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Data show that a heterozygous son of sevenless homolog 1 (SOS1) gene frameshift mutation (c.3266dup or c.3248dup) was identified in each patient.
The present study provides a first evidence of allelic imbalance of SOS1 and pinpoints this condition as a possible mechanism underlying a different penetrance of some SOS1-mutated alleles in unrelated carriers
In non-apoptotic cells, nuclear EGFR (Montrer EGFR Kits ELISA) induced SOS1 expression by directly binding to the SOS1 promoter.
findings suggest that targeting the Src (Montrer SRC Kits ELISA)/Abl (Montrer ABL1 Kits ELISA)/Sos1/Rac (Montrer AKT1 Kits ELISA) pathway may represent a double-edged sword to control both cancer-invasive capacities and cancer-related inflammation.
These data demonstrated the negative regulation between miR (Montrer MLXIP Kits ELISA)-146a and SOS1 and between miR (Montrer MLXIP Kits ELISA)-370 and GADD45beta (Montrer GADD45B Kits ELISA) and that these regulations are influenced by enterovirus 71 to induce apoptosis.
Combined rational design and a high throughput screening platform for identifying chemical inhibitors of a Ras-activating enzyme.
SOS1 and Ras regulate epithelial tight junction formation in the human airway through EMP1.
HGF (Montrer HGF Kits ELISA)-related mutation g.126,142-126,143insC in exon 21 was not found in any of the 6 affected individuals from three families.
Stabilized alpha helices of son of sevenless 1 directly inhibit wild-type and mutant forms of KRAS.
CIIA (Montrer VPS28 Kits ELISA) functions as a negative modulator of the SOS1-Ras signaling events initiated by peptide growth factors including EGF (Montrer EGF Kits ELISA).
The increased activity of the PI3K/AKT (Montrer AKT1 Kits ELISA) pathway led to downregulation of the surface receptor CD62L (Montrer SELL Kits ELISA) in Sos-1/2dKO T cells and a subsequent impairment in T-cell migration.
SUMOylation of Grb2 (Montrer GRB2 Kits ELISA) enhances the ERK (Montrer EPHB2 Kits ELISA) activity by increasing its binding with Sos1.
Data suggest that interactions between Sos1 (Son of Sevenless homolog 1) and Crk (Montrer CRK Kits ELISA) (proto-oncogene (Montrer RAB1A Kits ELISA) proteins c-crk (Montrer CRK Kits ELISA)) involve electrostatic interactions at binding sites.
ROS1 (Montrer ROS1 Kits ELISA) kinase activity and MEK1 (Montrer MAP2K1 Kits ELISA)/2-ERK1/2 (Montrer MAPK1/3 Kits ELISA) signaling regulates epithelial differentiation in the epididymis.
Sos1 has distinct roles in acting as a scaffold to oligomerize the adaptor protein LAT (Montrer LAT Kits ELISA), and in guanine nucleotide exchange activity
ezrin also is important for the activity of SOS itself. Ezrin interacts with GDP-Ras and with the Dbl homology (DH)/pleckstrin homology (PH) domains of SOS, bringing GDP-Ras to the proximity of the allosteric site of SOS.
Absolute counts of mature B and T cells in spleen and peripheral blood were unchanged in single-knockout mutants, while significantly reduced in Sos1/2 double-knockout mice.
Study shows that the ability of Sos1/Grb2 to appropriately regulate pluripotency and differentiation factors and to initiate primitive endoderm development requires collective binding of multiple Sos1/Grb2 domains to their protein and phospholipid ligands.
assessed the independent and combined roles for the RasGEFs Sos1, Sos2 (Montrer SOS2 Kits ELISA), and RasGRP1 (Montrer RASGRP1 Kits ELISA) during thymocyte development
This gene encodes a protein that is a guanine nucleotide exchange factor for RAS proteins, membrane proteins that bind guanine nucleotides and participate in signal transduction pathways. GTP binding activates and GTP hydrolysis inactivates RAS proteins. The product of this gene may regulate RAS proteins by facilitating the exchange of GTP for GDP. Mutations in this gene are associated with gingival fibromatosis 1 and Noonan syndrome type 4.
, gingival fibromatosis, hereditary, 1
, guanine nucleotide exchange factor
, son of sevenless homolog 1
, guanine nucleotide releasing factor
, ras guanine exchange factor
, son-of-sevenless 1
, Son of sevenless homolog 1