Curated Information
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Home > Curated Information Page > PubMed Id: 15805466
Mayer C, Bierhoff H, Grummt I (2005) The nucleolus as a stress sensor: JNK2 inactivates the transcription factor TIF-IA and down-regulates rRNA synthesis. Genes Dev 19, 933-41 15805466
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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T200-p - TIF1A (human)
Modsite: IARYVPstPWFLMPI SwissProt Entrez-Gene
Orthologous residues
TIF1A (human): T200‑p, TIF1A (mouse): T198‑p
Characterization
Methods used to characterize site in vivo [32P] bio-synthetic labeling, mutation of modification site, phosphoamino acid analysis, phosphopeptide mapping
Relevant cell lines - cell types - tissues:  U2OS (bone cell) [GR (human)]
Cellular systems studied:  cell lines
Species studied:  human
Enzymes shown to modify site in vitro
Type Enzyme
KINASE JNK2 (human)
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
H2O2 increase
anisomycin increase
Downstream Regulation
Effect of modification (function):  activity, inhibited, intracellular localization, molecular association, regulation
Effect of modification (process):  transcription, inhibited
Modification regulates interactions with: 
Interacting molecule Interacting domains Effect Consequences (function) Consequences (process) Detection assays
POLR1B (human) Disrupts co-immunoprecipitation
TAF1B (human) Disrupts co-immunoprecipitation