DLX3, Polyclonal Antibody

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Small volumes of anti-DLX3 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Polyclonal

Western Blot (WB), Immunohistochemistry (IHC)

Western blot analysis of extracts of various cell lines, using DLX3 Antibody at 1:1000 dilution.
Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (MBS128200) at 1:10000 dilution.
Lysates/proteins: 25ug per lane.
Blocking buffer: 3% nonfat dry milk in TBST.
Detection: ECL Basic Kit.
Exposure time: 90s.

287

distal-less homeobox 3

homeobox protein DLX-3

Homeobox protein DLX-3

DLX3_HUMAN

Many vertebrate homeo box-containing genes have been identified on the basis of their sequence similarity with Drosophila developmental genes. Members of the Dlx gene family contain a homeobox that is related to that of Distal-less (Dll), a gene expressed in the head and limbs of the developing fruit fly. The Distal-less (Dlx) family of genes comprises at least 6 different members, DLX1-DLX6. Trichodentoosseous syndrome (TDO), an autosomal dominant condition, has been correlated with DLX3 gene mutation. This gene is located in a tail-to-tail configuration with another member of the gene family on the long arm of chromosome 17. Mutations in this gene have been associated with the autosomal dominant conditions trichodentoosseous syndrome and amelogenesis imperfecta with taurodontism. [provided by RefSeq, Jul 2008]

DLX3: Likely to play a regulatory role in the development of the ventral forebrain. May play a role in craniofacial patterning and morphogenesis. Defects in DLX3 are a cause of trichodentoosseous syndrome (TDO). TDO is an autosomal dominant syndrome characterized by enamel hypoplasia and hypocalcification with associated strikingly curly hair. Defects in DLX3 are the cause of amelogenesis imperfecta type 4 (AI4); also known as amelogenesis imperfecta hypomaturation-hypoplastic type with taurodontism. AI4 is an autosomal dominant defect of enamel formation associated with enlarged pulp chambers. Belongs to the distal-less homeobox family.

Protein type: Transcription factor; DNA-binding

Chromosomal Location of Human Ortholog: 17q21

Cellular Component: nucleus

Molecular Function: sequence-specific DNA binding; chromatin binding; transcription factor activity

Biological Process: blood vessel development; positive regulation of transcription from RNA polymerase II promoter; odontogenesis of dentine-containing teeth; placenta development

Disease: Amelogenesis Imperfecta, Type Iv; Trichodentoosseous Syndrome

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