| Spred1 deficit promotes treatment resistance and transformation of chronic phase CML. | Spred1 deficit promotes treatment resistance and transformation of chronic phase CML.
Qiao J, Liang C, Zhao D, Nguyen LXT, Chen F, Suo S, Hoang DH, Pellicano F, Rodriguez IR, Elhajmoussa Y, Ghoda L, Yoshimura A, Stein AS, Ali H, Koller P, Perrotti D, Copland M, Han A, Zhang BA, Marcucci G., Free PMC Article | 02/19/2022 |
| Impaired instrumental learning in Spred1(-/-) mice, a model for a rare RASopathy. | Impaired instrumental learning in Spred1(-/-) mice, a model for a rare RASopathy.
Borrie SC, Horner AE, Yoshimura A, Legius E, Kopanitsa MV, Brems H. | 02/19/2022 |
| 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 |
| Exercise training increased endothelial progenitor cells function in experimental myocardial infarction mice and miR-126 expression, while Spred1 expression was significantly down-regulated. | TPPU enhanced exercise-induced epoxyeicosatrienoic acid concentrations to exert cardioprotection in mice after myocardial infarction.
Guo Y, Luo F, Zhang X, Chen J, Shen L, Zhu Y, Xu D., Free PMC Article | 10/12/2019 |
| The Spred1 deficiency mitigates hematopoietic stem cell (HSC) failure induced by infection mimetics and prolongs HSC lifespan, but it does not initiate leukemogenesis due to compensatory upregulation of Spred2. | Spred1 Safeguards Hematopoietic Homeostasis against Diet-Induced Systemic Stress.
Tadokoro Y, Hoshii T, Yamazaki S, Eto K, Ema H, Kobayashi M, Ueno M, Ohta K, Arai Y, Hara E, Harada K, Oshima M, Oshima H, Arai F, Yoshimura A, Nakauchi H, Hirao A. | 09/7/2019 |
| 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 |
| The data suggest that Spred1 negatively regulates group 2 innate lymphoid cell development and functions through the suppression of the Ras-ERK pathway. | Spred1, a Suppressor of the Ras-ERK Pathway, Negatively Regulates Expansion and Function of Group 2 Innate Lymphoid Cells.
Suzuki M, Morita R, Hirata Y, Shichita T, Yoshimura A. | 10/31/2015 |
| Microrna-126 was transported into recipient human coronary artery endothelial cells by endothelial microparticles and functionally regulated the target protein sprouty-related, EVH1 domain-containing protein 1 (SPRED1). | Endothelial microparticle-mediated transfer of MicroRNA-126 promotes vascular endothelial cell repair via SPRED1 and is abrogated in glucose-damaged endothelial microparticles.
Jansen F, Yang X, Hoelscher M, Cattelan A, Schmitz T, Proebsting S, Wenzel D, Vosen S, Franklin BS, Fleischmann BK, Nickenig G, Werner N. | 02/1/2014 |
| show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function | A shared molecular mechanism underlies the human rasopathies Legius syndrome and Neurofibromatosis-1.
Stowe IB, Mercado EL, Stowe TR, Bell EL, Oses-Prieto JA, Hernández H, Burlingame AL, McCormick F., Free PMC Article | 09/15/2012 |
| The results suggest that Spred1 negatively regulates mast cell activation, which is modulated by miR126. | miR126 positively regulates mast cell proliferation and cytokine production through suppressing Spred1.
Ishizaki T, Tamiya T, Taniguchi K, Morita R, Kato R, Okamoto F, Saeki K, Nomura M, Nojima Y, Yoshimura A. | 02/18/2012 |
| SPRED1 is a likely substrate of SHP2, whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK pathway. | Sprouty-related Ena/vasodilator-stimulated phosphoprotein homology 1-domain-containing protein (SPRED1), a tyrosine-protein phosphatase non-receptor type 11 (SHP2) substrate in the Ras/extracellular signal-regulated kinase (ERK) pathway.
Quintanar-Audelo M, Yusoff P, Sinniah S, Chandramouli S, Guy GR., Free PMC Article | 09/10/2011 |
| 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 |
| Spred1 is critical for normal cortical development, as it modulates progenitor self-renewal/proliferation and helps maintain the integrity and organization of germinal zones | Spred1, a negative regulator of Ras-MAPK-ERK, is enriched in CNS germinal zones, dampens NSC proliferation, and maintains ventricular zone structure.
Phoenix TN, Temple S., Free PMC Article | 01/21/2010 |
| TGF-beta mediates an inhibitory mechanism on CD8+ TILs involving TCR-signaling blockade and the upregulation of Spred-1. | TGF-beta modulates the functionality of tumor-infiltrating CD8+ T cells through effects on TCR signaling and Spred1 expression.
di Bari MG, Lutsiak ME, Takai S, Mostböck S, Farsaci B, Semnani RT, Wakefield LM, Schlom J, Sabzevari H., Free PMC Article | 01/21/2010 |
| Spred1 is required for synaptic plasticity and hippocampus-dependent learning. | Spred1 is required for synaptic plasticity and hippocampus-dependent learning.
Denayer E, Ahmed T, Brems H, Van Woerden G, Borgesius NZ, Callaerts-Vegh Z, Yoshimura A, Hartmann D, Elgersma Y, D'Hooge R, Legius E, Balschun D., Free PMC Article | 01/21/2010 |
| Spred1 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 |
| These data suggest that Spred-1 inhibits ERK activation in collaboration with Cav-1 | The Sprouty-related protein, Spred-1, localizes in a lipid raft/caveola and inhibits ERK activation in collaboration with caveolin-1.
Nonami A, Taketomi T, Kimura A, Saeki K, Takaki H, Sanada T, Taniguchi K, Harada M, Kato R, Yoshimura A. | 01/21/2010 |
| Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness by modulating IL-5 signaling in allergic asthma, without affecting helper T cell differentiation | Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness.
Inoue H, Kato R, Fukuyama S, Nonami A, Taniguchi K, Matsumoto K, Nakano T, Tsuda M, Matsumura M, Kubo M, Ishikawa F, Moon BG, Takatsu K, Nakanishi Y, Yoshimura A., Free PMC Article | 01/21/2010 |
| Spred-1 and Spred-2 were found to be expressed predominantly in brain | 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 |
| role in hematopoiesis | Spred-1 negatively regulates interleukin-3-mediated ERK/mitogen-activated protein (MAP) kinase activation in hematopoietic cells.
Nonami A, Kato R, Taniguchi K, Yoshiga D, Taketomi T, Fukuyama S, Harada M, Sasaki A, Yoshimura A. | 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 |