抗Human SOS1 抗体:
抗Mouse (Murine) SOS1 抗体:
抗Rat (Rattus) SOS1 抗体:
Human Monoclonal SOS1 Primary Antibody for IF, WB - ABIN535287
Xing, Hamaguchi: Effects of SHIP-1 on MMP2 secretion and invasion of SR3Y1 cells. in Journal of genetics and genomics = Yi chuan xue bao 2007
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Human Monoclonal SOS1 Primary Antibody for ELISA, WB - ABIN537102
Corbalan-Garcia, Yang, Degenhardt, Bar-Sagi: Identification of the mitogen-activated protein kinase phosphorylation sites on human Sos1 that regulate interaction with Grb2. in Molecular and cellular biology 1996
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Human Monoclonal SOS1 Primary Antibody for IF, ELISA - ABIN2476553
Scita, Tenca, Frittoli, Tocchetti, Innocenti, Giardina, Di Fiore: Signaling from Ras to Rac and beyond: not just a matter of GEFs. in The EMBO journal 2000
Transcriptional profiling reveals that the expression of mutant SOS1 leads to the upregulation of MYC target genes and genes associated with Ras transformation.
In the present study, we analyze the 14-3-3/SOS1 protein-protein interaction (PPI) by different biochemical assays and report the high resolution crystal structure of a 13-mer motif of SOS1 bound to 14-3-3 zeta
There was an additive effect of the alleles in the four genes associated with good growth response. For rs3110697 within IGFBP3, rs1045992 in CYP19A1 and rs2888586 in SOS1, the variant associated with better growth response showed higher transcriptional activity with r-hGH treatment
Noonan Syndrome mutations in SOS1 protein affects SOS1 translocation to the plasma membrane.
Disease-causing variants were identified in 0.6% (four of 692) of individuals with HCM, including three missense variants in the PTPN11, SOS1, and BRAF genes. Overall, 36 variants of uncertain significance (VUSs) were identified, averaging approximately 3VUSs/100 cases.
The overall VUS frequency was twice as high in prenatal specimens (58.1 vs. 29.3%). PTPN11 and SOS1 had a 1.5-fold higher VUS frequency in the prenatal cohort (10.7 vs. 7.4% and 95 vs. 61.1%, respectively). The diagnostic yield was 3.7% for prenatal samples, with a higher yield of 12.3% in fetuses with cystic hygroma as a sole finding, and 21.3% for postnatal
SOS1 is required for full transformation and critically contribute to the leukemogenic potential of BCR-ABL.
a distinct role of the C-terminal proline-rich (PR) domain of the full-length son of sevenless homolog 1 (SOS1) protein.
SOS1 was statistically significantly associated with gestational diabetes mellitus risk after adjusting for multiple comparisons
Findings identified p.Ser548Arg missense mutation in Son of Sevenless Homolog 1 (SOS1) in the boy, confirmed in his mother.
We report on a novel pathogenic mutation in the SOS1 gene and a large clinical spectrum in a Noonan syndrome family with ten genetically confirmed affected individuals.
Data indicate dynamic of H-Ras functional cycle as controlled by son of sevenless homolog 1 (Sos).
In summary, patients from two families with history of non-syndromic autosomal-dominant HGF from Malopolska and Mazovia provinces in Poland had not been affected by HGF type 1, caused by a single-cytosine insertion in exon 21 of the SOS-1 gene.
Mutation scanning of the entire coding sequence of SOS1 gene identified seven intronic variants and one new exonic substitution (c.138G > A). The seven common intronic variants were not considered to be of pathogenic importance. The exonic substitution c.138G > A was found to be absent in 100 ethnically matched normal control chromosomes, not expected to have functional significance based on prediction bioinformatics tool
Grb2-independent interactions are sufficient to retain human SOS on the membrane for many minutes, during which a single SOS molecule could processively activate thousands of Ras molecules.
a computational methodology that overlays any variant database onto the somatic mutations in all cancer exomes identified activating SOS1 mutations associated with Noonan syndrome as significantly altered in melanoma
Data show that a heterozygous son of sevenless homolog 1 (SOS1) gene frameshift mutation (c.3266dup or c.3248dup) was identified in each patient.
Ras.GDP weakly binds to the catalytic but not to the allosteric site of Sos.
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 induced SOS1 expression by directly binding to the SOS1 promoter.
Unique dependence on Sos1 in Kras (G12D) -induced leukemogenesis.
Sos1 disruption delayed the onset of tumor initiation, decreased tumor growth, and prevented malignant progression of papillomas in a DMBA (7,12-dimethylbenz[alpha]anthracene)/TPA (12-O-tetradecanoylphorbol-13-acetate)-induced skin carcinogenesis model.
a direct mechanistic link between Sos1 and control of intracellular oxidative stress, and demonstrate functional prevalence of Sos1 over Sos2 with regards to cellular proliferation and viability.
findings suggest that targeting the Src/Abl/Sos1/Rac pathway may represent a double-edged sword to control both cancer-invasive capacities and cancer-related inflammation.
The increased activity of the PI3K/AKT pathway led to downregulation of the surface receptor CD62L in Sos-1/2dKO T cells and a subsequent impairment in T-cell migration.
SUMOylation of Grb2 enhances the ERK activity by increasing its binding with Sos1.
Data suggest that interactions between Sos1 (Son of Sevenless homolog 1) and Crk (proto-oncogene proteins c-crk) 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, 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, and RasGRP1 during thymocyte development
Both heterozygous and homozygous Sos1E846K mutants showed many Noonan syndrome-associated phenotypes, including growth delay, distinctive facial dysmorphia, hematologic abnormalities, and cardiac defects.
Sos1 detected in neuronal cell body, dendrites and PSD, but not in presynaptic compartments by biochemical fractionation and immunohistochemistry (light microscopy and EM detection)
Sos1 is recruited into a multimolecular signaling complex by Abi1
Vav1 transduces TCR signals to Ras by controlling recruitment of RasGRP1 to the membrane and recruitment of Sos1 and -2 to the transmembrane adapter protein LAT.
the src-family kinases are responsible for the LHR-mediated phosphorylation of the EGFR and Shc, the formation of complexes containing Shc and Sos, the activation of Ras, and the phosphorylation of ERK1/2
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