Curated Information
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Curated Information Page
PubMed Id: 21701498 
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.
Fitzgerald JC, et al. (2012) Phosphorylation of HtrA2 by cyclin-dependent kinase-5 is important for mitochondrial function. Cell Death Differ 19, 257-66 21701498
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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S142-p - HTRA2 (human) ▲
Orthologous residues
HTRA2 (human): S142‑p, HTRA2 iso2 (human): S142‑p, HTRA2 (mouse): S142‑p
Characterization
 Methods used to characterize site in vivo:  mutation of modification site
 Disease tissue studied:  neuroblastoma
 Relevant cell lines - cell types - tissues:  293 (epithelial), SH-SY5Y (neural crest)
 Cellular systems studied:  cell lines
 Species studied:  human

S400-p - HTRA2 (human) ▲
Orthologous residues
HTRA2 (human): S400‑p, HTRA2 iso2 (human): ‑, HTRA2 (mouse): S400‑p
Characterization
 Methods used to characterize site in vivo:  immunoprecipitation, mutation of modification site, phospho-antibody, western blotting
 Disease tissue studied:  neuroblastoma
 Relevant cell lines - cell types - tissues:  293 (epithelial), SH-SY5Y (neural crest)
 Cellular systems studied:  cell lines
 Species studied:  human
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE CDK5 (human)
Upstream Regulation
 Potential in vivo enzymes for site: 
Type Enzyme Evidence Notes
KINASE CDK5 (human) genetic knockout/knockin of upstream enzyme, co-immunoprecipitation, phospho-antibody, pharmacological inhibitor of upstream enzyme, microscopy-colocalization, modification site within consensus motif, pharmacological activator of upstream enzyme, siRNA inhibition of enzyme
 Comments:  S142 is required for maximal phosphorylation of S400.
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
p38-alpha (human) increase
Downstream Regulation
 Comments:  S400 phosphorylation is important for mitochondrial function.

S400-p - HTRA2 (mouse) ▲
Orthologous residues
HTRA2 (human): S400‑p, HTRA2 iso2 (human): ‑, HTRA2 (mouse): S400‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'brain, cortex'
 Cellular systems studied:  tissue
 Species studied:  mouse
Associated Diseases
Diseases: Alterations: Comments:
Parkinson's disease decreased In a murine model G399S mutation had decreased S400 phosphorylation.


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