Curated Information
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Curated Information Page
PubMed Id: 9927609 
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.
Lew JY, et al. (1999) Increased site-specific phosphorylation of tyrosine hydroxylase accompanies stimulation of enzymatic activity induced by cessation of dopamine neuronal activity. Mol Pharmacol 55, 202-9 9927609
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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S19-p - TH (rat) ▲
Orthologous residues
TH (human): S19‑p, TH iso2 (human): S19‑p, TH iso3 (human): S19‑p, TH iso5 (human): S19‑p, TH (mouse): S19‑p, TH (rat): S19‑p, TH (cow): S19‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  adrenal cancer, pheochromocytoma, pituitary cancer
 Relevant cell lines - cell types - tissues:  'brain, striatum', AtT20 (pituitary cell), PC-12 (chromaffin)
 Cellular systems studied:  tissue
 Species studied:  rat
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
NSD-1015 no change compared to control
butyrolactone no change compared to control
butyrolactone, apomorphine no change compared to control
nerve damage increase cerbral hemitransection
apomorphine inhibit treatment-induced increase
butyrolactone increase
apomorphine butyrolactone no effect upon treatment-induced increase no dose-dependent inhibition

S31-p - TH (rat) ▲
Orthologous residues
TH (human): S62‑p, TH iso2 (human): S58‑p, TH iso3 (human): S31‑p, TH iso5 (human): S35‑p, TH (mouse): S31‑p, TH (rat): S31‑p, TH (cow): S31‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  adrenal cancer, pheochromocytoma, pituitary cancer
 Relevant cell lines - cell types - tissues:  'brain, striatum', AtT20 (pituitary cell), PC-12 (chromaffin)
 Cellular systems studied:  tissue
 Species studied:  rat
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
okadaic acid increase
haloperidol increase
nerve damage no change compared to control cerebral hemitransection
apomorphine no change compared to control
NSD-1015 no change compared to control
butyrolactone no change compared to control
butyrolactone, apomorphine no change compared to control
nerve damage no change compared to control cerebral hemitransection
apomorphine no change compared to control

S40-p - TH (rat) ▲
Orthologous residues
TH (human): S71‑p, TH iso2 (human): S67‑p, TH iso3 (human): S40‑p, TH iso5 (human): S44‑p, TH (mouse): S40‑p, TH (rat): S40‑p, TH (cow): S40‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Disease tissue studied:  adrenal cancer, pheochromocytoma, pituitary cancer
 Relevant cell lines - cell types - tissues:  'brain, striatum', AtT20 (pituitary cell), PC-12 (chromaffin)
 Cellular systems studied:  tissue
 Species studied:  rat
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
NSD-1015 no change compared to control
butyrolactone increase
apomorphine butyrolactone inhibit treatment-induced increase
nerve damage increase cerbral hemitransection
apomorphine inhibit treatment-induced increase


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