Curated Information
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Curated Information Page
PubMed Id: 12801934 
This page summarizes selected information from the article referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2012,40:D261-70). To learn more about the scope of PhosphoSitePlus®, click here.
Wang HY, Li W, Benedetti NJ, Lee DH (2003) Alpha 7 nicotinic acetylcholine receptors mediate beta-amyloid peptide-induced tau protein phosphorylation. J Biol Chem 278, 31547-53 12801934
Only sites from this record are displayed on this page. Click on the protein name to open the protein page, and on the RSD number to open the site page. For the complete dataset, click the download button, on the right.
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T181-p - Tau iso8 (human)
Orthologous residues
Tau (human): T498‑p, Tau iso2 (human): T123‑p, Tau iso3 (human): T87‑p, Tau iso5 (human): T181‑p, Tau iso6 (human): T123‑p, Tau iso7 (human): T152‑p, Tau iso8 (human): T181‑p, Tau (mouse): T473‑p, Tau iso3 (mouse): T170‑p, Tau iso7 (mouse): T112‑p, Tau (rat): T492‑p, Tau (cow): T172‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  neuroblastoma
 Relevant cell lines - cell types - tissues:  neuron:synaptosome, SK-N-MC (neural crest)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE ERK2 (human)
KINASE JNK1 (human)
KINASE JNK2 (human)
KINASE ERK1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
beta-amyloid 42 increase
methyllycaconitine beta-amyloid 42 inhibit treatment-induced increase
alpha-BTX beta-amyloid 42 inhibit treatment-induced increase
alpha-conotoxin MI beta-amyloid 42 no effect upon treatment-induced increase
mecamylamine beta-amyloid 42 no effect upon treatment-induced increase
atropine beta-amyloid 42 no effect upon treatment-induced increase
MSH beta-amyloid 42 no effect upon treatment-induced increase
beta-amyloid 42 nAChRA7 (human) inhibit treatment-induced increase antisense
nicotine increase
epibatidine increase
cytosine no change compared to control

S202-p - Tau iso8 (human)
Orthologous residues
Tau (human): S519‑p, Tau iso2 (human): S144‑p, Tau iso3 (human): S108‑p, Tau iso5 (human): S202‑p, Tau iso6 (human): S144‑p, Tau iso7 (human): S173‑p, Tau iso8 (human): S202‑p, Tau (mouse): S494‑p, Tau iso3 (mouse): S191‑p, Tau iso7 (mouse): S151‑p, Tau (rat): S513‑p, Tau (cow): S209‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  neuroblastoma
 Relevant cell lines - cell types - tissues:  neuron:synaptosome, SK-N-MC (neural crest)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE JNK2 (human)
KINASE JNK1 (human)
KINASE ERK1 (human)
KINASE ERK2 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
beta-amyloid 42 increase
methyllycaconitine beta-amyloid 42 inhibit treatment-induced increase
alpha-BTX beta-amyloid 42 inhibit treatment-induced increase
alpha-conotoxin MI beta-amyloid 42 no effect upon treatment-induced increase
mecamylamine beta-amyloid 42 no effect upon treatment-induced increase
atropine beta-amyloid 42 no effect upon treatment-induced increase
MSH beta-amyloid 42 no effect upon treatment-induced increase
beta-amyloid 42 nAChRA7 (human) inhibit treatment-induced increase antisense
nicotine increase
epibatidine increase
cytosine no change compared to control

T231-p - Tau iso8 (human)
Orthologous residues
Tau (human): T548‑p, Tau iso2 (human): T173‑p, Tau iso3 (human): T137‑p, Tau iso5 (human): T231‑p, Tau iso6 (human): T173‑p, Tau iso7 (human): T202‑p, Tau iso8 (human): T231‑p, Tau (mouse): T523‑p, Tau iso3 (mouse): T220‑p, Tau iso7 (mouse): T180‑p, Tau (rat): T542‑p, Tau (cow): T238‑p
Characterization
 Methods used to characterize site in vivo phospho-antibody, western blotting
 Disease tissue studied:  neuroblastoma
 Relevant cell lines - cell types - tissues:  neuron:synaptosome, SK-N-MC (neural crest)
 Cellular systems studied:  cell lines, primary cells
 Species studied:  human
 Enzymes shown to modify site in vitro
Type Enzyme
KINASE JNK2 (human)
KINASE JNK1 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
beta-amyloid 42 increase
methyllycaconitine beta-amyloid 42 inhibit treatment-induced increase
alpha-BTX beta-amyloid 42 inhibit treatment-induced increase
alpha-conotoxin MI beta-amyloid 42 no effect upon treatment-induced increase
mecamylamine beta-amyloid 42 no effect upon treatment-induced increase
atropine beta-amyloid 42 no effect upon treatment-induced increase
MSH beta-amyloid 42 no effect upon treatment-induced increase
beta-amyloid 42 nAChRA7 (human) inhibit treatment-induced increase antisense
nicotine increase
epibatidine increase
cytosine no change compared to control


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