| Dock5 Deficiency Promotes Proteinuric Kidney Diseases via Modulating Podocyte Lipid Metabolism. | Dock5 Deficiency Promotes Proteinuric Kidney Diseases via Modulating Podocyte Lipid Metabolism.
Qu H, Liu X, Zhu J, Xiong X, Li L, He Q, Wang Y, Yang G, Zhang L, Yang Q, Luo G, Zheng Y, Zheng H., Free PMC Article | 03/21/2024 |
| DOCK5 regulates energy balance and hepatic insulin sensitivity by targeting mTORC1 signaling. | DOCK5 regulates energy balance and hepatic insulin sensitivity by targeting mTORC1 signaling.
Lai Y, Zhao A, Tan M, Yang M, Lin Y, Li S, Song J, Zheng H, Zhu Z, Liu D, Liu C, Li L, Yang G., Free PMC Article | 05/8/2021 |
| The authors show that Dock5 is as a new regulator of microtubule dynamic instability in osteoclast through Rac-dependent and -independent pathways. | Dock5 is a new regulator of microtubule dynamic instability in osteoclasts.
Guimbal S, Morel A, Guérit D, Chardon M, Blangy A, Vives V. | 02/29/2020 |
| Dock5 and tensin 3 cooperate for osteoclast activity, to ensure the correct organization of podosomes. | Tensin 3 is a new partner of Dock5 that controls osteoclast podosome organization and activity.
Touaitahuata H, Morel A, Urbach S, Mateos-Langerak J, de Rossi S, Blangy A. | 08/5/2017 |
| Tensin3 is a versatile regulator of DOCK5 signaling and cell adhesion. (Review) | Tensins are versatile regulators of Rho GTPase signalling and cell adhesion.
Blangy A. | 03/11/2017 |
| together with DOCK2 contributes to chemotaxis, reactive oxygen species production, and extracellular trap formation | DOCK2 and DOCK5 act additively in neutrophils to regulate chemotaxis, superoxide production, and extracellular trap formation.
Watanabe M, Terasawa M, Miyano K, Yanagihara T, Uruno T, Sanematsu F, Nishikimi A, Côté JF, Sumimoto H, Fukui Y., Free PMC Article | 04/18/2015 |
| Dock1 and Dock5 are not the important exchange factors regulating Rac activity during the establishment and maintenance of the glomerular barrier | The Rac-specific exchange factors Dock1 and Dock5 are dispensable for the establishment of the glomerular filtration barrier in vivo.
Laurin M, Dumouchel A, Fukui Y, Côté JF., Free PMC Article | 01/17/2015 |
| results thus identify DOCK5 as a key signaling adaptor that orchestrates remodeling of the microtubule network essential for mast cell degranulation. | DOCK5 functions as a key signaling adaptor that links FcεRI signals to microtubule dynamics during mast cell degranulation.
Ogawa K, Tanaka Y, Uruno T, Duan X, Harada Y, Sanematsu F, Yamamura K, Terasawa M, Nishikimi A, Côté JF, Fukui Y., Free PMC Article | 09/6/2014 |
| The atypical Rac1 exchange factor Dock5 is necessary for osteoclast function both in vitro and in vivo. | The Rac1 exchange factor Dock5 is essential for bone resorption by osteoclasts.
Vives V, Laurin M, Cres G, Larrousse P, Morichaud Z, Noel D, Côté JF, Blangy A., Free PMC Article | 08/20/2011 |
| Generated an mDock5-specific antibody, which detected denatured and nascent forms of mDock5. Determined tissue-specific expression patterns and subcellular localization of mDock5 using this antibody. | Characterization of an mDock5-specific antibody and tissue-specific expression and subcellular localization of mDock5.
Kim E, Yoon JB, Kim Yoon S. | 07/19/2010 |
| Dock5 is dispensable for normal mouse embryogenesis and contribution of Dock5 toward myofiber development. | The atypical Rac activator Dock180 (Dock1) regulates myoblast fusion in vivo.
Laurin M, Fradet N, Blangy A, Hall A, Vuori K, Côté JF., Free PMC Article | 01/21/2010 |
| Cataract causing lr2 gene is found in the CXSD mouse, which is a recombinant inbred strain of BALB/c and STS mice | Fine localization of Nefl and Nef3 and its exclusion as candidate gene for lens rupture 2(lr2).
Rhee SD, Kim E, Yoon SK, Yang SD, Okumoto M, Han SS, Song CW. | 01/21/2010 |