Norbury Christopher C相关文献与解析，生知库

Suklabaidya Sujit, Mohanty Suchitra, Reider Irene E, White Jesse, Colter Dominic, McCormick Sarah M, Shembade Noula, Choi Young Bong, Norbury Christopher C, Harhaj Edward W

信号转导

STING

TAX1BP1

发表日期：2026

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HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis

HCMV感染会下调GPX4的表达并刺激脂质过氧化，但不会诱导铁死亡。

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/jvi.01851-24

Martin, Madison; Kumar, Rinki; Buchkovich, Nicholas J; Norbury, Christopher C

The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.

HCMV 被膜蛋白 UL88 可降解 MyD88 并降低先天免疫激活

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/jvi.00414-25

Kumar Rinki, Reider Irene E, Martin Madison, Simpson Julia S, Buchkovich Nicholas J, Norbury Christopher C

其它

发表日期：2025

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A Novel Proteoglycan-4 Isoform Drives Skeletal Regeneration

一种新型蛋白聚糖-4亚型驱动骨骼再生

期刊:

影响因子:

doi:10.1101/2025.09.15.676417

Tantawy, Mohamed; Khajuria, Deepak K; Norbury, Christopher C; Kamal, Fadia; Elbarbary, Reyad A

发表日期：2025

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An increase in glycoprotein concentration on extracellular virions dramatically alters vaccinia virus infectivity and pathogenesis without impacting immunogenicity

细胞外病毒颗粒上糖蛋白浓度的增加会显著改变痘苗病毒的感染性和致病性，但不会影响其免疫原性。

期刊:PLoS Pathogens

影响因子:4.9

doi:10.1371/journal.ppat.1010177

Monticelli, Stephanie R; Bryk, Peter; Brewer, Matthew G; Aguilar, Hector C; Norbury, Christopher C; Ward, Brian M

Peptide-MHC-I from Endogenous Antigen Outnumber Those from Exogenous Antigen, Irrespective of APC Phenotype or Activation

内源性抗原产生的肽-MHC-I 数量多于外源性抗原产生的肽-MHC-I，与 APC 表型或激活状态无关。

期刊:PLoS Pathogens

影响因子:4.9

doi:10.1371/journal.ppat.1004941

Sei, Janet J; Haskett, Scott; Kaminsky, Lauren W; Lin, Eugene; Truckenmiller, Mary E; Bellone, Clifford J; Buller, R Mark; Norbury, Christopher C

APC

发表日期：2015

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Redundant Function of Plasmacytoid and Conventional Dendritic Cells Is Required To Survive a Natural Virus Infection

浆细胞样树突状细胞和常规树突状细胞的冗余功能对于在自然病毒感染中存活至关重要

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/JVI.01024-15

Kaminsky, Lauren W; Sei, Janet J; Parekh, Nikhil J; Davies, Michael L; Reider, Irene E; Krouse, Tracy E; Norbury, Christopher C

MyD88-dependent immunity to a natural model of vaccinia virus infection does not involve Toll-like receptor 2

MyD88依赖性免疫对痘苗病毒感染自然模型的免疫反应不涉及Toll样受体2。

期刊:Journal of Virology

影响因子:3.8

doi:10.1128/JVI.02776-13

Davies, Michael L; Sei, Janet J; Siciliano, Nicholas A; Xu, Ren-Huan; Roscoe, Felicia; Sigal, Luis J; Eisenlohr, Laurence C; Norbury, Christopher C

Crosstalk between the type 1 interferon and nuclear factor kappa B pathways confers resistance to a lethal virus infection

I型干扰素和核因子κB通路之间的相互作用赋予机体对致命病毒感染的抵抗力。

期刊:Cell Host & Microbe

影响因子:18.7

doi:10.1016/j.chom.2013.04.015

Rubio, Daniel; Xu, Ren-Huan; Remakus, Sanda; Krouse, Tracy E; Truckenmiller, Mary Ellen; Thapa, Roshan J; Balachandran, Siddharth; Alcamí, Antonio; Norbury, Christopher C; Sigal, Luis J

Corticosterone impairs dendritic cell maturation and function

皮质酮会损害树突状细胞的成熟和功能。

期刊:Immunology

影响因子:5

doi:10.1111/j.1365-2567.2007.02637.x

Elftman, Michael D; Norbury, Christopher C; Bonneau, Robert H; Truckenmiller, Mary E

Negative feedback regulation of STING signaling by TAX1BP1-directed Golgiphagy.

TAX1BP1 介导的高尔基吞噬作用对 STING 信号传导的负反馈调节。

HCMV infection downregulates GPX4 and stimulates lipid peroxidation but does not induce ferroptosis

HCMV感染会下调GPX4的表达并刺激脂质过氧化，但不会诱导铁死亡。

The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.

HCMV 被膜蛋白 UL88 可降解 MyD88 并降低先天免疫激活

A Novel Proteoglycan-4 Isoform Drives Skeletal Regeneration

一种新型蛋白聚糖-4亚型驱动骨骼再生

An increase in glycoprotein concentration on extracellular virions dramatically alters vaccinia virus infectivity and pathogenesis without impacting immunogenicity

细胞外病毒颗粒上糖蛋白浓度的增加会显著改变痘苗病毒的感染性和致病性，但不会影响其免疫原性。

Peptide-MHC-I from Endogenous Antigen Outnumber Those from Exogenous Antigen, Irrespective of APC Phenotype or Activation

内源性抗原产生的肽-MHC-I 数量多于外源性抗原产生的肽-MHC-I，与 APC 表型或激活状态无关。

Redundant Function of Plasmacytoid and Conventional Dendritic Cells Is Required To Survive a Natural Virus Infection

浆细胞样树突状细胞和常规树突状细胞的冗余功能对于在自然病毒感染中存活至关重要

MyD88-dependent immunity to a natural model of vaccinia virus infection does not involve Toll-like receptor 2

MyD88依赖性免疫对痘苗病毒感染自然模型的免疫反应不涉及Toll样受体2。

Crosstalk between the type 1 interferon and nuclear factor kappa B pathways confers resistance to a lethal virus infection

I型干扰素和核因子κB通路之间的相互作用赋予机体对致命病毒感染的抵抗力。

Corticosterone impairs dendritic cell maturation and function

皮质酮会损害树突状细胞的成熟和功能。