Gao Shenglin相关文献与解析，生知库 | 链接生命科学的每一步

Identification of a novel and high-affinity cyclic peptide targeting Keap1 for inflammation treatment by a combined virtual screening strategy.

通过结合虚拟筛选策略，鉴定出一种靶向 Keap1 的新型高亲和力环状肽，用于炎症治疗。

期刊:Journal of Enzyme Inhibition and Medicinal Chemistry

影响因子:5.4

doi:10.1080/14756366.2025.2574023

Gao Shenglin, Shi Xiaokai, Yang Shudan, Wang Yuting, Wang Qian, Yang Minyan

炎症/感染

KEAP1

Immunology/Inflammation

炎症

发表日期：2025

文献求助收藏

Transcriptional Regulation of NUPR1 by MYH11 Activates PI3â K/AKT and Promotes Bladder Cancer Progression Through Ferroptosis and M2 Polarization of Macrophages.

MYH11 对 NUPR1 的转录调控激活 PI3K/AKT，并通过铁死亡和巨噬细胞的 M2 极化促进膀胱癌的进展

期刊:Technology in Cancer Research & Treatment

影响因子:2.8

doi:10.1177/15330338241305434

Zhang Lifeng, Zhang Li, Shi Zebin, Mi Yuanyuan, Zhang Lei, Shi Xiaokai, Gao Shenglin, Zuo Li

Asymmetrically PEGylated and amphipathic heptamethine indocyanine dyes potentiate radiotherapy of renal cell carcinoma via mitochondrial targeting

不对称聚乙二醇化两亲性七甲川吲哚菁染料通过靶向线粒体增强肾细胞癌的放射治疗效果

期刊:Journal of Nanobiotechnology

影响因子:10.6

doi:10.1186/s12951-024-03012-3

Zifei Wu # ,Xie Huang # ,Chuan Wu ,Yan Zhou ,Mingquan Gao ,Shenglin Luo ,Qiang Xiang ,Weidong Wang ,Rong Li

STUB1 is acetylated by KAT5 and alleviates myocardial ischemia-reperfusion injury through LATS2-YAP-β-catenin axis

STUB1被KAT5乙酰化并通过LATS2-YAP-β-catenin轴减轻心肌缺血-再灌注损伤

期刊:Communications Biology

影响因子:5.2

doi:10.1038/s42003-024-06086-9

Can Liu, Zhongxuan Gui, Cheng An, Fei Sun, Xiaotian Gao, Shenglin Ge

Targeted Inhibition of Matrix Metalloproteinase-8 Prevents Aortic Dissection in a Murine Model

靶向抑制基质金属蛋白酶-8可预防小鼠模型中的主动脉夹层

期刊:Cells

影响因子:5.1

doi:10.3390/cells11203218

Chengxin Zhang ，Kaiyuan Niu ，Meixia Ren ，Xinmiao Zhou ，Zhisheng Yang ，Mei Yang ，Xinxin Wang ，Jun Luo ，Yue Shao ，Cheng Zhang ，Dan Chen ，Shan Gao ，Shenglin Ge ，Qingchen Wu ，Qingzhong Xiao

发表日期：2022

文献求助收藏

Identification of a Novel Ferroptosis-Related Gene Signature for Prediction of Prognosis in Bladder Urothelial Carcinoma

鉴定一种新的铁死亡相关基因特征用于预测膀胱尿路上皮癌的预后

期刊:Bladder Cancer

影响因子:1.2

doi:10.3233/BLC-211522

Shi, Xiaokai; Zhou, Xiao; Zhang, Lei; Yue, Chuang; Gao, Shenglin; Cheng, Jiasheng; Zuo, Li; Zhang, Lifeng

Signature for Prostate Cancer Based on Autophagy-Related Genes and a Nomogram for Quantitative Risk Stratification

基于自噬相关基因的前列腺癌特征及定量风险分层列线图

期刊:Disease Markers

影响因子:

doi:10.1155/2022/7598942

Wen, Chenghao; Ge, Qintao; Dai, Bangshun; Li, Jiawei; Yang, Feixiang; Meng, Jialin; Gao, Shenglin; Fan, Song; Zhang, Li

Tumor immune microenvironment-based classifications of bladder cancer for enhancing the response rate of immunotherapy

基于肿瘤免疫微环境的膀胱癌分类可提高免疫治疗的反应率

期刊:Molecular Therapy-Oncolytics

影响因子:5.3

doi:10.1016/j.omto.2021.02.001

Meng, Jialin; Lu, Xiaofan; Zhou, Yujie; Zhang, Meng; Ge, Qintao; Zhou, Jun; Hao, Zongyao; Gao, Shenglin; Yan, Fangrong; Liang, Chaozhao

ARIH2 Ubiquitination Regulates NUPR1 to Inhibit Ferroptosis in Bladder Cancer

ARIH2泛素化调控NUPR1以抑制膀胱癌中的铁死亡

Gαi3: a crucial biomarker and therapeutic target in bladder cancer

Gαi3：膀胱癌的关键生物标志物和治疗靶点

Identification of a novel and high-affinity cyclic peptide targeting Keap1 for inflammation treatment by a combined virtual screening strategy.

