Cell Signaling Technology

Product Pathways - Neuroscience

CK1δ Antibody #12417

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Endogenous 44 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

CK1δ Antibody recognizes endogenous levels of total CK1δ protein. This antibody does not cross-react with CK1ε.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human CK1δ protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using CK1δ Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing Myc-tagged full-length human CK1δ (CK1δ-Myc; +) or Myc-tagged full-length human CK1ε (CK1ε-Myc; +), using CK1δ Antibody (upper) or Myc-Tag (71D10) Rabbit mAb #2278 (lower).

Background

Casein Kinase I (CK1 or CKI) is the name given to a family of kinases consisting of multiple isoforms (α, α', β, γ1-3, δ, and ε) with a conserved N-terminal kinase domain and a variable C-terminal sequence that determines subcellular localization and regulates enzyme activity (1-3). Indeed, multiple inhibitory autophosphorylation sites have been identified near the C terminus of CK1ε (3). This ubiquitously expressed family of protein kinases has been implicated in multiple processes including DNA repair, cell morphology, and Wnt signaling (4). Perhaps the best understood role of CK1 is to provide the priming phosphorylation of β-catenin at Ser45 to produce the consensus GSK-3 substrate motif (S/T-X-X-X-pS) (4).

CK1δ is involved in many cellular processes such as differentiation (5), cell growth and apoptosis (6-8), and control of the circadian rhythm (9).

  1. Gross, S.D. and Anderson, R.A. (1998) Cell. Signal. 10, 699-711.
  2. Vancura, A. et al. (1994) J. Biol. Chem. 269, 19271-19278.
  3. Gietzen, K.F. and Virshup, D.M. (1999) J. Biol. Chem. 274, 32063-32070.
  4. Polakis, P. (2002) Curr. Biol. 12, R499-R501.
  5. Bryja, V. et al. (2007) J Cell Sci 120, 586-95.
  6. Knippschild, U. et al. (2005) Onkologie 28, 508-14.
  7. Knippschild, U. et al. (1997) Oncogene 15, 1727-36.
  8. Brockschmidt, C. et al. (2008) Gut 57, 799-806.
  9. Vanselow, K. and Kramer, A. (2007) Cold Spring Harb Symp Quant Biol 72, 167-76.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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