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Home > Curated Information Page > PubMed Id: 19595710
Kadoyama K, et al. (2009) Disease-dependent reciprocal phosphorylation of serine and tyrosine residues of c-Met/HGF receptor contributes disease retardation of a transgenic mouse model of ALS. Neurosci Res 65, 194-200 19595710
This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.
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S983-p - Met (mouse)
Modsite: PHLDRLVsARSVsPT SwissProt Entrez-Gene
Orthologous residues
Met (human): S985‑p, Met iso2 (human): S1003‑p, Met (mouse): S983‑p, Met (rat): S986‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  neuron
Cellular systems studied:  primary cells
Species studied:  mouse
Comments:  G93A/HGF transgenic mice (ALS model mice)
Upstream Regulation
Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
PHOSPHATASE PPP2CA (mouse) activation of upstream enzyme
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HGF (human) decrease in G93A transgenic mice (ALS model mice)
Downstream Regulation
Effect of modification (function):  enzymatic activity, inhibited
Associated Diseases
Diseases Alterations Comments
ALS decreased

Y1228-p - Met (mouse)
Modsite: FGLArDMyDKEyysV SwissProt Entrez-Gene
Orthologous residues
Met (human): Y1230‑p, Met iso2 (human): Y1248‑p, Met (mouse): Y1228‑p, Met (rat): Y1231‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  neuron
Cellular systems studied:  primary cells
Species studied:  mouse
Comments:  G93A/HGF transgenic mice (ALS model mice)
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HGF (human) increase in G93A transgenic mice (ALS model mice)
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced
Associated Diseases
Diseases Alterations Comments
ALS increased

Y1232-p - Met (mouse)
Modsite: rDMyDKEyysVHNKt SwissProt Entrez-Gene
Orthologous residues
Met (human): Y1234‑p, Met iso2 (human): Y1252‑p, Met (mouse): Y1232‑p, Met (rat): Y1235‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  neuron
Cellular systems studied:  primary cells
Species studied:  mouse
Comments:  G93A/HGF transgenic mice (ALS model mice)
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HGF (human) increase in G93A transgenic mice (ALS model mice)
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced
Associated Diseases
Diseases Alterations Comments
ALS increased

Y1233-p - Met (mouse)
Modsite: DMyDKEyysVHNKtG SwissProt Entrez-Gene
Orthologous residues
Met (human): Y1235‑p, Met iso2 (human): Y1253‑p, Met (mouse): Y1233‑p, Met (rat): Y1236‑p
Characterization
Methods used to characterize site in vivo phospho-antibody, western blotting
Relevant cell lines - cell types - tissues:  neuron
Cellular systems studied:  primary cells
Species studied:  mouse
Comments:  G93A/HGF transgenic mice (ALS model mice)
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
HGF (human) increase in G93A transgenic mice (ALS model mice)
Downstream Regulation
Effect of modification (function):  enzymatic activity, induced
Associated Diseases
Diseases Alterations Comments
ALS increased