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近期使用MCE产品发表高分文章锦集

    MCE (MedChemExpress) 是全球领先的科研化学品和生物活性化合物供应商。MCE 的产品范围覆盖各类抑制剂、激动剂、化合物库、天然产物、细胞因子及多种生化试剂盒。“确保客户拿到的每一个产品的质量” 是 MCE 的核心理念。现将 MCE 客户近期发表的部分高分文章作一分享,MCE 您科研路上做贴心的伙伴!
 
    The molecular landscape of ETMR at diagnosis and relapse.
 
    Pamiparib purchased from MCE.
 
    多层菊形团样胚胎性肿瘤 (ETMR) 是一种预后普遍较差的侵袭性儿科胚胎性脑肿瘤。研究团队收集了 193 个原发性 ETMR 和 23 个匹配复发样本,以研究其基因组图谱。研究发现,驱动器 C19MC 未被频繁扩增的肿瘤患者中,存在 DICER1 或者其他 microRNA 相关的胚系突变。全基因组测序表明,肿瘤的单核苷酸变异 (SNV) 总体复发率较低,但 R-loop 结构的广泛存在,导致普遍的基因组不稳定。研究表明,R-loop 相关的染色体不稳定可由 DICER1 功能缺失引起。原发肿瘤与匹配的复发样本的比较显示,结构变异的保守性很强,而 SNV 的保守性却很低。此外,许多新获得的 SNV 与顺铂治疗相关的突变信号有关。最后,研究证明了用拓扑异构酶和 PARP 抑制剂靶向 R-loop 可能是 ETMR 的有效治疗对策。
 
    Researchers found that patients with tumours in which the proposed driver C19MC2-4 was not amplified frequently had germline mutations in DICER1 or other microRNA-related aberrations such as somatic amplification of miR-17-92 (alsoknown as MIR17HG). Whole-genome sequencing revealed that tumours had an overalllow recurrence of single-nucleotide variants (SNVs), but showed prevalentgenomic instability caused by widespread occurrence of R-loop structures. Weshow that R-loop-associated chromosomal instability can be induced by the lossof DICER1 function. Comparison of primary tumours and matched relapse samples showed a strong conservation of structural variants, but low conservation ofSNVs. Moreover, many newly acquired SNVs are associated with a mutational signature related to cisplatin treatment. Finally, Researchers show that targeting R-loops with topoisomerase and PARP inhibitors might be an effective treatment strategy for this deadly disease.
 
    Metabolic Control of Astrocyte Pathogenic Activity via cPLA2-MAVS. 
 
    Miglustat hydrochloride  purchased from MCE.
 
    代谢已被证明可以调控外周免疫,但对其在中枢神经系统 (CNS) 炎症中的作用知之甚少。通过结合蛋白质组,代谢组,转录组,和摄动研究, 研究者发现 cPLA2-MAVS 通过代谢调控星形胶质细胞的致病性。
 
 
    A Translation-Activating Function of MIWI/piRNA during Mouse Spermiogenesis. 
 
    Cycloheximide purchased from MCE.
 
    精子发生是一个高度协调发育过程,在此过程中染色质浓缩使转录与翻译解耦。生精 mRNAs 转录较早并以翻译惰性状态保存,直到翻译需要。然而,目前仍不清楚在精子发生过程中这种抑制的 mRNA 如何被激活。作者团队之前已报道过,在精子形成后期,MIWI/piRNA 机制负责 mRNA 的消除,为产生精子做准备。本次研究意外地发现同样的机制还负责激活部分生精 mRNA 的翻译,以协调向精子的形态转化。这种作用需要 piRNA 与 3'UTR 中靶标 mRNA 的特定碱基配对相互作用,与顺式作用 AU- 富含元件偶联来激活翻译,使 MIWI/piRNA/eIF3f/HuR 超复合体以发育阶段特异性方式成核。这些发现揭示了 piRNA 系统在翻译激活中的关键作用,这在精子细胞发育是必需的。
 
    Researchers unexpectedly discover that the MIWI/piRNA machinery is responsible for activating translation of a subset of spermiogenic mRNAs to coordinate with morphological transformation into spermatozoa. Such action requires specific base-pairing interactions of piRNAs with target mRNAs in their 3' UTRs, which activates translation through coupling with cis-acting AU-rich elements to nucleate the formation of a MIWI/piRNA/eIF3f/HuR super-complex in a developmental stage-specific manner. These findings reveal acritical role of the piRNA system in translation activation, and that is functionally required for spermatid development.
 
    The ADP/ATP translocase drives mitophagy independent of nucleotide exchange.
 
    CCCP purchased from MCE.
 
