日期:
2020 年 — 2026 年
2020
2021
2022
2023
2024
2025
2026
影响因子:

Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response

疾病相关的 RNF186 对 ATF6 的泛素化促进了先天性受体诱导的未折叠蛋白反应

Kishu Ranjan, Matija Hedl, Saloni Sinha, Xuchen Zhang, Clara Abraham

TNFSF15 Promotes Antimicrobial Pathways in Human Macrophages and These Are Modulated by TNFSF15 Disease-Risk Variants

TNFSF15 促进人类巨噬细胞中的抗菌途径,这些途径受 TNFSF15 疾病风险变异的调节

Rui Sun, Matija Hedl, Clara Abraham

Unbiased Label-Free Quantitative Proteomics of Cells Expressing Amyotrophic Lateral Sclerosis (ALS) Mutations in CCNF Reveals Activation of the Apoptosis Pathway: A Workflow to Screen Pathogenic Gene Mutations

CCNF 中表达肌萎缩侧索硬化症 (ALS) 突变的细胞的无偏无标记定量蛋白质组学揭示了细胞凋亡途径的激活:筛查致病基因突变的工作流程

Flora Cheng, Alana De Luca, Alison L Hogan, Stephanie L Rayner, Jennilee M Davidson, Maxinne Watchon, Claire H Stevens, Sonia Sanz Muñoz, Lezanne Ooi, Justin J Yerbury, Emily K Don, Jennifer A Fifita, Maria D Villalva, Hannah Suddull, Tyler R Chapman, Thomas J Hedl, Adam K Walker, Shu Yang, Marco Mo

Riluzole does not ameliorate disease caused by cytoplasmic TDP-43 in a mouse model of amyotrophic lateral sclerosis

利鲁唑不能改善肌萎缩侧索硬化症小鼠模型中细胞质 TDP-43 引起的疾病

Amanda L Wright, Paul A Della Gatta, Sheng Le, Britt A Berning, Prachi Mehta, Kelly R Jacobs, Hossai Gul, Rebecca San Gil, Thomas J Hedl, Winonah R Riddell, Owen Watson, Sean S Keating, Juliana Venturato, Roger S Chung, Julie D Atkin, Albert Lee, Bingyang Shi, Catherine A Blizzard, Marco Morsch, Ada

IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes

IL23 诱导 IL23R 循环并扩增人类巨噬细胞中先天受体诱导的信号和细胞因子,而 IBD 保护性 IL23R R381Q 变体会调节这些结果

Rui Sun, Matija Hedl, Clara Abraham

Myeloid Cell-Intrinsic IRF5 Promotes T Cell Responses through Multiple Distinct Checkpoints In Vivo, and IRF5 Immune-Mediated Disease Risk Variants Modulate These Myeloid Cell Functions

髓系细胞内在 IRF5 通过体内多个不同的检查点促进 T 细胞反应,IRF5 免疫介导的疾病风险变异调节这些髓系细胞功能

Jie Yan, Matija Hedl, Clara Abraham

Disease Risk-Associated Genetic Variants in STAT1 and STAT4 Function in a Complementary Manner to Increase Pattern-Recognition Receptor-Induced Outcomes in Human Macrophages

STAT1 和 STAT4 中与疾病风险相关的遗传变异以互补的方式发挥作用,从而增强人类巨噬细胞中模式识别受体诱导的结果

Matija Hedl, Rui Sun, Clara Abraham

LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes

LACC1是NOD2诱导的、内质网应激介导的人类巨噬细胞先天免疫结果所必需的,而LACC1风险变异体调节这些结果

Chen Huang ,Matija Hedl ,Kishu Ranjan ,Clara Abraham

STAT3 and STAT5 Signaling Thresholds Determine Distinct Regulation for Innate Receptor-Induced Inflammatory Cytokines, and STAT3/ STAT5 Disease Variants Modulate These Outcomes

STAT3 和 STAT5 信号阈值决定先天受体诱导的炎症细胞因子的不同调节,STAT3/STAT5 疾病变异调节这些结果

Matija Hedl, Rui Sun, Chen Huang, Clara Abraham

Twist1 and Twist2 Induce Human Macrophage Memory upon Chronic Innate Receptor Treatment by HDAC-Mediated Deacetylation of Cytokine Promoters

Twist1 和 Twist2 通过 HDAC 介导的细胞因子启动子去乙酰化在慢性先天受体治疗后诱导人类巨噬细胞记忆

Rui Sun, Matija Hedl, Clara Abraham