the tumor microenvironment and enhances anti-PD-1 immunotherapy efficacy in colorectal cancer liver metastasis</strong></span></p> <p><span style="color: #262626;">該項(xiàng)研究發(fā)現(xiàn)了腫瘤相關(guān)巨噬細(xì)胞高表達(dá)的SPHK1在結(jié)直腸癌肝轉(zhuǎn)移(CRLM)發(fā)生和進(jìn)展中作用機(jī)制,并提示聯(lián)合SPHK1阻斷劑和抗PD-1治療可能成為一種有前途的治療方案。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>Luminex細(xì)胞因子檢測服務(wù)</strong></span><span style="color: #0987e0;">,助力解析了腫瘤細(xì)胞通過分泌趨化因子征募SPHK1+ TAMs,為揭示SPHK1調(diào)控腫瘤免疫微環(huán)境的機(jī)制提供了關(guān)鍵證據(jù)。</span></p> <section><img src="https://img.medsci.cn/1adfab29dec6f345ba7d92f6ea722120b7bad1867cd78f1361cbb357b712322b.jpg" /></section> </section> </section> </section> </section> </section> </section> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>13</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:華中科技大學(xué)同濟(jì)醫(yī)學(xué)院附屬協(xié)和醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>Sci Bull  (IF: 21.1)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Initial cardioplegic flush with crystalloid cardioplegia improves donor heart preservation and function via NR4A3 upregulation and metabolic reprogramming</strong></span></p> <p><span style="color: #262626;">該項(xiàng)研究提出了一種創(chuàng)新的供體心臟獲取和保存方法,使用晶體停搏液(CC)聯(lián)合威斯康星大學(xué)(UW)保存液。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>PEX100信號通路磷酸化抗體芯片檢測分析服務(wù)</strong></span><span style="color: #0987e0;">,精準(zhǔn)解析了CC+UW干預(yù)下心肌細(xì)胞信號通路的動態(tài)變化,揭示了該方法通過抑制NF-κB通路激活,減少炎癥反應(yīng)與能量消耗,提升心臟保存效果。</span></p> <section><img src="https://img.medsci.cn/779e5b4980f645ec7123aa933f79176ee3bfdf639b1db7bc3dcf9799f3f936fa.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section> <section></section> </section> <section> <section style="color: #0987e0;"><strong>14</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:中國人民解放軍總醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>J Clin Invest  (IF: 13.6)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>Asparagine drives immune evasion in bladder cancer via RIG-I stability and type I IFN signaling</strong></span></p> <p><span style="color: #262626;">這項(xiàng)研究發(fā)現(xiàn)了在膀胱癌中,天然代謝物天冬酰胺可以直接結(jié)合RIG-I,促進(jìn)其降解,從而抑制IFN信號和抗腫瘤免疫。提出了左旋天冬酰胺酶聯(lián)合抗PD-1治療的新策略。</span></p> <p><span style="color: #0987e0;">華盈生物提供的</span><span style="color: #ff0000;"><strong> Luminex細(xì)胞因子檢測服務(wù)</strong></span><span style="color: #0987e0;">協(xié)助團(tuán)隊(duì)解析了腫瘤細(xì)胞與免疫微環(huán)境的互作機(jī)制。通過高通量篩選多種細(xì)胞因子與趨化因子,發(fā)現(xiàn)了抑制天冬酰胺可促進(jìn)腫瘤細(xì)胞分泌CCL5,從而招募CD8+ T細(xì)胞浸潤,增強(qiáng)抗腫瘤免疫的分子機(jī)制。</span></p> <section><img src="https://img.medsci.cn/dc2139766ca2f6fa042924c5897485525b35c9188b358aceffeb0c218a6e543e.jpg" /></section> </section> </section> </section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>15</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:復(fù)旦大學(xué)附屬中山醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong>J Exp Clin Cancer Res (IF:12.8)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>The DCDC2/ENO1 axis promotes tumor progression and immune evasion in intrahepatic cholangiocarcinoma via activating FGL1-LAG3 checkpoint</strong></span></p> <p><span style="color: #262626;">該研究揭示了DCDC2是肝內(nèi)膽管癌(ICC)的新型腫瘤相關(guān)抗原,其通過穩(wěn)定ENO1蛋白,一方面促進(jìn)腫瘤進(jìn)展,另一方面通過FGL1-LAG3檢查點(diǎn)抑制CD8+T細(xì)胞功能。靶向該軸為ICC診斷和治療提供了新策略。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>20K人類蛋白組芯片自身抗體篩選的檢測服務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了血清中DCDC2自身抗體可作為早期診斷ICC的生物標(biāo)志物。這為解析DCDC2是一種新型腫瘤相關(guān)抗原提供了強(qiáng)有力的證據(jù)支持。</span></p> <section><img src="https://img.medsci.cn/7db1b06444854e787cb6411ca60238c1f794e614b1f9408d364fdf1e78082773.jpg" /></section> </section> </section> </section> </section> </section> </section> <section data-tools="135編輯器" data-id="157292"> <section> <section> <section> <section> <section> <section> <section style="color: #0987e0;"><strong>16</strong></section> </section> </section> </section> </section> <section> <section style="color: #333333;" data-autoskip="1"> <p><span style="color: #262626;"><strong>合作單位</strong>:中山大學(xué)孫逸仙紀(jì)念醫(yī)院</span></p> <p><span style="color: #262626;"><strong>期刊名稱</strong>:</span><span style="color: #ff0000;"><strong><span class="">eBioMedicine</span> (IF: 10.8)</strong></span></p> <p><span style="color: #262626;"><strong>文章標(biāo)題</strong>:</span><span style="color: #262626;"><strong>TCL1A in naïve B cells as a therapeutic target for type 1 diabetes</strong></span></p> <p><span style="color: #262626;">本研究發(fā)現(xiàn)了T1D患者早期B細(xì)胞的功能異常,尤其是naïve B細(xì)胞比例增加,且其AKT激酶共激活因子TCL1A表達(dá)上調(diào)。