+ |
AKT |
phosphorylation
|
TBC1D4 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-245268 |
Ser588 |
RMRGRLGsVDSFERS |
Mus musculus |
3T3-L1 Cell |
pmid |
sentence |
11994271 |
To determine directly whether AS160 was a substrate for Akt, we examined the phosphorylation of recombinant AS160, as well as mutant forms with Ser-588, Thr-642, or both converted to Ala, by recombinant Akt 1. |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-148342 |
Thr642 |
QFRRRAHtFSHPPSS |
Homo sapiens |
|
pmid |
sentence |
16880201 |
14-3-3 proteins interact with as160 in an insulin- and akt-dependent manner via an akt phosphorylation site, thr-642. |
|
Publications: |
2 |
Organism: |
Mus Musculus, Homo Sapiens |
+ |
AKT1 |
phosphorylation
|
TBC1D4 |
0.756 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252494 |
Thr642 |
QFRRRAHtFSHPPSS |
Homo sapiens |
|
pmid |
sentence |
16880201 |
14-3-3 proteins interact with as160 in an insulin- and akt-dependent manner via an akt phosphorylation site, thr-642. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
AKT1 | down-regulates
phosphorylation
|
TBC1D4 |
0.756 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252594 |
|
|
Homo sapiens |
|
pmid |
sentence |
12637568 |
Recently, we identified a 160-kda protein in adipocytes, designated as160, that is phosphorylated by the insulin-activated kinase akt |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle |
+ |
AKT | down-regulates
phosphorylation
|
TBC1D4 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-99300 |
|
|
Homo sapiens |
|
pmid |
sentence |
12637568 |
Recently, we identified a 160-kda protein in adipocytes, designated as160, that is phosphorylated by the insulin-activated kinase akt |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle |
+ |
TBC1D4 | down-regulates
|
SLC2A4 |
0.655 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-99303 |
|
|
Homo sapiens |
|
pmid |
sentence |
12637568 |
These findings strongly indicate that insulin-stimulated phosphorylation of as160 is required for glut4 translocation and that this phosphorylation signals translocation through inactivation of the rab gap function. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |