Our Abpromise guarantee covers the use of ab16982 in the following tested applications.

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

  • Applications


  • Form

  • Additional notes

    - First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions.
    - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer.
    - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent.
    - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised.
    - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.

    Information available upon request.

General Info

  • Alternative names

    • DKFZp761G1421
    • KIAA1938
    • MRD5
    • Neuronal RasGAP
    • OTTHUMP00000064825
    • p135 SynGAP
    • Ras GTPase activating protein SynGAP
    • Ras GTPase-activating protein SynGAP
    • RASA 1
    • RASA 5
    • RASA1
    • RASA5
    • Synaptic Ras GAP 1
    • Synaptic Ras GTPase activating protein
    • Synaptic Ras GTPase activating protein 1
    • Synaptic Ras GTPase activating protein 1 homolog
    • Synaptic Ras GTPase activating protein 135kDa
    • Synaptic Ras GTPase-activating protein 1
    • Synaptic Ras-GAP 1
    • SYNGAP 1
    • SYNGAP1
    see all
  • Function

    Major constituent of the PSD essential for postsynaptic signaling. Inhibitory regulator of the Ras-cAMP pathway. Member of the NMDAR signaling complex in excitatory synapses, it may play a role in NMDAR-dependent control of AMPAR potentiation, AMPAR membrane trafficking and synaptic plasticity. Regulates AMPAR-mediated miniature excitatory postsynaptic currents. May be involved in certain forms of brain injury, leading to long-term learning and memory deficits.
  • Involvement in disease

    Defects in SYNGAP1 are the cause of mental retardation autosomal dominant type 5 (MRD5) [MIM:612621]. Mental retardation is characterized by significantly sub-average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period. MRD5 patients show global developmental delay with delayed motor development, hypotonia, moderate-to-severe mental retardation, and severe language impairment. Autism can be present in some patients.
  • Sequence similarities

    Contains 1 C2 domain.
    Contains 1 PH domain.
    Contains 1 Ras-GAP domain.
  • Post-translational

    Phosphorylated by CaM-kinase II. Dephosphorylated upon NMDA receptor activation or SYNGAP1/MPDZ complex disruption.
  • Information by UniProt


ab16982 has not yet been referenced specifically in any publications.

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