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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 (show EGFR Proteins) induced SOS1 expression by directly binding to the SOS1 promoter.
findings suggest that targeting the Src (show SRC Proteins)/Abl (show ABL1 Proteins)/Sos1/Rac (show AKT1 Proteins) 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 (show MLXIP Proteins)-146a and SOS1 and between miR (show MLXIP Proteins)-370 and GADD45beta (show GADD45B Proteins) 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 (show HGF Proteins)-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 (show VPS28 Proteins) functions as a negative modulator of the SOS1-Ras signaling events initiated by peptide growth factors including EGF (show EGF Proteins).
Increased expression of SOS1 increases NFkappaB activation in several types of cancer cells, and ablation of SOS1 inhibits EGF-induced NFkappaB activation in these cells, indicating that SOS1 is a component of the pathway connecting EGFR to NFkappaB activation.
The increased activity of the PI3K/AKT (show AKT1 Proteins) pathway led to downregulation of the surface receptor CD62L (show SELL Proteins) in Sos-1/2dKO T cells and a subsequent impairment in T-cell migration.
SUMOylation of Grb2 (show GRB2 Proteins) enhances the ERK (show EPHB2 Proteins) activity by increasing its binding with Sos1.
Data suggest that interactions between Sos1 (Son of Sevenless homolog 1) and Crk (show CRK Proteins) (proto-oncogene (show RAB1A Proteins) proteins c-crk (show CRK Proteins)) involve electrostatic interactions at binding sites.
ROS1 kinase activity and MEK1/2-ERK1/2 signaling regulates epithelial differentiation in the epididymis.
Sos1 has distinct roles in acting as a scaffold to oligomerize the adaptor protein LAT (show LAT Proteins), 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 (show SOS2 Proteins), and RasGRP1 (show RASGRP1 Proteins) 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