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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Sprouty-related, EVH1 domain containing 1

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). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Sprouty, NF1, ERK, MAPK, Spred-2
Papers on SPRED1
Interaction between a domain of a negative regulator of the RAS-ERK pathway, SPRED1, and the GTPase-Activating Protein-Related Domain of neurofibromin is implicated in Legius Syndrome and Neurofibromatosis Type 1.
Yoshimura et al., Japan. In J Biol Chem, Jan 2016
UNASSIGNED: Constitutional heterozygous loss-of-function mutations in the SPRED1 gene cause a phenotype known as Legius syndrome, which consists of symptoms of multiple cafe-au-lait macules, axillary freckling, learning disabilities and macrocephaly.
Overexpression and knockout of miR-126 both promote leukemogenesis.
Chen et al., Chicago, United States. In Blood, Nov 2015
Mechanistically, miR-126 overexpression activates genes that are highly expressed in LSCs/LICs and/or primitive hematopoietic stem/progenitor cells, likely through targeting ERRFI1 and SPRED1, whereas miR-126 knockout activates genes that are highly expressed in committed, more differentiated hematopoietic progenitor cells, presumably through inducing FZD7 expression.
Downregulation of MicroRNA-126 Contributes to the Failing Right Ventricle in Pulmonary Arterial Hypertension.
Bonnet et al., Québec, Canada. In Circulation, Oct 2015
miR-126 downregulation was associated with increased Sprouty-related EVH1 domain-containing protein 1 (SPRED-1), leading to decreased activation of RAF (phosphorylated RAF/RAF) and mitogen-activated protein kinase (MAPK); (phosphorylated MAPK/MAPK), thus inhibiting the vascular endothelial growth factor pathway.
CIC inactivating mutations identify aggressive subset of 1p19q codeleted gliomas.
Sanson et al., Paris, France. In Ann Neurol, Sep 2015
Moreover, a truncating CIC mutation resulted in a defect of nuclear targeting of CIC protein to the nucleus in a human glioma cell line expressing IDH1(R132H) and overexpression of CCND1 and other new target genes of CIC, such as DUSP4 and SPRED1.
Genomic profiling screens small molecules of metastatic prostate carcinoma.
Sun et al., Beijing, China. In Oncol Lett, Sep 2015
In addition, KPNA4, SYT1, PLCB1, SPRED1, MBNL2, RNF165, MEF2C, MBNL1, ZFP36L1 and CELF2, were found to be likely to play significant roles in the process of metastatic prostate carcinoma.
Family with Legius syndrome (neurofibromatosis type 1-like syndrome).
Mitsuhashi et al., Tokyo, Japan. In J Dermatol, Jul 2015
Mutation analysis revealed a mutation of c.349C>T resulting in p.Arg117* in the SPRED1 gene as the cause of the Legius syndrome.
Legius syndrome: case report and review of literature.
Berti et al., Trieste, Italy. In Ital J Pediatr, 2014
The diagnosis was confirmed by the finding of a mutation in SPRED1 gene, a feedback regulator of RAS/MAPK signaling.
Mutation in NRAS in familial Noonan syndrome--case report and review of the literature.
Bondeson et al., Uppsala, Sweden. In Bmc Med Genet, 2014
Comprehensive mutation analysis of NF1, PTPN11, SOS1, CBL, BRAF, RAF1, SHOC2, MAP2K2, MAP2K1, SPRED1, NRAS, HRAS and KRAS was performed using targeted next-generation sequencing.
Identification and Validation of Protein Biomarkers of Response to Neoadjuvant Platinum Chemotherapy in Muscle Invasive Urothelial Carcinoma.
Netto et al., Kingston, Canada. In Plos One, 2014
The combination of GDPD3 and SPRED1 resulted in a multivariate classification tree that was significantly associated with NAC response status (Goodman-Kruskal γ = 0.85 p<0.0001) in our independent NAC treated MIBC cohort.
[Relationship between Spred1 and acute myeloid leukemia].
Zhang et al., Shenyang, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2013
SPRED1 protein coded by SPRED1 gene, a kind of tumors suppressor, belongs to Sprouty related protein family and mainly distributes in human brain.
Legius syndrome, an Update. Molecular pathology of mutations in SPRED1.
Legius et al., Leuven, Belgium. In Keio J Med, 2012
In 2007 we reported that some individuals with multiple CALMs have a heterozygous mutation in the SPRED1 gene and have NF1-like syndrome, or Legius syndrome.
Review and update of SPRED1 mutations causing Legius syndrome.
Messiaen et al., Leuven, Belgium. In Hum Mutat, 2012
Legius syndrome is caused by germline loss-of-function SPRED1 mutations, resulting in overactivation of the RAS-MAPK signal transduction cascade.
A shared molecular mechanism underlies the human rasopathies Legius syndrome and Neurofibromatosis-1.
McCormick et al., San Francisco, United States. In Genes Dev, 2012
show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function
Interaction of the receptor FGFRL1 with the negative regulator Spred1.
Trueb et al., Bern, Switzerland. In Cell Signal, 2011
Interaction of FGFRL1 with Spred1 increases the proportion of the receptor at the plasma membrane.
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.
Guy et al., Singapore, Singapore. In J Biol Chem, 2011
SPRED1 is a likely substrate of SHP2, whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK pathway.
Identification of five novel SPRED1 germline mutations in Legius syndrome.
Upadhyaya et al., In Clin Genet, 2011
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
miR126 positively regulates mast cell proliferation and cytokine production through suppressing Spred1.
Yoshimura et al., Tokyo, Japan. In Genes Cells, 2011
The results suggest that Spred1 negatively regulates mast cell activation, which is modulated by miR126.
Clinical and mutational spectrum of neurofibromatosis type 1-like syndrome.
Legius et al., Birmingham, United States. In Jama, 2009
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.
Germline loss-of-function mutations in SPRED1 cause a neurofibromatosis 1-like phenotype.
Legius et al., Leuven, Belgium. In Nat Genet, 2007
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.
Spred is a Sprouty-related suppressor of Ras signalling.
Yoshimura et al., Fukuoka, Japan. In Nature, 2001
Here we describe two structurally similar tyrosine kinase substrates, Spred-1 and Spred-2.
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