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

Cardiac REDD1 alters glucose and fatty acid metabolic gene expression via an mTORC1-independent, PPARα-dependent mechanism and drives hypertrophic growth

心脏 REDD1 通过一种不依赖于 mTORC1、依赖于 PPARα 的机制改变葡萄糖和脂肪酸代谢基因的表达,并驱动肥大生长。

Wheeler, Mason; Renick, Jamie; Fawbush, Roslyn; McAlpin, Emily; Stevens, Shaunaci; Sreedevi, Karthi; Warren, Junco; Dennis, Michael; Pfleger, Jessica

Podocyte-Specific Expression of the Stress Response Protein REDD1 Is Necessary for Diabetes-Induced Podocytopenia

足细胞特异性表达应激反应蛋白REDD1是糖尿病诱导的足细胞减少症所必需的

Sunilkumar, Siddharth; Yerlikaya, Esma I; Toro, Allyson L; Chen, Han; Zhou, Yandong; Gill, Donald L; Kimball, Scot R; Dennis, Michael D

Targeting REDD1 in Podocytes: A Promising Strategy for Mitigating Diabetic Kidney Injury

靶向足细胞中的REDD1:缓解糖尿病肾损伤的一种有前景的策略

Bohovyk, Ruslan; Staruschenko, Alexander

Deletion of the stress response protein REDD1 prevents sodium iodate-induced RPE damage and photoreceptor loss

删除应激反应蛋白REDD1可预防碘酸钠诱导的RPE损伤和感光细胞丢失。

Subrahmanian, Sandeep M; Yerlikaya, Esma I; Sunilkumar, Siddharth; Toro, Allyson L; McCurry, Christopher M; Grillo, Stephanie L; Barber, Alistair J; Sundstrom, Jeffrey M; Dennis, Michael D

Bone mesenchymal stem cells attenuate hepatic stellate cell activation and liver fibrosis through REDD1/autophagy pathway

骨髓间充质干细胞通过REDD1/自噬通路减弱肝星状细胞活化和肝纤维化。

Tingjuan Huang ,Lina Nie ,Haichao Diao ,Ziyi Shang ,Qizhi Shuai ,Jun Xu ,Jun Xie

REDD1-dependent GSK3β signaling in podocytes promotes canonical NF-κB activation in diabetic nephropathy

在糖尿病肾病中,足细胞中 REDD1 依赖的 GSK3β 信号通路促进经典 NF-κB 通路的激活。

Sunilkumar, Siddharth; Yerlikaya, Esma I; VanCleave, Ashley; Subrahmanian, Sandeep M; Toro, Allyson L; Kimball, Scot R; Dennis, Michael D

REDD1 Affects Proliferation, Apoptosis, Migration, and Colony Formation via p-ERK and p-JNK Signaling in Lung Adenocarcinoma Cells Under Hypoxia

在缺氧条件下,REDD1通过p-ERK和p-JNK信号通路影响肺腺癌细胞的增殖、凋亡、迁移和克隆形成。

Fang, Xiaoyu; Wang, Xuezhao; Liu, Xiansheng; He, Yuanzhou

Corrigendum to "Iron depletion suppresses mTORC1-directed signalling in intestinal Caco-2 cells via induction of REDD1" [Cellular Signalling, 28: (2016) 412-424]

对“铁耗竭通过诱导 REDD1 抑制肠道 Caco-2 细胞中 mTORC1 定向信号传导”的更正 [Cellular Signalling, 28: (2016) 412-424]

Watson, Ailsa; Lipina, Christopher; McArdle, Harry J; Taylor, Peter M; Hundal, Harinder S

REDD1 attenuates cholestatic liver fibrosis and suppresses PI3K/AKT/mTOR pathway.

REDD1 可减轻胆汁淤积性肝纤维化并抑制 PI3K/AKT/mTOR 通路。

Li Xiaonan, Liu Xin, Shi Xinrui, Li Zixu, Shuai Qizhi, Huang Tingjuan, Liu Yun, Ren Junjie

REDD1 Is a Promising Therapeutic Target to Combat the Development of Diabetes Complications: A Report on Research Supported by Pathway to Stop Diabetes

REDD1 是对抗糖尿病并发症发展的一个有前景的治疗靶点:由“阻止糖尿病之路”项目资助的研究报告

Sunilkumar, Siddharth; Dennis, Michael D