Cell Signaling Technology

Product Pathways - Tyrosine Kinase/ Adaptors

Phospho-ALK (Tyr1604) Antibody #3341

Applications Reactivity MW (kDa) Source
W IP H 80 NPM-ALK. 200 ALK. Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

Phospho-ALK (Tyr1604) Antibody detects ALK only when phosphorylated at tyrosine 1604 (equivalent to Tyr664 of NPM-ALK).

Source / Purification

Polyclonal antibodies are produced by immunizing rabbits with a synthetic phospho-peptide (KLH-coupled) corresponding to residues surrounding Tyr1604 of human ALK. Antibodies are purified by protein A and peptide affinity chromatography

Western Blotting

Western Blotting

Western blot analysis of extracts from Sup-M2 cells, using Phospho-ALK (Tyr1604) Antibody (A, B) or ALK Antibody (C,D). The phospho-specificity of the antibody was characterized by treating the membrane with calf intestinal alkaline phosphatase (CIP) (B,D) after Western transfer. (Sup-M2 cells provided by Dr. Stephan W. Morris, St. Jude Children's Research Hospital, Tennessee.)

Background

Anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor for pleiotrophin (PTN), a growth factor involved in embryonic brain development (1-3). In ALK-expressing cells, PTN induces phosphorylation of both ALK and the downstream effectors IRS-1, Shc, PLCγ and PI3 kinase (1). ALK was originally discovered as an NPM (nucleophosmin)-ALK fusion protein produced by a translocation (4). The NPM-ALK fusion protein is a constitutively active oncogenic tyrosine kinase associated with anaplastic lymphoma (4). Activation of PLCγ by NPM-ALK has been suggested to be a crucial step for its mitogenic activity and may be important in the pathogenesis of anaplastic lymphomas. (5).

Phosphorylated Tyr664 of NPM-ALK (equivalent to Tyr1604 of full length ALK) is required for the interaction with PLCgamma (5). Site-directed mutagenesis of this tyrosine residue results in the loss of oncogenic activity of NPM-ALK (5).

  1. Stoica, G.E. et al. (2001) J. Biol. Chem. 276, 16772-16779.
  2. Iwahara, T. et al. (1997) Oncogene 14, 439-449.
  3. Morris, S.W. et al. (1997) Oncogene 14, 2175-2188.
  4. Morris, S.W. et al. (1994) Science 263, 1281-1284.
  5. Bai, R.Y. et al. (1998) Mol. Cell Biol. 18, 6951-6961.

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