Curated Information
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Home > Curated Information Page > PubMed Id: 16600022
Liu HK, et al. (2006) Functional characterisation of the regulation of CAAT enhancer binding protein alpha by GSK-3 phosphorylation of Threonines 222/226. BMC Mol Biol 7, 14 16600022
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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T222-p - C/EBP-alpha (rat)
Modsite: HLQPGHPtPPPtPVP SwissProt Entrez-Gene
Orthologous residues
C/EBP‑alpha (human): T226‑p, C/EBP‑alpha (mouse): T222‑p, C/EBP‑alpha (rat): T222‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  liver cancer
Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), AD293 (epithelial), H4IIe (hepatic)
Cellular systems studied:  cell lines
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CHIR99021 decrease
GSK3A (human) increase Minor increase (1.2x)
insulin increase
Downstream Regulation
Effect of modification (function):  activity, inhibited
Effect of modification (process):  transcription, altered
Comments:  In 3T3L1 preadipocytes, mutation of T222/T226 to alanines increased transcription at CBE-containing promoter (as compared to WT C/EBP-alpha). S230A had a similar effect as the double T->A mutation. The triple alanine mutation had the highest transcription of the reporter gene. S230A did not reduce T222/226 phosphorylation (although CHIR99021 inhibitor did).

T226-p - C/EBP-alpha (rat)
Modsite: GHPtPPPtPVPsPHP SwissProt Entrez-Gene
Orthologous residues
C/EBP‑alpha (human): T230‑p, C/EBP‑alpha (mouse): T226‑p, C/EBP‑alpha (rat): T226‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  liver cancer
Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), AD293 (epithelial), H4IIe (hepatic)
Cellular systems studied:  cell lines
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
CHIR99021 decrease
GSK3A (human) increase Minor increase (1.2x)
insulin increase
Downstream Regulation
Effect of modification (function):  activity, inhibited
Effect of modification (process):  transcription, altered
Comments:  In 3T3L1 preadipocytes, mutation of T222/T226 to alanines increased transcription at CBE-containing promoter (as compared to WT C/EBP-alpha). S230A had a similar effect as the double T->A mutation. The triple alanine mutation had the highest transcription of the reporter gene. S230A did not reduce T222/226 phosphorylation (although CHIR99021 inhibitor did).

S230-p - C/EBP-alpha (rat)
Modsite: PPPtPVPsPHPAPAM SwissProt Entrez-Gene
Orthologous residues
C/EBP‑alpha (human): S234‑p, C/EBP‑alpha (mouse): S230‑p, C/EBP‑alpha (rat): S230‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  liver cancer
Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), AD293 (epithelial), H4IIe (hepatic)
Cellular systems studied:  cell lines
Species studied:  human, mouse, rat
Downstream Regulation
Effect of modification (function):  activity, inhibited
Effect of modification (process):  transcription, altered
Comments:  In 3T3L1 preadipocytes, mutation of T222/T226 to alanines increased transcription at CBE-containing promoter (as compared to WT C/EBP-alpha). S230A had a similar effect as the double T->A mutation. The triple alanine mutation had the highest transcription of the reporter gene. S230A did not reduce T222/226 phosphorylation (although CHIR99021 inhibitor did).

S21-p - GSK3A (rat)
Modsite: SGRARtssFAEPGGG SwissProt Entrez-Gene
Orthologous residues
GSK3A (human): S21‑p, GSK3A (mouse): S21‑p, GSK3A (rat): S21‑p, GSK3A (cow): S21‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  liver cancer
Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), AD293 (epithelial), H4IIe (hepatic)
Cellular systems studied:  cell lines
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
CHIR99021 no change compared to control

S9-p - GSK3B (rat)
Modsite: SGRPRTTsFAESCKP SwissProt Entrez-Gene
Orthologous residues
GSK3B (human): S9‑p, GSK3B iso2 (human): S9‑p, GSK3B (mouse): S9‑p, GSK3B (rat): S9‑p, GSK3B (rabbit): S9‑p
Characterization
Methods used to characterize site in vivo mutation of modification site, phospho-antibody, western blotting
Disease tissue studied:  liver cancer
Relevant cell lines - cell types - tissues:  3T3-L1 (fibroblast), AD293 (epithelial), H4IIe (hepatic)
Cellular systems studied:  cell lines
Species studied:  human, mouse, rat
Upstream Regulation
Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
CHIR99021 no change compared to control