通过结合虚拟筛选策略，鉴定出一种靶向 Keap1 的新型高亲和力环状肽，用于炎症治疗。

Transcriptional Regulation of NUPR1 by MYH11 Activates PI3â K/AKT and Promotes Bladder Cancer Progression Through Ferroptosis and M2 Polarization of Macrophages.

MYH11 对 NUPR1 的转录调控激活 PI3K/AKT，并通过铁死亡和巨噬细胞的 M2 极化促进膀胱癌的进展

Asymmetrically PEGylated and amphipathic heptamethine indocyanine dyes potentiate radiotherapy of renal cell carcinoma via mitochondrial targeting

不对称聚乙二醇化两亲性七甲川吲哚菁染料通过靶向线粒体增强肾细胞癌的放射治疗效果

STUB1 is acetylated by KAT5 and alleviates myocardial ischemia-reperfusion injury through LATS2-YAP-β-catenin axis

STUB1被KAT5乙酰化并通过LATS2-YAP-β-catenin轴减轻心肌缺血-再灌注损伤

Targeted Inhibition of Matrix Metalloproteinase-8 Prevents Aortic Dissection in a Murine Model

靶向抑制基质金属蛋白酶-8可预防小鼠模型中的主动脉夹层

Identification of a Novel Ferroptosis-Related Gene Signature for Prediction of Prognosis in Bladder Urothelial Carcinoma

鉴定一种新的铁死亡相关基因特征用于预测膀胱尿路上皮癌的预后

Signature for Prostate Cancer Based on Autophagy-Related Genes and a Nomogram for Quantitative Risk Stratification

基于自噬相关基因的前列腺癌特征及定量风险分层列线图

Tumor immune microenvironment-based classifications of bladder cancer for enhancing the response rate of immunotherapy

基于肿瘤免疫微环境的膀胱癌分类可提高免疫治疗的反应率

ARIH2 Ubiquitination Regulates NUPR1 to Inhibit Ferroptosis in Bladder Cancer

ARIH2泛素化调控NUPR1以抑制膀胱癌中的铁死亡

Gαi3: a crucial biomarker and therapeutic target in bladder cancer

Gαi3：膀胱癌的关键生物标志物和治疗靶点

Identification of a novel and high-affinity cyclic peptide targeting Keap1 for inflammation treatment by a combined virtual screening strategy.

通过结合虚拟筛选策略，鉴定出一种靶向 Keap1 的新型高亲和力环状肽，用于炎症治疗。

Transcriptional Regulation of NUPR1 by MYH11 Activates PI3â K/AKT and Promotes Bladder Cancer Progression Through Ferroptosis and M2 Polarization of Macrophages.

MYH11 对 NUPR1 的转录调控激活 PI3K/AKT，并通过铁死亡和巨噬细胞的 M2 极化促进膀胱癌的进展

Asymmetrically PEGylated and amphipathic heptamethine indocyanine dyes potentiate radiotherapy of renal cell carcinoma via mitochondrial targeting

不对称聚乙二醇化两亲性七甲川吲哚菁染料通过靶向线粒体增强肾细胞癌的放射治疗效果

STUB1 is acetylated by KAT5 and alleviates myocardial ischemia-reperfusion injury through LATS2-YAP-β-catenin axis

STUB1被KAT5乙酰化并通过LATS2-YAP-β-catenin轴减轻心肌缺血-再灌注损伤

Targeted Inhibition of Matrix Metalloproteinase-8 Prevents Aortic Dissection in a Murine Model

靶向抑制基质金属蛋白酶-8可预防小鼠模型中的主动脉夹层

Identification of a Novel Ferroptosis-Related Gene Signature for Prediction of Prognosis in Bladder Urothelial Carcinoma

鉴定一种新的铁死亡相关基因特征用于预测膀胱尿路上皮癌的预后

Signature for Prostate Cancer Based on Autophagy-Related Genes and a Nomogram for Quantitative Risk Stratification

基于自噬相关基因的前列腺癌特征及定量风险分层列线图

Tumor immune microenvironment-based classifications of bladder cancer for enhancing the response rate of immunotherapy

基于肿瘤免疫微环境的膀胱癌分类可提高免疫治疗的反应率

Transcriptional Regulation of NUPR1 by MYH11 Activates PI3â K/AKT and Promotes Bladder Cancer Progression Through Ferroptosis and M2 Polarization of Macrophages.