Overview

  • Product name

    Anti-SOX10 antibody [BC34]
    See all SOX10 primary antibodies
  • Description

    Mouse monoclonal [BC34] to SOX10
  • Host species

    Mouse
  • Tested applications

    Suitable for: IHC-Pmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Recombinant fragment corresponding to Human SOX10 (N terminal).

  • Positive control

    • Human melanoma.
  • General notes

    This product was changed from ascites to tissue culture supernatant on 14/07/17. The following lots are from ascites and are still in stock as of [14/07/17] – [GR300901]. Lot numbers higher than [GR300901] will be from tissue culture supernatant. Please note that the dilutions may need to be adjusted accordingly.

Properties

Applications

Our Abpromise guarantee covers the use of ab195364 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
IHC-P 1/100 - 1/200. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.

Target

  • Function

    Transcription 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 specificity

    Expressed in fetal brain and in adult brain, heart, small intestine and colon.
  • Involvement in disease

    Defects 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 similarities

    Contains 1 HMG box DNA-binding domain.
  • Cellular localization

    Cytoplasm. Nucleus.
  • Information by UniProt
  • Database links

  • Alternative names

    • DOM antibody
    • DOM antibody
    • Dominant megacolon mouse human homolog of antibody
    • MGC15649 antibody
    • PCWH antibody
    • SOX 10 antibody
    • SOX10 antibody
    • SOX10_HUMAN antibody
    • SRY (sex determining region Y) box 10 antibody
    • SRY (sex determining region Y) box 10 antibody
    • SRY box 10 antibody
    • SRY box containing gene 10 antibody
    • SRY related HMG box gene 10 antibody
    • SRY related HMG box gene 10 antibody
    • Transcription factor SOX 10 antibody
    • Transcription factor SOX-10 antibody
    • WS2E antibody
    • WS4 antibody
    • WS4C antibody
    see all

Images

  • Immunohistochemical analysis of formalin/PFA-fixed paraffin-embedded spindle cell melanoma (DAB, left image) and pigmented melanoma (fast red, right image) labeling SOX10 with ab195364 at a 1/100 dilution.

References

ab195364 has not yet been referenced specifically in any publications.

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