    线粒体稳态取决于线粒体,线粒体的程序性降解。已知只有少数蛋白质参与线粒体吞噬。该文章首次阐述了腺苷转运蛋白 ANT (Adenine Nucleotide Translocator) 对线粒体自噬的重要作用。
 
    详细见往期ADP/ATP 转位酶驱使线粒体自噬
 
 
    Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis.
 
    Emricasan (IDN-6556) purchased from MCE.
 
    caspase-8 是外源性凋亡的启动半胱天冬酶,并抑制由 RIPK3 和 MLKL 介导的坏死性凋亡。该研究表明,酶活失效的 CASP8 (C362S) 的表达通过诱导坏死性凋亡和细胞焦亡诱导小鼠胚胎致死。与 Casp8-/-小鼠类似,在内皮细胞坏死性凋亡导致心血管缺陷后 Casp8C362S/C362S小鼠胚胎死亡。缺乏 MLKL 挽救了心血管疾病表型,但意外地导致了 Casp8c362/c362 小鼠围产期死亡率升高,这表明 CASP8 (C362S) 在胚胎发育的后期引起坏死性凋亡非依赖性死亡。肠上皮细胞中 caspase-8 催化活性特异性缺失引起肠道炎症与小鼠 Casp8 敲除结果相似。肠道细胞 caspase-8 特异性缺失小鼠中,敲除 Mlk1 抑制坏死性凋亡会严重加重肠道炎症,并且引起过早的致死性。CASP8 (C362S) 的表达触发了 ASC 斑点的形成,caspase-1 的活化和 IL-1β 的分泌。在Casp8C362S/C362SMlkl-/-Asc-/- 或 Casp8C362S/C362SMlkl-/-Casp1-/- 小鼠中,胚胎致死率和过早死亡都完全得到挽救,表明当坏死性凋亡被阻断时,炎性小体的活化促进CASP8 (C362S) 介导的组织病理。因此,因此,caspase-8 是控制细胞凋亡、坏死性凋亡和细胞焦亡的分子开关,在胚胎发育和成人时期防止组织损伤。
 
    Researchers show that the expression ofenzymatically inactive CASP8 (C362S) causes embryonic lethality in mice by inducing necroptosis and pyroptosis. Similar to Casp8-/- mice, Casp8C362S/C362S mouse embryos died after endothelial cell necroptosis leading to cardiovascular defects. MLKL deficiency rescued the cardiovascular phenotypebut unexpectedly caused perinatal lethality in Casp8C362S/C362S mice, indicating that CASP8 (C362S) causes necroptosis-independent death at laterstages of embryonic development. Specific loss of the catalytic activity of caspase-8 in intestinal epithelial cells induced intestinal inflammation similar to intestinal epithelial cell-specific Casp8 knockout mice. Inhibition of necroptosis by additional deletion of Mlkl severely aggravated intestinal inflammation and caused premature lethality in Mlkl knockout mice with specific loss of caspase-8 catalytic activity in intestinal epithelial cells. Expression of CASP8 (C362S) triggered the formation of ASC specks, activation of caspase-1 and secretion of IL-1β. Both embryonic lethality and premature death were completely rescued in Casp8C362S/C362S Mlkl-/- Asc-/- or Casp8C362S/C362SMlkl-/-Casp1-/- mice, indicating that the activation of the inflammasome promotes CASP8(C362S)-mediated tissue pathology when necroptosis is blocked. Therefore, caspase-8 represents the molecular switch that controls apoptosis, necroptosis and pyroptosis, and prevents tissue damage during embryonic development and adulthood.
 
    The fungal mycobiome promotes pancreatic oncogenesis via activation of MBL.
 
    GemcitabineAmphotericin B purchased from MCE.
 
    细菌性营养不良伴随着结肠癌和肝癌等恶性肿瘤的癌变,并且最近与胰腺导管腺癌 (PDA) 的发病机理有关。该文章证明了真菌从肠腔迁移到胰腺与胰腺导管腺癌 (Pancreatic ductal adenocarcinoma, PDA) 的发病机制有关。 
 
    详细见往期:Nature | 真菌菌群通过激活 MBL 促进胰腺癌发生
 
    Stress-Induced Metabolic Disorder in Peripheral CD4+ T Cells Leads to Anxiety-like Behavior.
 
    Forodesine hydrochloride purchased from MCE.
 
    身体或精神上的压力会导致大脑神经可塑性,并增加患抑郁症和焦虑症的风险。应激暴露导致外周T淋巴细胞功能障碍。然而,尚未充分建立在情绪障碍中外周T淋巴细胞的病理作用和潜在的调节机制。文章表明,频繁应激通过扰乱外周 CD4+ T 细胞代谢导致焦虑、抑郁样行为,增加患焦虑症、抑郁症的风险。
 
    详细见往期:Cell | 应激引起的外周CD4+ T细胞代谢紊乱能够导致焦虑行为

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