| SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes. | SPRED2 Is a Novel Regulator of Autophagy in Hepatocellular Carcinoma Cells and Normal Hepatocytes.
Wang T, Gao T, Fujisawa M, Ohara T, Sakaguchi M, Yoshimura T, Matsukawa A., Free PMC Article | 07/18/2024 |
| microRNA-141-3p mediates epithelial cell proliferation, apoptosis, and epithelial-mesenchymal transition and alleviates pulmonary fibrosis in mice via Spred2. | microRNA-141-3p mediates epithelial cell proliferation, apoptosis, and epithelial-mesenchymal transition and alleviates pulmonary fibrosis in mice via Spred2.
Zhu L, Chen M, Wang W, Zhu J, Wu H. | 11/22/2023 |
| LncRNA TUG1 reverses LPS-induced cell apoptosis and inflammation of macrophage via targeting MiR-221-3p/SPRED2 axis. | LncRNA TUG1 reverses LPS-induced cell apoptosis and inflammation of macrophage via targeting MiR-221-3p/SPRED2 axis.
Hu L, Ye H, Liao J. | 05/22/2021 |
| Spred2-deficiency enhances the proliferation of lung epithelial cells and alleviates pulmonary fibrosis induced by bleomycin. | Spred2-deficiency enhances the proliferation of lung epithelial cells and alleviates pulmonary fibrosis induced by bleomycin.
Kawara A, Mizuta R, Fujisawa M, Ito T, Li C, Nakamura K, Sun C, Kuwabara M, Kitabatake M, Yoshimura T, Matsukawa A., Free PMC Article | 01/9/2021 |
| Using established mice lines deficient for either or both Spred 1 and Spred 2, we demonstrate their role in regulating lens development by negatively regulating ERK1/2 activity. | The negative regulatory Spred1 and Spred2 proteins are required for lens and eye morphogenesis.
Wazin F, Lovicu FJ. | 07/25/2020 |
| SPRED2 deficiency impairs autophagy, leading to cardiac dysfunction and life-threatening arrhythmias. | SPRED2 deficiency elicits cardiac arrhythmias and premature death via impaired autophagy.
Ullrich M, Aßmus B, Augustin AM, Häbich H, Abeßer M, Martin Machado J, Werner F, Erkens R, Arias-Loza AP, Umbenhauer S, Wagner H, Benz PM, Unger A, Linke WA, Frantz S, Baba HA, Kuhn M, Schuh K. | 06/27/2020 |
| we showed that Spred2-deficiency promotes obesity, adipose tissue inflammation, and insulin resistance, possibly via enhanced adipose tissue inflammation caused by enhanced macrophage activation. | Spred2 Regulates High Fat Diet-Induced Adipose Tissue Inflammation, and Metabolic Abnormalities in Mice.
Ohkura T, Yoshimura T, Fujisawa M, Ohara T, Marutani R, Usami K, Matsukawa A., Free PMC Article | 12/21/2019 |
| Spred2-deficiency protects mice from polymicrobial sepsis via increased activation of the ERK/MAPK pathway and subsequent increase in innate immune responses. | Spred2-deficiecy Protects Mice from Polymicrobial Septic Peritonitis by Enhancing Inflammation and Bacterial Clearance.
Itakura J, Sato M, Ito T, Mino M, Fushimi S, Takahashi S, Yoshimura T, Matsukawa A., Free PMC Article | 06/29/2019 |
| Spred2-/- mice developed severer acute liver injury with increased levels of TNFalpha and IL-1beta in the livers. | Spred2 Deficiency Exacerbates D-Galactosamine/Lipopolysaccharide -induced Acute Liver Injury in Mice via Increased Production of TNFα.
Yang X, Fujisawa M, Yoshimura T, Ohara T, Sato M, Mino M, San TH, Gao T, Kunkel SL, Matsukawa A., Free PMC Article | 11/17/2018 |
| It is a known inhibitor of ERK1/2 signaling, which influences the severity of lung ischemia reperfusion injury. | SPRED2 deficiency may lead to lung ischemia-reperfusion injury via ERK1/2 signaling pathway activation.
Okada M, Yamane M, Yamamoto S, Otani S, Miyoshi K, Sugimoto S, Matsukawa A, Toyooka S, Oto T, Miyoshi S. | 11/3/2018 |
| Spred2 plays an important role in the regulation of colonic epithelial cell proliferation and inflammation by potentially down-regulating the activation of ERK. | A Novel Role of Spred2 in the Colonic Epithelial Cell Homeostasis and Inflammation.
Takahashi S, Yoshimura T, Ohkura T, Fujisawa M, Fushimi S, Ito T, Itakura J, Hiraoka S, Okada H, Yamamoto K, Matsukawa A., Free PMC Article | 05/26/2018 |
| Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer | Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer: a working hypothesis.
