Recombinant Human Sprouty-related, EVH1 domain-containing protein 1 (SPRED1)

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Code CSB-EP773600HU
MSDS
Size US$306
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP773600HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) SPRED1.
  • Based on the SEQUEST from database of E.coli host and target protein, the LC-MS/MS Analysis result of CSB-EP773600HU could indicate that this peptide derived from E.coli-expressed Homo sapiens (Human) SPRED1.
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Product Details

Purity
Greater than 85% as determined by SDS-PAGE.
Target Names
SPRED1
Uniprot No.
Research Area
Signal Transduction
Alternative Names
EVH1 domain-containing protein 1; EVH1/Sprouty domain containing protein; FLJ33903; hSpred 1; hSpred1; NFLS; PPP1R147; protein phosphatase 1 regulatory subunit 147; SPRE1_HUMAN; SPRED 1; Spred-1; spred1; Sprouty related EVH1 domain containing 1; sprouty related EVH1 domain containing protein 1; Sprouty related protein 1 with EVH 1 domain; Sprouty-related; Suppressor of Ras/MAPK activation
Species
Homo sapiens (Human)
Source
E.coli
Expression Region
2-444aa
Target Protein Sequence
SEETATSDNDNSYARVRAVVMTRDDSSGGWLPLGGSGLSSVTVFKVPHQEENGCADFFIRGERLRDKMVVLECMLKKDLIYNKVTPTFHHWKIDDKKFGLTFQSPADARAFDRGIRRAIEDISQGCPESKNEAEGADDLQANEEDSSSSLVKDHLFQQETVVTSEPYRSSNIRPSPFEDLNARRVYMQSQANQITFGQPGLDIQSRSMEYVQRQISKECGSLKSQNRVPLKSIRHVSFQDEDEIVRINPRDILIRRYADYRHPDMWKNDLERDDADSSIQFSKPDSKKSDYLYSCGDETKLSSPKDSVVFKTQPSSLKIKKSKRRKEDGERSRCVYCQERFNHEENVRGKCQDAPDPIKRCIYQVSCMLCAESMLYHCMSDSEGDFSDPCSCDTSDDKFCLRWLALVALSFIVPCMCCYVPLRMCHRCGEACGCCGGKHKAAG
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
70.3 kDa
Protein Length
Full Length of Mature Protein
Tag Info
N-terminal 10xHis-SUMO-tagged and C-terminal Myc-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.
Description

Amino acids 2-444 form the expressed segment for recombinant Human SPRED1. The theoretical molecular weight of the SPRED1 protein is 70.3 kDa. This SPRED1 recombinant protein is manufactured in e.coli. Fusion of the N-terminal 10xHis-SUMO tag and C-terminal Myc tag into the SPRED1 encoding gene fragment was conducted, allowing for easier detection and purification of the SPRED1 protein in subsequent stages.

Human sprouty-related, EVH1 domain-containing protein 1 (SPRED1) primarily functions as a negative regulator of the RAS-MAPK signaling pathway, crucial for cellular proliferation and differentiation. SPRED1 inhibits the activation of RAF kinases, attenuating downstream signaling. In medical research, SPRED1 is associated with Neurofibromatosis Type 1 (NF1) and Legius syndrome, providing insights into these genetic disorders. In cancer biology, SPRED1's role in suppressing MAPK signaling may have implications for tumor development and progression. Investigating SPRED1 contributes to understanding its regulatory functions, offering potential applications in cancer research, and developmental biology, and providing a molecular basis for therapeutic interventions targeting aberrant RAS-MAPK signaling pathways.

Customer Reviews and Q&A

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 Q&A
Q:

We plan to use SPRED1 as a target for in-vitro phosphorylation. Is the product suitable for the purpose?

A:
Thanks for your inquiry.We haven't tested the activity of this protein yet. The protein we provide is full length of mature protein which can be used in the customer's research in theory, but we can't guarantee 100%.
We suggest you to purchase a small size to have a try first.
It is mentioned in the literature that the author used Spred1 (EVH1) and mutated forms (T102→R, W31→C) expressed in E. coli strain BL21 Star (DE3) for their research and achieved the purpose of the research.
Here is the link of the literature: http://www.pnas.org/content/113/27/7497

Target Background

Function
Tyrosine kinase substrate that inhibits growth-factor-mediated activation of MAP kinase. Negatively regulates hematopoiesis of bone marrow. Inhibits fibroblast growth factor (FGF)-induced retinal lens fiber differentiation, probably by inhibiting FGF-mediated phosphorylation of ERK1/2. Attenuates actin stress fiber formation via inhibition of TESK1-mediated phosphorylation of cofilin. Inhibits TGFB-induced epithelial-to-mesenchymal transition in lens epithelial cells.
Gene References into Functions
  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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Involvement in disease
Neurofibromatosis 1-like syndrome (NFLS)
Subcellular Location
Cell membrane; Peripheral membrane protein. Membrane, caveola; Peripheral membrane protein. Nucleus. Note=Localized in cholesterol-rich membrane raft/caveola fractions.
Tissue Specificity
Weakly expressed in embryonic cell line HEK293.
Database Links

HGNC: 20249

OMIM: 609291

KEGG: hsa:161742

STRING: 9606.ENSP00000299084

UniGene: Hs.525781

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