| Long noncoding RNA LOC646029 functions as a ceRNA to suppress ovarian cancer progression through the miR-627-3p/SPRED1 axis. | Long noncoding RNA LOC646029 functions as a ceRNA to suppress ovarian cancer progression through the miR-627-3p/SPRED1 axis.
Zhao P, Wang Y, Yu X, Nan Y, Liu S, Li B, Cui Z, Liu Z. | 12/20/2023 |
| SPOCK2 and SPRED1 function downstream of EZH2 to impede the malignant progression of lung adenocarcinoma in vitro and in vivo. | SPOCK2 and SPRED1 function downstream of EZH2 to impede the malignant progression of lung adenocarcinoma in vitro and in vivo.
Liu Y, Fan X, Jiang C, Xu S., Free PMC Article | 03/16/2023 |
| SPRED1 deletion confers resistance to MAPK inhibition in melanoma. | SPRED1 deletion confers resistance to MAPK inhibition in melanoma.
Ablain J, Liu S, Moriceau G, Lo RS, Zon LI., Free PMC Article | 09/18/2021 |
| A Study on the Expression of SPRED1 and PBRM1 (Baf180) and their Clinical Significances in Patients with Gastric Cancer. | A Study on the Expression of SPRED1 and PBRM1 (Baf180) and their Clinical Significances in Patients with Gastric Cancer.
Liu W, Fang S, Zuo G. | 07/24/2021 |
| Moyamoya syndrome in a child with Legius syndrome: Introducing a cerebral vasculopathy to the SPRED1 phenotype? | Moyamoya syndrome in a child with Legius syndrome: Introducing a cerebral vasculopathy to the SPRED1 phenotype?
Pabst L, Carroll J, Lo W, Truxal KV. | 07/3/2021 |
| Constitutional mismatch repair deficiency is the diagnosis in 0.41% of pathogenic NF1/SPRED1 variant negative children suspected of sporadic neurofibromatosis type 1. | Constitutional mismatch repair deficiency is the diagnosis in 0.41% of pathogenic NF1/SPRED1 variant negative children suspected of sporadic neurofibromatosis type 1.
Perez-Valencia JA, Gallon R, Chen Y, Koch J, Keller M, Oberhuber K, Gomes A, Zschocke J, Burn J, Jackson MS, Santibanez-Koref M, Messiaen L, Wimmer K., Free PMC Article | 05/8/2021 |
| Simultaneous Detection of NF1, SPRED1, LZTR1, and NF2 Gene Mutations by Targeted NGS in an Italian Cohort of Suspected NF1 Patients. | Simultaneous Detection of NF1, SPRED1, LZTR1, and NF2 Gene Mutations by Targeted NGS in an Italian Cohort of Suspected NF1 Patients.
Bianchessi D, Ibba MC, Saletti V, Blasa S, Langella T, Paterra R, Cagnoli GA, Melloni G, Scuvera G, Natacci F, Cesaretti C, Finocchiaro G, Eoli M., Free PMC Article | 03/20/2021 |
| These data provide structural insight into the interaction of Spred1 and neurofibromin. | Pathogenic Mutations Associated with Legius Syndrome Modify the Spred1 Surface and Are Involved in Direct Binding to the Ras Inactivator Neurofibromin.
Führer S, Tollinger M, Dunzendorfer-Matt T. | 06/20/2020 |
| SPRED1 is down-regulated by E2 and negatively correlated to ER status in BC cells. SPRED1 was a new direct target of miR-196a which participated in miR-196a-promoted BC development and was suppressed by ligand-activated ER-alpha signal pathway. | Estrogen-induced miR-196a elevation promotes tumor growth and metastasis via targeting SPRED1 in breast cancer.
Jiang CF, Shi ZM, Li DM, Qian YC, Ren Y, Bai XM, Xie YX, Wang L, Ge X, Liu WT, Zhen LL, Liu LZ, Jiang BH., Free PMC Article | 08/3/2019 |
| Aberrant methylation statuses of the SPRED1 promoter regions are associated with the downregulation of gene transcription in acute myeloid leukemia. | A Pilot Study of Aberrant CpG Island Hypermethylation of SPRED1 in Acute Myeloloid Leukemia.
Sun J, Zhang J, Wang Y, Li Y, Zhang R., Free PMC Article | 06/8/2019 |
| this study establishes SPRED1 as a major tumor suppressor gene in mucosal melanoma. | Human tumor genomics and zebrafish modeling identify SPRED1 loss as a driver of mucosal melanoma.
