The Rabbit Polyclonal anti-DCLK2 antibody (ABIN7214526) specifically detects DCLK2 in WB, ELISA and IF.
The antibody is reactive with Human and Mouse samples.
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,IF 1:200-1:1000,ELISA 1:10000,Not yet tested in other applications.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % sodium azide.
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
-20 °C
Storage Comment
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Expiry Date
12 months
Target
DCLK2
(Doublecortin-Like Kinase 2 (DCLK2))
Alternative Name
DCAMKL2
Background
DCLK2, DCAMKL2, DCDC3B, DCK2, Serine/threonine-protein kinase DCLK2, CaMK-like CREB regulatory kinase 2, CL2, CLICK-II, CLICK2, Doublecortin domain-containing protein 3B, Doublecortin-like and CAM kinase-like 2, Doublecortin-like kinase 2DCLK2 encodes a member of the protein kinase superfamily and the doublecortin family. Doublecortin like kinase 2 encoded by DCLK2 contains two N-terminal doublecortin domains, which bind microtubules and regulate microtubule polymerization, a C-terminal serine/threonine protein kinase domain, which shows substantial homology to Ca2+/calmodulin-dependent protein kinase, and a serine/proline-rich domain in between the doublecortin and the protein kinase domains, which mediates multiple protein-protein interactions. The microtubule-polymerizing activity of the encoded protein is independent of its protein kinase activity. Mouse studies show that the DCX gene, another family member, and DCLK2 share function in the establishment of hippocampal organization and that their absence results in a severe epileptic phenotype and lethality, as described in human patients with lissencephaly. Multiple alternatively spliced transcript variants have been identified.