Cell Signaling Technology

Product Pathways - Tyrosine Kinase / Adaptors

APS Antibody #4832

Applications Reactivity Sensitivity MW (kDa) Source
W IHC-P H M Endogenous 90 to 95 Rabbit

Applications Key:  W=Western Blotting  IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:  H=Human  M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

APS Antibody detects endogenous levels of total APS. This antibody does not cross-react with other adaptor/docking proteins.

Source / Purification

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

Western Blotting

Western Blotting

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

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using APS Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma, using APS Antibody.


IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human non-Hodgkin's lymphoma, using APS Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma, using APS Antibody in the presence of control peptide (left) or antigen specific peptide (right).

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human prostate carcinoma, showing cytoplasmic localization using APS Antibody.


Background

APS is an SH2 and PH domain-containing adaptor protein closely related to Lnk and SH2-B (1). APS was identified as a substrate for many receptor tyrosine kinases including TrkA, insulin receptor, c-Kit and PDGF receptor (2). Tyrosine phosphorylation of APS provides docking sites for downstrean signaling components, mediating diverse signaling pathways. APS plays quite different roles in RTK signaling. Overexpression of APS has been shown to inhibit PDGF-induced mitogenicity, which may result from APS/c-Cbl-mediated PDGF receptor degradation (3). However, APS promotes enhanced mitogenicity in response to insulin stimulation (4). The striking difference in APS-mediated signaling between the different RTKs could lie in the mode of interaction with the respective receptor.

  1. Liu, J. et al. (2002) Mol. Cell. Biol. 22, 3599-3609.
  2. Qian, X. and Ginty, D. (2001) Mol. Cell. Biol. 21, 1613-1620.
  3. Wollberg, P. et al. (2003) Biochem. J. 370, 1033-1038.
  4. Ahmed, Z. and Pillay, T.S. (2001) Biochem. Soc. Trans. 29, 529-534.

Application References

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Companion Products

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

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