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Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer
SPREDs promote self-renewal and inhibit mesodermal differentiation of murine ES cells by selective suppression of the ERK/MAPK signaling pathway in pluripotent cells
The data suggest that Spred1 negatively regulates group 2 innate lymphoid cell development and functions through the suppression of the Ras-ERK pathway.
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).
show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function
The results suggest that Spred1 negatively regulates mast cell activation, which is modulated by miR126.
SPRED1 is a likely substrate of SHP2, whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK pathway.
Data show that both SPRED1 and SPRED2 inhibit the ability of DYRK1A to phosphorylate its substrates.
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.
role in hematopoiesis
Spred-1 and Spred-2 were found to be expressed predominantly in brain
Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness by modulating IL-5 signaling in allergic asthma, without affecting helper T cell differentiation
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.
These data suggest that Spred-1 inhibits ERK activation in collaboration with Cav-1
Spred1 is essential for embryonic lymphangiogenesis by regulating VEGFR3 signaling.
Spred1 is required for synaptic plasticity and hippocampus-dependent learning.
TGF-beta mediates an inhibitory mechanism on CD8+ TILs involving TCR-signaling blockade and the upregulation of Spred-1.
Spred1 is critical for normal cortical development, as it modulates progenitor self-renewal/proliferation and helps maintain the integrity and organization of germinal zones
this study establishes SPRED1 as a major tumor suppressor gene in mucosal melanoma.
The EVH1 domain of Spred1 binds to the noncatalytic portion of the GAP-related domain of neurofibromin.
Results provide genetic evidence that miR-126, through its target gene Spred-1, plays a critical role in the development of retinal vascular layers.
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.
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.
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.
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.
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
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.
SPRED1 seems to play an important role in recruiting neurofibromin to the plasma membrane. (Review)
Older age and deletions of IKZF1 and SPRED1 were also associated with poor overall survival of pediatric B-cell precursor acute lymphoblastic leukemia.
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.
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.
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.
Interaction of FGFRL1 with Spred1 increases the proportion of the receptor at the plasma membrane.
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
The protein encoded by this gene is a member of the Sprouty family of proteins and is phosphorylated by tyrosine kinase in response to several growth factors. The encoded protein can act as a homodimer or as a heterodimer with SPRED2 to regulate activation of the MAP kinase cascade. Defects in this gene are a cause of neurofibromatosis type 1-like syndrome (NFLS).
sprouty-related, EVH1 domain-containing protein 1
, sprouty-related protein with EVH-1 domain 1
, sprouty-related, EVH1 domain containing 1
, sprouty-related, EVH1 domain-containing protein 1-like
, sprouty-related protein 1 with EVH-1 domain
, suppressor of Ras/MAPK activation
, sprouty protein with EVH-1 domain 1, related sequence