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Doublecortin antibody (DCX) (AA 413-417)

Details for Product anti-DCX Antibody No. ABIN871730, Supplier: Login to see
Antigen
  • DCX
  • DBCN
  • DC
  • LISX
  • SCLH
  • XLIS
  • Dbct
  • 18C15.5
Epitope
AA 413-417
17
14
6
5
5
4
3
3
3
3
2
2
2
2
2
1
1
1
1
1
1
1
1
1
1
1
Reactivity
Human, Mouse (Murine), Rat (Rattus)
113
67
43
9
6
3
3
2
1
1
1
1
Host
Rabbit
85
27
24
Clonality
Polyclonal
Conjugate
This Doublecortin antibody is un-conjugated
5
4
4
4
4
4
2
Application
Western Blotting (WB)
121
74
36
22
12
11
11
3
3
3
2
1
Supplier
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Immunogen Peptide sequence around AA 413-417 ( P-T-S-P-G) derived from Human Doublecortin. Antibodies were produced by immunizing rabbits with synthetic peptide and KLH conjugates.
Specificity The antibody detects endogenous level of total Doublecortin protein.
Purification Affinity purified
Alternative Name Doublecortin (DCX Antibody Abstract)
Background Seems 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.
Molecular Weight 40-45 kDa
Gene ID 1641
NCBI Accession NP_000546
UniProt O43602
Pathways
Application Notes Western blotting: 1:500-1:1000
Restrictions For Research Use only
Format Liquid
Concentration 1 mg/mL
Buffer Phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02 % sodium azide and 50 % glycerol.
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage 4 °C/-20 °C
Storage Comment Store at -20 °C for long term preservation (recommended). Store at 4 °C for short term use.
Background publications Pilz, Matsumoto, Minnerath et al.: "LIS1 and XLIS (DCX) mutations cause most classical lissencephaly, but different patterns of malformation." in: Human molecular genetics, Vol. 7, Issue 13, pp. 2029-37, 1999 (PubMed).

des Portes, Pinard, Billuart et al.: "A novel CNS gene required for neuronal migration and involved in X-linked subcortical laminar heterotopia and lissencephaly syndrome." in: Cell, Vol. 92, Issue 1, pp. 51-61, 1998 (PubMed).