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The EVH1 domain of Spred1 binds to the noncatalytic portion of the GAP-related domain of neurofibromin.
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Results provide genetic evidence that miR-126, through its target gene Spred-1, plays a critical role in the development of retinal vascular layers.
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In one case we identified a nonsense mutation c.46C>T (p.Arg16*) in exon 2 of SPRED1 gene, confirming diagnosis of Legius syndrome. This mutation was reported previously.
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PURA may be a potential target of miR-144 and observed downregulation of PURA may be caused by increased expression of miR-144. The other predicted target of miR-144 SPRED1, was found to be downregulated in 69 per cent EC tissues as compared to matched distant non-malignant tissues.
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This study constitutes the first report from Japan of Legius syndrome occurring in siblings. Mutation analysis showed a mutation of c.349C>T resulting in p.Arg117* in exon 4.
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Data suggest SPRED1 EVH1 domain interacts with NF1 GRD domain [N-term. 16AA/C-term. 20AA of GTPase-activating protein-related domain]; SPRED1 EVH1 and NF1 GRD mutations observed in Legius syndrome reduce binding affinity between EVH1/GRD domains.
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Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer
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SPRED1 decreased expression correlated with genetic features of AML. Our study reveals a new mechanism which contributes to deregulate RAS MAPK pathway in the vast majority of paediatric AMLs
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Antisense-mediated knockdown (anti-miR) revealed that miR-206/21 coordinately promote RAS-ERK signaling and the corresponding cell phenotypes by inhibiting translation of the pathway suppressors RASA1 and SPRED1.
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SPRED1 seems to play an important role in recruiting neurofibromin to the plasma membrane. (Review)
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Older age and deletions of IKZF1 and SPRED1 were also associated with poor overall survival of pediatric B-cell precursor acute lymphoblastic leukemia.
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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).
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Based on our current understanding of KIT and SPRED1 protein interactions, we propose that cafe-au-lait macules and freckling may be seen in some patients with piebaldism and does not necessarily represent coexistence of neurofibromatosis type 1.
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Data indicate that upregulated miR-126 upon coxsackievirus B3 (CVB3) infection targets SPRED1, LRP6, and WRCH1 genes, mediating cross-talk between ERK1/2 and Wnt/beta-catenin pathways, and thus promoting viral replication.
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Sixty-three mutations and deletions are definitely pathogenic or most likely pathogenic, eight SPRED1 mutations are probably benign rare variants, and 17 SPRED1 missense mutations are still unclassified. Review.
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show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function
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Interaction of FGFRL1 with Spred1 increases the proportion of the receptor at the plasma membrane.
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a cohort of 115 NF1-like patients were screened for SPRED1 gene mutations and six mutations were identified. 12 potentially pathogenic SPRED1 mutations have been detected in 200 such NF1-like patients
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SPRED1 is a likely substrate of SHP2, whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK pathway.
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Sprouty and Spred proteins are negative regulators of the ERK/Elk-1 pathway activation induced not only by growth-factors, but also by reactive lipidic mediators.
