Product nameAnti-Doublecortin antibody [EPR10936]
See all Doublecortin primary antibodies
DescriptionRabbit monoclonal [EPR10936] to Doublecortin
Tested applicationsSuitable for: WB, IPmore details
Unsuitable for: Flow Cyt,ICC/IF or IHC-P
Species reactivityReacts with: Human
Does not react with: Mouse, Rat
Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) within Human Doublecortin aa 400 to the C-terminus (Cysteine residue). The exact sequence is proprietary.
Database link: O43602
- Human fetal brain and SH-SY5Y lysates. Immunoprecipitation pellet from Human fetal brain lysate.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.20
Preservative: 0.01% Sodium azide
Constituents: 9% PBS, 40% Glycerol, 0.05% BSA, 50% Tissue culture supernatant
PurityTissue culture supernatant
Our Abpromise guarantee covers the use of ab172631 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 49 kDa.|
|IP||1/10 - 1/100.|
FunctionSeems to be required for initial steps of neuronal dispersion and cortex lamination during cerebral cortex development. May act by competing with the putative neuronal protein kinase DCAMKL1 in binding to a target protein. May in that way participate in a signaling pathway that is crucial for neuronal interaction before and during migration, possibly as part of a calcium ion-dependent signal transduction pathway. May be part with LIS-1 of an overlapping, but distinct, signaling pathways that promote neuronal migration.
Tissue specificityHighly expressed in neuronal cells of fetal brain (in the majority of cells of the cortical plate, intermediate zone and ventricular zone), but not expressed in other fetal tissues. In the adult, highly expressed in the brain frontal lobe, but very low expression in other regions of brain, and not detected in heart, placenta, lung, liver, skeletal muscles, kidney and pancreas.
Involvement in diseaseDefects in DCX are the cause of lissencephaly X-linked type 1 (LISX1) [MIM:300067]; also called X-LIS or LIS. LISX1 is a classic lissencephaly characterized by mental retardation and seizures that are more severe in male patients. Affected boys show an abnormally thick cortex with absent or severely reduced gyri. Clinical manifestations include feeding problems, abnormal muscular tone, seizures and severe to profound psychomotor retardation. Female patients display a less severe phenotype referred to as 'doublecortex'.
Defects in DCX are the cause of subcortical band heterotopia X-linked (SBHX) [MIM:300067]; also known as double cortex or subcortical laminar heterotopia (SCLH). SBHX is a mild brain malformation of the lissencephaly spectrum. It is characterized by bilateral and symmetric plates or bands of gray matter found in the central white matter between the cortex and cerebral ventricles, cerebral convolutions usually appearing normal.
Note=A chromosomal aberration involving DCX is found in lissencephaly. Translocation t(X;2)(q22.3;p25.1).
Sequence similaritiesContains 2 doublecortin domains.
- Information by UniProt
- DBCN antibody
- Dbct antibody
- DC antibody
All lanes : Anti-Doublecortin antibody [EPR10936] (ab172631) at 1/1000 dilution
Lane 1 : Human fetal brain lysate
Lane 2 : SH-SY5Y lysate
Lysates/proteins at 10 µg per lane.
Predicted band size: 49 kDa
Western blot analysis on immunoprecipitation pellet from (Lane 1) Human fetal brain lysate or (Lane 2) 1XPBS (negative control) using ab172631 at a 1/10 dilution and HRP-conjugated anti-rabbit IgG preferentially detecting the non-reduced form of rabbit IgG.
ab172631 has not yet been referenced specifically in any publications.