Curated Information
Javascript is not enabled on this browser. This site will not work properly without Javascript.
PhosphoSitePlus Homepage Cell Signaling Technology
PhosphoSitePlus
HomeAbout PhosphoSiteUsing PhosphoSiteCuration ProcessContact
NIH-logos NIGMS Logo NIAAA Logo NCI Logo NIH Logo
Curated Information Page
PubMed Id: 15461588 
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.
Murray JT, et al. (2004) Identification of filamin C as a new physiological substrate of PKBalpha using KESTREL. Biochem J 384, 489-94 15461588
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.
Download Sites

T308-p - Akt1 (human) ▲
Orthologous residues
Akt1 (human): T308‑p, Akt1 (mouse): T308‑p, Akt1 (rat): T308‑p, Akt1 (fruit fly): T423‑p, Akt1 (cow): T308‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'muscle, skeletal', 'muscle, smooth', C2C12 (myoblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  cardiac muscle
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
insulin PDK1 (mouse) increase impaired in PDK1 -/- mice

S473-p - Akt1 (human) ▲
Orthologous residues
Akt1 (human): S473‑p, Akt1 (mouse): S473‑p, Akt1 (rat): S473‑p, Akt1 (fruit fly): S586‑p, Akt1 (cow): S473‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'muscle, skeletal', 'muscle, smooth', C2C12 (myoblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  cardiac muscle
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF increase
rapamycin EGF no effect upon treatment-induced increase
PD184352 EGF no effect upon treatment-induced increase
wortmannin EGF inhibit treatment-induced increase
wortmannin, rapamycin EGF inhibit treatment-induced increase
PD184352, wortmannin EGF inhibit treatment-induced increase
PD184352, rapamycin EGF no effect upon treatment-induced increase
insulin increase
rapamycin insulin no effect upon treatment-induced increase
PD184352 insulin no effect upon treatment-induced increase
wortmannin insulin inhibit treatment-induced increase
wortmannin, rapamycin insulin inhibit treatment-induced increase
PD184352, wortmannin insulin inhibit treatment-induced increase
PD184352, rapamycin insulin no effect upon treatment-induced increase

S2233-p - FLNC (human) ▲
Orthologous residues
FLNC (human): S2233‑p, FLNC (mouse): S2234‑p, FLNC (rat): S2234‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'muscle, skeletal', 'muscle, smooth', C2C12 (myoblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  cardiac muscle
 Enzymes shown to modify site in vitro: 
Type Enzyme
KINASE Akt1 (human)
KINASE Akt2 (human)
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
insulin increase
rapamycin insulin no effect upon treatment-induced increase
PD184352 insulin no effect upon treatment-induced increase
wortmannin insulin inhibit treatment-induced increase
wortmannin, rapamycin insulin inhibit treatment-induced increase
PD184352, wortmannin insulin inhibit treatment-induced increase
PD184352, rapamycin insulin no effect upon treatment-induced increase
EGF increase
EGF increase
rapamycin EGF no effect upon treatment-induced increase
PD184352 EGF no effect upon treatment-induced increase
wortmannin EGF inhibit treatment-induced increase
wortmannin, rapamycin EGF inhibit treatment-induced increase
PD184352, wortmannin EGF inhibit treatment-induced increase
PD184352, rapamycin EGF no effect upon treatment-induced increase
insulin increase
rapamycin insulin no effect upon treatment-induced increase
PD184352 insulin no effect upon treatment-induced increase
wortmannin insulin inhibit treatment-induced increase
wortmannin, rapamycin insulin inhibit treatment-induced increase
PD184352, wortmannin insulin inhibit treatment-induced increase
PD184352, rapamycin insulin no effect upon treatment-induced increase
insulin PDK1 (mouse) increase impaired in PDK1 -/- mice

S235-p - S6 (human) ▲
Orthologous residues
S6 (human): S235‑p, S6 (mouse): S235‑p, S6 (rat): S235‑p
Characterization
 Methods used to characterize site in vivo:  phospho-antibody, western blotting
 Relevant cell lines - cell types - tissues:  'muscle, skeletal', 'muscle, smooth', C2C12 (myoblast)
 Cellular systems studied:  cell lines
 Species studied:  human, mouse
 Comments:  cardiac muscle
Upstream Regulation
 Treatments, proteins and their effect on site modification: 
Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes
EGF no change compared to control
insulin no change compared to control
rapamycin decrease
PD184352 no change compared to control
wortmannin no change compared to control
wortmannin, rapamycin decrease
PD184352, wortmannin no change compared to control
PD184352, rapamycin decrease


Home  |  Curator Login With enhanced literature mining using Linguamatics I2E I2E Logo Produced by 3rd Millennium  |  Design by Digizyme
©2003-2013 Cell Signaling Technology, Inc.