Product nameAnti-SOX10 antibody
See all SOX10 primary antibodies
DescriptionRabbit polyclonal to SOX10
SpecificityAntibody was raised using a synthetic peptide corresponding to Sox8. However, this antibody demonstrates cross reactivity against Sox10. Does not cross react with SOX9
Tested applicationsSuitable for: ICC/IF, IHC-Fr, WBmore details
Species reactivityReacts with: Mouse, Chicken
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Our Abpromise guarantee covers the use of ab27655 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||1/1000 - 1/5000.|
|IHC-Fr||1/5000. Fix with 4% paraformaldehyde for 2h at 4C.|
|WB||Use a concentration of 1 µg/ml. Detects a band of approximately 56 kDa (predicted molecular weight: 50 kDa).|
FunctionTranscription factor that seems to function synergistically with the POU domain protein TST-1/OCT6/SCIP. Could confer cell specificity to the function of other transcription factors in developing and mature glia.
Tissue specificityExpressed in fetal brain and in adult brain, heart, small intestine and colon.
Involvement in diseaseDefects in SOX10 are the cause of Waardenburg syndrome type 2E (WS2E) [MIM:611584]. WS2 is a genetically heterogeneous, autosomal dominant disorder characterized by sensorineural deafness, pigmentary disturbances, and absence of dystopia canthorum. The frequency of deafness is higher in WS2 than in WS1.
Defects in SOX10 are a cause of Waardenburg syndrome type 4C (WS4C) [MIM:613266]; also known as Waardenburg-Shah syndrome. WS4C is characterized by the association of Waardenburg features (depigmentation and deafness) and the absence of enteric ganglia in the distal part of the intestine (Hirschsprung disease).
Defects in SOX10 are a cause of Yemenite deaf-blind hypopigmentation syndrome (YDBHS) [MIM:601706]. YDBHS consists of cutaneous hypopigmented and hyperpigmented spots and patches, microcornea, coloboma and severe hearing loss. Another case observed in a girl with similar skin symptoms and hearing loss but without microcornea or coloboma is reported as a mild form of this syndrome.
Defects in SOX10 are the cause of peripheral demyelinating neuropathy, central dysmyelinating leukodystrophy, Waardenburg syndrome, and Hirschsprung disease (PCWH) [MIM:609136]; also called neurologic variant of Waardenburg-Shah syndrome. PCWH is a rare, complex and more severe neurocristopathy that includes features of 4 distinct syndromes: peripheral demyelinating neuropathy, central dysmyelinating leukodystrophy, Waardenburg syndrome, and Hirschsprung disease.
Sequence similaritiesContains 1 HMG box DNA-binding domain.
Cellular localizationCytoplasm. Nucleus.
- Information by UniProt
- DOM antibody
- DOM antibody
- Dominant megacolon mouse human homolog of antibody
Sections through the trunk of E4 chick embryos fixed in 4 % paraformaldehyde and stained with anti-SOX10 (ab27655) diluted 1/5000. Secondary antibody was FITC-conjugated donkey anti-rabbit. ab27655 stains the embryonic neural crest cells which can be seen migrating into the dorsal root ganglion.
All lanes : Anti-SOX10 antibody (ab27655) at 1/500 dilution
Lane 1 : Brain (Mouse) Tissue Lysate
Lane 2 : Heart (Mouse) Tissue Lysate
Lysates/proteins at 10 µg per lane.
All lanes : Goat polyclonal to Rabbit IgG - H&L - Pre-Adsorbed (HRP) at 1/3000 dilution
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 50 kDa
Observed band size: 56 kDa why is the actual band size different from the predicted?
Additional bands at: 100 kDa, 74 kDa. We are unsure as to the identity of these extra bands.
Exposure time: 8 minutes
SOX10 contains a number of potential phosphorylation sites (SwissProt) which may explain its migration at a higher molecular weight than predicted.
This product has been referenced in:
- Pelletier J et al. Generation and characterization of polyclonal and monoclonal antibodies to human NTPDase2 including a blocking antibody. Purinergic Signal 13:293-304 (2017). Read more (PubMed: 28409324) »
- Chen Y et al. GSK3ß inhibition accelerates axon debris clearance and new axon remyelination. Am J Transl Res 8:5410-5420 (2016). Read more (PubMed: 28078012) »