Description

Specifications

Our Abpromise guarantee covers the use of ab215114 in the following tested applications.

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

  • Applications

    Blocking - Blocking peptide for Anti-beta III Tubulin antibody [EP1569Y] - Neuronal Marker (Alexa Fluor® 555) (ab202519)

  • Form

    Lyophilised
  • Additional notes

    This is the blocking peptide for ab202519.

    - 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. Store at -20°C.

General Info

  • Alternative names

    • beta 3 tubulin
    • beta 4
    • beta-4
    • CDCBM
    • CDCBM1
    • CFEOM3
    • CFEOM3A
    • FEOM3
    • M(beta)3
    • M(beta)6
    • MC1R
    • Neuron specific beta III Tubulin
    • Neuron-specific class III beta-tubulin
    • QccE-11995
    • QccE-15186
    • TBB3_HUMAN
    • Tubb 3
    • TUBB3
    • TUBB4
    • Tubulin beta 3
    • Tubulin beta 3 chain
    • Tubulin beta 4
    • Tubulin beta III
    • Tubulin beta-3 chain
    • Tubulin beta-4 chain
    • Tubulin beta-III
    • tuj 1
    • tuj1
    see all
  • Function

    Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha-chain. TUBB3 plays a critical role in proper axon guidance and mantainance.
  • Tissue specificity

    Expression is primarily restricted to central and peripheral nervous system.
  • Involvement in disease

    Defects in TUBB3 are the cause of congenital fibrosis of extraocular muscles type 3A (CFEOM3A) [MIM:600638]. A congenital ocular motility disorder marked by restrictive ophthalmoplegia affecting extraocular muscles innervated by the oculomotor and/or trochlear nerves. It is clinically characterized by anchoring of the eyes in downward gaze, ptosis, and backward tilt of the head. Congenital fibrosis of extraocular muscles type 3 presents as a non-progressive, autosomal dominant disorder with variable expression. Patients may be bilaterally or unilaterally affected, and their oculo-motility defects range from complete ophthalmoplegia (with the eyes fixed in a hypo- and exotropic position), to mild asymptomatic restrictions of ocular movement. Ptosis, refractive error, amblyopia, and compensatory head positions are associated with the more severe forms of the disorder. In some cases the ocular phenotype is accompanied by additional features including developmental delay, corpus callosum agenesis, basal ganglia dysmorphism, facial weakness, polyneuropathy.
  • Sequence similarities

    Belongs to the tubulin family.
  • Domain

    The highly acidic C-terminal region may bind cations such as calcium.
  • Post-translational
    modifications

    Some glutamate residues at the C-terminus are polyglutamylated. This modification occurs exclusively on glutamate residues and results in polyglutamate chains on the gamma-carboxyl group. Also monoglycylated but not polyglycylated due to the absence of functional TTLL10 in human. Monoglycylation is mainly limited to tubulin incorporated into axonemes (cilia and flagella) whereas glutamylation is prevalent in neuronal cells, centrioles, axonemes, and the mitotic spindle. Both modifications can coexist on the same protein on adjacent residues, and lowering glycylation levels increases polyglutamylation, and reciprocally. The precise function of such modifications is still unclear but they regulate the assembly and dynamics of axonemal microtubules.
  • Cellular localization

    Cytoplasm > cytoskeleton.
  • Information by UniProt

References

ab215114 has not yet been referenced specifically in any publications.

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