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Jiao-Hui Wu

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Articles 21
Citations 450
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Recent Articles
1.
Zhang L, Wu J, Jean-Charles P, Murali P, Zhang W, Jazic A, et al.
J Biol Chem . 2023 Jun; 299(7):104911. PMID: 37311534
Reversible lysine-63 (K63) polyubiquitination regulates proinflammatory signaling in vascular smooth muscle cells (SMCs) and plays an integral role in atherosclerosis. Ubiquitin-specific peptidase 20 (USP20) reduces NFκB activation triggered by proinflammatory...
2.
Wu J, Zhang L, Nepliouev I, Brian L, Huang T, Snow K, et al.
Cardiovasc Res . 2021 Apr; 118(3):772-784. PMID: 33914863
Aims: The F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation, and pro-inflammatory signalling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis. Methods And Results: SM22-Cre+/Dbnflox/flox/Ldlr-/- (SMC-Dbn-/-/Ldlr-/-) and...
3.
Jean-Charles P, Wu J, Zhang L, Kaur S, Nepliouev I, Stiber J, et al.
Arterioscler Thromb Vasc Biol . 2018 Oct; 38(10):2295-2305. PMID: 30354204
Objective- Signaling that activates NFκB (nuclear factor κB) in smooth muscle cells (SMCs) is integral to atherosclerosis and involves reversible ubiquitination that activates proteins downstream of proatherogenic receptors. Deubiquitination of...
4.
Zhang L, Wu J, Huang T, Nepliouev I, Brian L, Zhang Z, et al.
Cardiovasc Res . 2018 Jun; 114(13):1806-1815. PMID: 29931051
Aims: The actin-binding protein Drebrin is up-regulated in response to arterial injury and reduces smooth muscle cell (SMC) migration and proliferation through its interaction with the actin cytoskeleton. We, therefore,...
5.
Zhang L, Wu J, Otto J, Gurley S, Hauser E, Shenoy S, et al.
Cardiovasc Res . 2017 Oct; 113(13):1551-1559. PMID: 29048463
Aims: Chronic kidney disease (CKD) is a powerful independent risk factor for cardiovascular events, including vein graft failure. Because CKD impairs the clearance of small proteins, we tested the hypothesis...
6.
Smith J, Alagesan P, Desai N, Pack T, Wu J, Inoue A, et al.
Mol Pharmacol . 2017 Jun; 92(2):136-150. PMID: 28559424
Biased agonism, the ability of different ligands for the same receptor to selectively activate some signaling pathways while blocking others, is now an established paradigm for G protein-coupled receptor signaling....
7.
Stiber J, Wu J, Zhang L, Nepliouev I, Zhang Z, Bryson V, et al.
Arterioscler Thromb Vasc Biol . 2016 Mar; 36(5):984-93. PMID: 27013612
Objective: Vascular smooth muscle cell (SMC) migration is regulated by cytoskeletal remodeling as well as by certain transient receptor potential (TRP) channels, nonselective cation channels that modulate calcium influx. Proper...
8.
Jean-Charles P, Zhang L, Wu J, Han S, Brian L, Freedman N, et al.
J Biol Chem . 2016 Feb; 291(14):7450-64. PMID: 26839314
Toll-like receptor 4 (TLR4) promotes vascular inflammatory disorders such as neointimal hyperplasia and atherosclerosis. TLR4 triggers NFκB signaling through the ubiquitin ligase TRAF6 (tumor necrosis factor receptor-associated factor 6). TRAF6...
9.
Wu J, Fanaroff A, Sharma K, Smith L, Brian L, Eipper B, et al.
Arterioscler Thromb Vasc Biol . 2013 Jan; 33(4):702-8. PMID: 23288169
Objective: Kalirin is a multifunctional protein that contains 2 guanine nucleotide exchange factor domains for the GTPases Rac1 and RhoA. Variants of KALRN have been associated with atherosclerosis in humans,...
10.
Han S, Xiao K, Kim J, Wu J, Wisler J, Nakamura N, et al.
J Cell Biol . 2012 Nov; 199(5):817-30. PMID: 23166351
Lysosomal degradation of ubiquitinated β(2)-adrenergic receptors (β(2)ARs) serves as a major mechanism of long-term desensitization in response to prolonged agonist stimulation. Surprisingly, the βAR antagonist carvedilol also induced ubiquitination and...