文献库，生知库 | 链接生命科学的每一步

Jagdish Chandra Joshi ，Bhagwati Joshi ，Cuiping Zhang ，Somenath Banerjee ，Vigneshwaran Vellingiri ，Vijay Avin Balaji Raghunathrao ，Mumtaz Anwar ，Tejas Pravin Rokade ，Lianghui Zhang ，Ruhul Amin ，Yuanlin Song ，Dolly Mehta

IFNγ

免疫/内分泌

RGS2

发表日期：2025

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RGS2 is an innate immune checkpoint for TLR4 and Gαq-mediated IFNγ generation and lung injury

RGS2是TLR4和Gαq介导的IFNγ生成和肺损伤的固有免疫检查点。

期刊:

影响因子:

doi:10.1101/2023.09.22.559016

Joshi, Jagdish Chandra; Joshi, Bhagwati; Zhang, Cuiping; Banerjee, Somenath; Vellingiri, Vigneshwaran; Raghunathrao, Vijay Avin Balaji; Zhang, Lianghui; Amin, Ruhul; Song, Yuanlin; Mehta, Dolly

Regulation of cGAS Activity and Downstream Signaling

cGAS活性及其下游信号的调控

期刊:Cells

影响因子:5.2

doi:10.3390/cells11182812

Joshi, Bhagwati; Joshi, Jagdish Chandra; Mehta, Dolly

信号转导

发表日期：2022

文献求助收藏

Protease-activated receptor 2 promotes clearance of Pseudomonas aeruginosa infection by inducing cAMP-Rac1 signaling in alveolar macrophages

蛋白酶激活受体2通过诱导肺泡巨噬细胞中的cAMP-Rac1信号通路促进铜绿假单胞菌感染的清除

期刊:Frontiers in Pharmacology

影响因子:4.8

doi:10.3389/fphar.2022.874197

Rayees, Sheikh; Joshi, Jagdish Chandra; Joshi, Bhagwati; Vellingiri, Vigneshwaran; Banerjee, Somenath; Mehta, Dolly

SPHK2-Generated S1P in CD11b+ Macrophages Blocks STING to Suppress the Inflammatory Function of Alveolar Macrophages

CD11b+巨噬细胞中SPHK2生成的S1P阻断STING以抑制肺泡巨噬细胞的炎症功能

期刊:Cell Reports

影响因子:7.5

doi:10.1016/j.celrep.2020.02.112

Jagdish C Joshi ，Bhagwati Joshi ，Ian Rochford ，Sheikh Rayees ，Md Zahid Akhter ，Sukriti Baweja ，Koteshwara Rao Chava ，Mohammad Tauseef ，Hazem Abdelkarim ，Viswanathan Natarajan ，Vadim Gaponenko ，Dolly Mehta

Macrophage TLR4 and PAR2 Signaling: Role in Regulating Vascular Inflammatory Injury and Repair

巨噬细胞TLR4和PAR2信号通路：在调节血管炎症损伤和修复中的作用

期刊:Frontiers in Immunology

影响因子:5.9

doi:10.3389/fimmu.2020.02091

Rayees, Sheikh; Rochford, Ian; Joshi, Jagdish Chandra; Joshi, Bhagwati; Banerjee, Somenath; Mehta, Dolly

PAR2-Mediated cAMP Generation Suppresses TRPV4-Dependent Ca(2+) Signaling in Alveolar Macrophages to Resolve TLR4-Induced Inflammation.

PAR2 介导的 cAMP 生成抑制肺泡巨噬细胞中 TRPV4 依赖的 Ca(2+) 信号传导，从而消除 TLR4 诱导的炎症

期刊:Cell Reports

影响因子:6.9

doi:10.1016/j.celrep.2019.03.053

Rayees Sheikh, Joshi Jagdish Chandra, Tauseef Mohammad, Anwar Mumtaz, Baweja Sukriti, Rochford Ian, Joshi Bhagwati, Hollenberg Morley D, Reddy Sekhar P, Mehta Dolly

RGS2 is an innate immune checkpoint for suppressing Gαq-mediated IFNγ generation and lung injury

RGS2 是一种先天免疫检查点，可抑制 Gαq 介导的 IFNγ 生成和肺损伤。

RGS2 is an innate immune checkpoint for TLR4 and Gαq-mediated IFNγ generation and lung injury

RGS2是TLR4和Gαq介导的IFNγ生成和肺损伤的固有免疫检查点。

Regulation of cGAS Activity and Downstream Signaling

cGAS活性及其下游信号的调控

Protease-activated receptor 2 promotes clearance of Pseudomonas aeruginosa infection by inducing cAMP-Rac1 signaling in alveolar macrophages

蛋白酶激活受体2通过诱导肺泡巨噬细胞中的cAMP-Rac1信号通路促进铜绿假单胞菌感染的清除

SPHK2-Generated S1P in CD11b+ Macrophages Blocks STING to Suppress the Inflammatory Function of Alveolar Macrophages

CD11b+巨噬细胞中SPHK2生成的S1P阻断STING以抑制肺泡巨噬细胞的炎症功能

Macrophage TLR4 and PAR2 Signaling: Role in Regulating Vascular Inflammatory Injury and Repair

巨噬细胞TLR4和PAR2信号通路：在调节血管炎症损伤和修复中的作用

PAR2-Mediated cAMP Generation Suppresses TRPV4-Dependent Ca(2+) Signaling in Alveolar Macrophages to Resolve TLR4-Induced Inflammation.

PAR2 介导的 cAMP 生成抑制肺泡巨噬细胞中 TRPV4 依赖的 Ca(2+) 信号传导，从而消除 TLR4 诱导的炎症