DKK1 Antibody
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
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Primary Accession | O54908 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 29298 Da |
Gene ID | 13380 |
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Application & Usage | Western blotting (0.5-4 µg/ml). However, the optimal conditions should be determined individually. The antibody detects ~35 kDa Dkk1 of human, mouse and rat origins. |
Other Names | DKK-1 , DKK1 , SK , dickkopf homolog 1 , dickkopf-1 , dickkopf-1 like |
Target/Specificity | DKK1 |
Antibody Form | Liquid |
Appearance | Colorless liquid |
Formulation | 100 µg (0.5 mg/ml) affinity purified rabbit polyclonal antibody in phosphate buffered saline (PBS), pH 7.2, containing 30% glycerol, 0.5% BSA, 0.01% thimerosal. |
Handling | The antibody solution should be gently mixed before use. |
Reconstitution & Storage | -20 °C |
Background Descriptions | |
Precautions | DKK1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | Dkk1 |
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Function | Antagonizes canonical Wnt signaling by inhibiting LRP5/6 interaction with Wnt and by forming a ternary complex with the transmembrane protein KREMEN that promotes internalization of LRP5/6 (PubMed:18524778). Inhibits the pro-apoptotic function of KREMEN1 in a Wnt-independent manner, and has anti-apoptotic activity (PubMed:26206087). Plays a role in limb development; attenuates Wnt signaling in the developing limb to allow normal limb patterning (PubMed:18505822). |
Cellular Location | Secreted. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Xenopus Dickkopf (Dkk)-1 was initially discovered as a Wnt antagonist that plays an important role in head formation. By far, four members of Dkk have been identified in mammals. Each Dkk molecule contains two conserved cysteine-rich domains. Recent studies showed that the second Cys-rich domains of Dkk1 and Dkk2 inhibited Wnt-3a-activated signaling, whereas the first Cys-rich domains had no effects. In addition, the second Cys-rich domain of Dkk-2, but not that of Dkk-1, was able to activate the canonical pathway in the presence of LRP6, and this LRP-dependent signaling does not require Dvl.
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