Ablain J, Xu M, Rothschild H, Jordan RC, Mito JK, Daniels BH, Bell CF, Joseph NM, Wu H, Bastian BC, Zon LI, Yeh I., Free PMC Article | 04/13/2019 |
| The EVH1 domain of Spred1 binds to the noncatalytic portion of the GAP-related domain of neurofibromin. | The neurofibromin recruitment factor Spred1 binds to the GAP related domain without affecting Ras inactivation.
Dunzendorfer-Matt T, Mercado EL, Maly K, McCormick F, Scheffzek K., Free PMC Article | 07/29/2017 |
| Results provide genetic evidence that miR-126, through its target gene Spred-1, plays a critical role in the development of retinal vascular layers. | Strand and Cell Type-specific Function of microRNA-126 in Angiogenesis.
Zhou Q, Anderson C, Hanus J, Zhao F, Ma J, Yoshimura A, Wang S., Free PMC Article | 06/24/2017 |
| 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. | The first Slovak Legius syndrome patient carrying the SPRED1 gene mutation.
Sekelska M, Briatkova L, Olcak T, Bolcekova A, Ilencikova D, Kadasi L, Zatkova A. | 06/24/2017 |
| 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. | Potential diagnostic implications of miR-144 overexpression in human oesophageal cancer.
Sharma P, Saraya A, Sharma R., Free PMC Article | 06/3/2017 |
| 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. | Family with Legius syndrome (neurofibromatosis type 1-like syndrome).
Sakai N, Maeda T, Kawakami H, Uchiyama M, Harada K, Tsuboi R, Mitsuhashi Y. | 12/17/2016 |
| 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. | Interaction between a Domain of the Negative Regulator of the Ras-ERK Pathway, SPRED1 Protein, and the GTPase-activating Protein-related Domain of Neurofibromin Is Implicated in Legius Syndrome and Neurofibromatosis Type 1.
Hirata Y, Brems H, Suzuki M, Kanamori M, Okada M, Morita R, Llano-Rivas I, Ose T, Messiaen L, Legius E, Yoshimura A., Free PMC Article | 07/16/2016 |
| 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 |
| 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 | SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia.
Pasmant E, Gilbert-Dussardier B, Petit A, de Laval B, Luscan A, Gruber A, Lapillonne H, Deswarte C, Goussard P, Laurendeau I, Uzan B, Pflumio F, Brizard F, Vabres P, Naguibvena I, Fasola S, Millot F, Porteu F, Vidaud D, Landman-Parker J, Ballerini P. | 04/11/2015 |
| 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. | MicroRNAs 206 and 21 cooperate to promote RAS-extracellular signal-regulated kinase signaling by suppressing the translation of RASA1 and SPRED1.
Sharma SB, Lin CC, Farrugia MK, McLaughlin SL, Ellis EJ, Brundage KM, Salkeni MA, Ruppert JM., Free PMC Article | 02/14/2015 |
| SPRED1 seems to play an important role in recruiting neurofibromin to the plasma membrane. (Review) | Legius syndrome, an Update. Molecular pathology of mutations in SPRED1.
Brems H, Legius E. | 06/28/2014 |
| Older age and deletions of IKZF1 and SPRED1 were also associated with poor overall survival of pediatric B-cell precursor acute lymphoblastic leukemia. | Deletions of IKZF1 and SPRED1 are associated with poor prognosis in a population-based series of pediatric B-cell precursor acute lymphoblastic leukemia diagnosed between 1992 and 2011.
Olsson L, Castor A, Behrendtz M, Biloglav A, Forestier E, Paulsson K, Johansson B. | 04/12/2014 |
| 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 |
| 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. | Association of Piebaldism, multiple café-au-lait macules, and intertriginous freckling: clinical evidence of a common pathway between KIT and sprouty-related, ena/vasodilator-stimulated phosphoprotein homology-1 domain containing protein 1 (SPRED1).
Chiu YE, Dugan S, Basel D, Siegel DH., Free PMC Article | 01/18/2014 |
| 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. | MiR-126 promotes coxsackievirus replication by mediating cross-talk of ERK1/2 and Wnt/β-catenin signal pathways.
Ye X, Hemida MG, Qiu Y, Hanson PJ, Zhang HM, Yang D., Free PMC Article | 01/11/2014 |