• Product nameAnti-SOS1 antibody [SOS-1]
    See all SOS1 primary antibodies
  • Description
    Mouse monoclonal [SOS-1] to SOS1
  • SpecificityThis antibody reacts with human SOS1, an ubiquitously expressed 150 kDa intracellular protein.
  • Tested applicationsSuitable for: FPIA, ICC/IF, WB, ELISAmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse
  • Immunogen

    Synthetic peptide:


    , corresponding to amino acids 1315-1333 of Human SOS1

  • Positive control
    • HeLa human cervix carcinoma cell line, K562 human Caucasian chronic myeloid leukemia cell line or RAJI human Burkitt lymphoma cell line. IF/ICC: HeLa cell line.



Our Abpromise guarantee covers the use of ab64595 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
FPIA Use 1µg for 106 cells.
ICC/IF Use a concentration of 10 µg/ml.
WB Use a concentration of 1 µg/ml. Detects a band of approximately 150 kDa (predicted molecular weight: 152 kDa).
ELISA Use at an assay dependent concentration.


  • FunctionPromotes the exchange of Ras-bound GDP by GTP.
  • Tissue specificityExpressed in gingival tissues.
  • Involvement in diseaseDefects in SOS1 are the cause of gingival fibromatosis 1 (GGF1) [MIM:135300]; also known as GINGF1. Gingival fibromatosis is a rare overgrowth condition characterized by a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of maxillary and mandibular keratinized gingiva. GGF1 is usually transmitted as an autosomal dominant trait, although sporadic cases are common.
    Defects in SOS1 are the cause of Noonan syndrome type 4 (NS4) [MIM:610733]. NS4 is an autosomal dominant disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS4 is associated with juvenile myelomonocytic leukemia (JMML). SOS1 mutations engender a high prevalence of pulmonary valve disease; atrial septal defects are less common.
  • Sequence similaritiesContains 1 DH (DBL-homology) domain.
    Contains 1 N-terminal Ras-GEF domain.
    Contains 1 PH domain.
    Contains 1 Ras-GEF domain.
  • Information by UniProt
  • Database links
  • Alternative names
    • alternate SOS1 antibody
    • GF1 antibody
    • GGF1 antibody
    • GINGF antibody
    • gingival fibromatosis antibody
    • gingival fibromatosis hereditary 1 antibody
    • Guanine nucleotide exchange factor antibody
    • HGF antibody
    • NS4 antibody
    • Son of sevenless homolog 1 (Drosophila) antibody
    • Son of sevenless homolog 1 antibody
    • SOS Ras/Rac guanine nucleotide exchange factor 1 antibody
    • SOS-1 antibody
    • Sos1 antibody
    • SOS1_HUMAN antibody
    see all

Anti-SOS1 antibody [SOS-1] images

  • ICC/IF image of ab64595 stained HeLa cells. The cells were 4% formaldehyde fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab64595, 10µg/ml) overnight at +4°C. The secondary antibody (green) was ab96879, DyLight® 488 goat anti-mouse IgG (H+L) used at a 1/250 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM

  • All lanes : Anti-SOS1 antibody [SOS-1] (ab64595) at 1 µg/ml

    Lane 1 : K562 human Caucasian chronic myeloid leukemia cell line
    Lane 2 : RAJI human Burkitt lymphoma cell line

    Performed under reducing conditions.

    Predicted band size : 152 kDa
    Observed band size : 150 kDa (why is the actual band size different from the predicted?)

References for Anti-SOS1 antibody [SOS-1] (ab64595)

ab64595 has not yet been referenced specifically in any publications.

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