SPRED1 Antibody, FITC conjugated

1. The EVH1 domain of Spred1 binds to the noncatalytic portion of the GAP-related domain of neurofibromin. PMID: 27313208
2. Results provide genetic evidence that miR-126, through its target gene Spred-1, plays a critical role in the development of retinal vascular layers. PMID: 27203443
3. 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. PMID: 28150585
4. 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. PMID: 27748283
5. 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. PMID: 25981987
6. 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. PMID: 26635368
7. Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer PMID: 26075267
8. 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 PMID: 24469042
9. 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. PMID: 25202123
10. SPRED1 seems to play an important role in recruiting neurofibromin to the plasma membrane. (Review) PMID: 24334617
11. Older age and deletions of IKZF1 and SPRED1 were also associated with poor overall survival of pediatric B-cell precursor acute lymphoblastic leukemia. PMID: 23823658
12. 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). PMID: 24014835
13. 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. PMID: 23016555
14. 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. PMID: 22753041
15. show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function PMID: 22751498
16. 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 PMID: 21649642
17. SPRED1 is a likely substrate of SHP2, whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK pathway. PMID: 21531714
18. 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. PMID: 21364986
19. The frequency of SPRED1 mutations in patients meeting diagnostic criteria for neurofibromatosis 1 in a hospital-based clinic is 1% to 2%. The likelihood an individual is harboring a SPRED1 mutation increases with age. PMID: 20179001
20. no evidence of leukemogenic SPRED1 involement in juvenile myelomonocytic leukemia PMID: 20339110
21. 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. PMID: 15683364
22. reduction of Spred expression in hepatocellular carcinoma (HCC) is one of the causes of the acquisition of malignant features. Thus, Spred could be not only a novel prognostic factor but also a new therapeutic target for human HCC PMID: 16652141
23. Studies show that the clinical features of the reported disorder resemble those of neurofibromatosis type 1 provide the first report of mutations of SPRED1 (SPROUTY)/SPRED family of genes) in human disease. PMID: 17704776
24. enhanced TESK1 activity results in increased stress fibers (via phospho-cofilin), but this can be blocked by elevating Spred1 PMID: 18216281
25. Linkage analysis of SPRED1 excluded its involvement in Cafe-au-lait spots in a patient with a severe form of Noonan syndrome. PMID: 19120036
26. SPRED1 mutations occurred with a prevalence of 0.5% in NF1 patients and in 5% of NF1 patients displaying an NF1-like phenotype. PMID: 19366998
27. Unrelated mild NF1 patients were screened for mutations of the SPRED1-3 and the SPRY1-4 genes. SPRED1 mutations were identified in 6 cases. PMID: 19443465
28. A high SPRED1 mutation detection rate was found in NF1 mutation-negative families with an autosomal dominant phenotype of CALMs (cafe au lait macules)with or without freckling and no other NF1 features. PMID: 19920235

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HGNC: 20249

OMIM: 609291

KEGG: hsa:161742

STRING: 9606.ENSP00000299084

UniGene: Hs.525781