Assinder SJ, Beniamen D, Lovicu FJ., Free PMC Article | 03/5/2016 |
| SPREDs promote self-renewal and inhibit mesodermal differentiation of murine ES cells by selective suppression of the ERK/MAPK signaling pathway in pluripotent cells | SPREDs (Sprouty related proteins with EVH1 domain) promote self-renewal and inhibit mesodermal differentiation in murine embryonic stem cells.
Mühl B, Hägele J, Tasdogan A, Loula P, Schuh K, Bundschu K. | 01/2/2016 |
| Spred-2 controls the development of lipopolysaccharide-induced lung inflammation. | Spred-2 deficiency exacerbates lipopolysaccharide-induced acute lung inflammation in mice.
Xu Y, Ito T, Fushimi S, Takahashi S, Itakura J, Kimura R, Sato M, Mino M, Yoshimura A, Matsukawa A., Free PMC Article | 06/20/2015 |
| Spred-2 negatively regulates APAP-hepatotoxicity under the control of Kupffer cells and NK cells. | Spred-2 deficiency exacerbates acetaminophen-induced hepatotoxicity in mice.
Wakabayashi H, Ito T, Fushimi S, Nakashima Y, Itakura J, Qiuying L, Win MM, Cuiming S, Chen C, Sato M, Mino M, Ogino T, Makino H, Yoshimura A, Matsukawa A. | 11/17/2012 |
| Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis. | Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.
Ullrich M, Bundschu K, Benz PM, Abesser M, Freudinger R, Fischer T, Ullrich J, Renné T, Walter U, Schuh K., Free PMC Article | 05/21/2011 |
| Data show that both SPRED1 and SPRED2 inhibit the ability of DYRK1A to phosphorylate its substrates. | Direct association of Sprouty-related protein with an EVH1 domain (SPRED) 1 or SPRED2 with DYRK1A modifies substrate/kinase interactions.
Li D, Jackson RA, Yusoff P, Guy GR., Free PMC Article | 02/26/2011 |
| SPRED2 is likely involved in the regulation of dynamic developmental processes. | Spred2 expression during mouse development.
Tuduce IL, Schuh K, Bundschu K. | 02/5/2011 |
| findings suggest a critical function for NBR1 in the regulation of receptor trafficking and provide a mechanism for down-regulation of signaling by Spred2 via NBR1. | Spred2 interaction with the late endosomal protein NBR1 down-regulates fibroblast growth factor receptor signaling.
Mardakheh FK, Yekezare M, Machesky LM, Heath JK., Free PMC Article | 01/21/2010 |
| Spred2 is essential for embryonic lymphangiogenesis by regulating VEGFR3 signaling. | Spreds are essential for embryonic lymphangiogenesis by regulating vascular endothelial growth factor receptor 3 signaling.
Taniguchi K, Kohno R, Ayada T, Kato R, Ichiyama K, Morisada T, Oike Y, Yonemitsu Y, Maehara Y, Yoshimura A., Free PMC Article | 01/21/2010 |
| Spred-2 functions as a negative regulator of aorta-gonad-mesonephros hematopoiesis by inhibiting hematopoietic cytokine signaling. | Spred-2 suppresses aorta-gonad-mesonephros hematopoiesis by inhibiting MAP kinase activation.
Nobuhisa I, Kato R, Inoue H, Takizawa M, Okita K, Yoshimura A, Taga T., Free PMC Article | 01/21/2010 |
| Spred-1 and Spred-2 were found to be expressed predominantly in brain. It becomes most likely that Spred-2 is involved in the regulation of secretory pathways | Expression and subcellular localization of Spred proteins in mouse and human tissues.
Engelhardt CM, Bundschu K, Messerschmitt M, Renné T, Walter U, Reinhard M, Schuh K. | 01/21/2010 |
| We show here that Spred-1 and Spred-2 appear to have distinct mechanisms whereby they induce their effects, as the Sprouty domain of Spred-1 is not required to block MAPK (mitogen-activated protein kinase) activation, while that of Spred-2 is required. | Distinct requirements for the Sprouty domain for functional activity of Spred proteins.
King JA, Straffon AF, D'Abaco GM, Poon CL, I ST, Smith CM, Buchert M, Corcoran NM, Hall NE, Callus BA, Sarcevic B, Martin D, Lock P, Hovens CM., Free PMC Article | 01/21/2010 |
| These data suggest that Spreds are key regulators of RhoA-mediated cell motility and signal transduction. Furthermore, our study suggests that the induction of Spreds could be a novel strategy for preventing cancer cell metastasis. | The Sprouty-related protein, Spred, inhibits cell motility, metastasis, and Rho-mediated actin reorganization.
Miyoshi K, Wakioka T, Nishinakamura H, Kamio M, Yang L, Inoue M, Hasegawa M, Yonemitsu Y, Komiya S, Yoshimura A. | 01/21/2010 |