靶向TCL1A能降低naïve B細(xì)胞數(shù)量,改善葡萄糖耐量。該成果為T1D治療提供了新的潛在靶點(diǎn)和治療策略。</span></p> <p><span style="color: #0987e0;">華盈生物為該研究提供了</span><span style="color: #ff0000;"><strong>PEX100信號通路磷酸化抗體芯片檢測服務(wù)</strong></span><span style="color: #0987e0;">,助力研究團(tuán)隊(duì)發(fā)現(xiàn)了TCL1A主要調(diào)PI3K/AKT途徑,揭示了TCL1A可以通過AKT2途徑調(diào)節(jié)B細(xì)胞的生存和增殖,促進(jìn)了T1D中自身反應(yīng)性B細(xì)胞的存活。</span></p> <p><img src="https://img.medsci.cn/8ef86fdfb78281e5795f6d7f0e7282e9ca46308a09120cd5e030c6d8c050ea11.jpg" /></p> </section> </section> </section> </section> </section> <p><span style="color: #262626;">回顧過去一年,我們倍感榮幸能夠參與到這場深刻改變生命科學(xué)認(rèn)知邊界的進(jìn)程中。從揭示疾病機(jī)制的分子基礎(chǔ),到繪制組織功能的時(shí)空圖譜,每一項(xiàng)令人矚目的研究成果背后,都標(biāo)志著我們對生命復(fù)雜性的理解又邁出了堅(jiān)實(shí)的一步。</span></p> <p><span style="color: #262626;">展望未來,生命科學(xué)的探索將向著更整合、更動態(tài)、更空間精準(zhǔn)的方向不斷深化。我們將繼續(xù)以前瞻性的視野,持續(xù)迭代與拓展我們的技術(shù)平臺——無論是蛋白組覆蓋的廣度和深度、還是空間分辨率與單細(xì)胞精度的極限,我們都將不懈追求。我們堅(jiān)信,蛋白組學(xué),特別是其空間與動態(tài)維度,將是解鎖下一輪生物學(xué)突破的核心鑰匙。</span></p> <p><span style="color: #262626;">我們期待,在新的一年里,繼續(xù)以最堅(jiān)實(shí)的技術(shù)平臺、最專業(yè)的科學(xué)支持與最開放的協(xié)作精神,與每一位致力于探索未知的科學(xué)家并肩前行。讓我們攜手,共同將更多的科學(xué)假設(shè)轉(zhuǎn)化為顛覆性的發(fā)現(xiàn),在描繪生命奧秘的宏偉藍(lán)圖上,增添更多決定性的筆觸。</span></p> <section> <section style="color: #0987e0000;"></section> <p style="color: #595959;"><span style="color: #0987e0;"><strong>業(yè)務(wù)咨詢400-869-2936或17316301592(微信同號)</strong></span></p> <section style="color: #0987e0000;" data-role="title" data-tools="135編輯器" data-id="101167"> <section> <section> <section> <section> <section style="color: #ffffff;" data-brushtype="text"> <p><span style="color: #000000;"><strong>相關(guān)文獻(xiàn)</strong></span></p> </section> </section> </section> </section> </section> </section> <p><span style="color: #262626;">1.Zhang, Y., et al., Cancer cells co-opt an inter-organ neuroimmune circuit to escape immune surveillance. Cell, 2025. 188(24):6754-6773.e29.</span></p> <p><span style="color: #262626;">2.Wang, X., et al., An iPSC-derived CD19/BCMA CAR-NK therapy in a patient with systemic sclerosis. Cell, 2025. 188(16):4225-4238.e12.</span></p> <p><span style="color: #262626;">3.Song, H., et al., Targeting tumor monocyte-intrinsic PD-L1 by rewiring STING signaling and enhancing STING agonist therapy. Cancer Cell, 2025. 43(3):503-518.e10.</span></p> <p><span style="color: #262626;">4.Wang, G.Z., et al., Characterization of the extrinsic and intrinsic signatures and therapeutic vulnerability of small cell lung cancers. Signal Transduct Target Ther, 2025. 10(1):290.</span></p> <p><span style="color: #262626;">5.Luo, Z., et al., A novel long-acting C5a-blocking cyclic peptide prevents sepsis-induced organ dysfunction via effective blockade of the inflammatory cascade. Signal Transduct Target Ther, 2025. 10(1):362.</span></p> <p><span style="color: #262626;">6.Li, M., et al., Clinical investigation on nebulized human umbilical cord MSC-derived extracellular vesicles for pulmonary fibrosis treatment. Signal Transduct Target Ther, 2025. 10(1):179.</span></p> <p><span style="color: #262626;">7.Dong, R., et al., TGM2-mediated histone serotonylation promotes HCC progression via MYC signalling pathway. J Hepatol, 2025. 83(1):105-118.</span></p> <p><span style="color: #262626;">8.Hu, M., et al., Gut microbial-derived N-acetylmuramic acid alleviates colorectal cancer via the AKT1 pathway. Gut, 2025. 74(8):1230-1245.</span></p> <p><span style="color: #262626;">9.Chen, L., et al., High-content screening identifies ganoderic acid A as a senotherapeutic to prevent cellular senescence and extend healthspan in preclinical models. 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