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The protein encoded by SPRED1 is a member of the Sprouty family of proteins and is phosphorylated by tyrosine kinase in response to several growth factors. Additionally we are shipping SPRED1 Proteins (3) and many more products for this protein.
Showing 10 out of 111 products:
Human Polyclonal SPRED1 Primary Antibody for EIA, IHC (p) - ABIN500796
Yoshida, Hisamoto, Akiba, Koga, Nakamura, Tokunaga, Hanada, Kumemura, Maeyama, Harada, Ogata, Yano, Kojiro, Ueno, Yoshimura, Sata: Spreds, inhibitors of the Ras/ERK signal transduction, are dysregulated in human hepatocellular carcinoma and linked to the malignant phenotype of tumors. in Oncogene 2006
Show all 4 references for ABIN500796
Human Polyclonal SPRED1 Primary Antibody for EIA, IHC (p) - ABIN356945
King, Straffon, DAbaco, Poon, I, Smith, Buchert, Corcoran, Hall, Callus, Sarcevic, Martin, Lock, Hovens: Distinct requirements for the Sprouty domain for functional activity of Spred proteins. in The Biochemical journal 2005
Show all 2 references for ABIN356945
Human Polyclonal SPRED1 Primary Antibody for FACS, WB - ABIN650630
Brems, Chmara, Sahbatou, Denayer, Taniguchi, Kato, Somers, Messiaen, De Schepper, Fryns, Cools, Marynen, Thomas, Yoshimura, Legius: Germline loss-of-function mutations in SPRED1 cause a neurofibromatosis 1-like phenotype. in Nature genetics 2007
Show all 2 references for ABIN650630
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 (show MAPK1 Antibodies) 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 (show EPHB2 Antibodies) 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 (show NF1 Antibodies), the NF1 (show NF1 Antibodies) 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 (show PTPN11 Antibodies), whose tyrosine dephosphorylation is required to attenuate the inhibitory action of SPRED1 in the Ras/ERK (show EPHB2 Antibodies) pathway.
Data show that both SPRED1 and SPRED2 (show SPRED2 Antibodies) inhibit the ability of DYRK1A (show DYRK1A Antibodies) to phosphorylate its substrates.
These data suggest that Spreds are key regulators of RhoA (show RHOA Antibodies)-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.
Spred-1 and Spred-2 (show SPRED2 Antibodies) were found to be expressed predominantly in brain
Data suggest SPRED1 EVH1 domain interacts with NF1 (show NF1 Antibodies) GRD domain [N-term. 16AA/C-term. 20AA of GTPase-activating protein (show RASA1 Antibodies)-related domain]; SPRED1 EVH1 and NF1 (show NF1 Antibodies) GRD mutations observed in Legius syndrome reduce binding affinity between EVH1/GRD domains.
SPRED1 decreased expression correlated with genetic features of AML (show RUNX1 Antibodies). Our study reveals a new mechanism which contributes to deregulate RAS MAPK (show MAPK1 Antibodies) pathway in the vast majority of paediatric AMLs
Antisense-mediated knockdown (anti-miR (show MLXIP Antibodies)) revealed that miR (show MLXIP Antibodies)-206/21 coordinately promote RAS-ERK (show EPHB2 Antibodies) signaling and the corresponding cell phenotypes by inhibiting translation of the pathway suppressors RASA1 (show RASA1 Antibodies) and SPRED1.
SPRED1 seems to play an important role in recruiting neurofibromin (show NF1 Antibodies) to the plasma membrane. (Review)
Older age and deletions of IKZF1 (show IKZF1 Antibodies) 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 (show NF1 Antibodies).
Data indicate that upregulated miR (show MLXIP Antibodies)-126 upon coxsackievirus B3 (CVB3) infection targets SPRED1, LRP6 (show LRP6 Antibodies), and WRCH1 (show RHOU Antibodies) genes, mediating cross-talk between ERK1/2 (show MAPK1/3 Antibodies) and Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) 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.
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