| + |
DAB2IP | down-regulates activity 
binding
|
14-3-3 |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254773 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27858941 |
DAB2IP then displaces the inhibitory binding between ASK1 and 14-3-3 protein, favoring ASK1 activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
YAP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-169719 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21084559 |
Phosphorylation of yap ser127 and of the corresponding sites in yki and taz generates a protein-binding motif for the 14-3-3 family proteins, which, upon binding by a 14-3-3 protein, leads to their cytoplasmic retention. One protein that associates with 14-3-3 in an akt-dependent manner is shown here to be the yes-associated protein (yap), which is phosphorylated by akt at serine 127, leading to binding to 14-3-3. Akt promotes yap localization to the cytoplasm, resulting in loss from the nucleus where it functions as a coactivator of transcription factors including p73. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-97481 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 12535517 |
One protein that associates with 14-3-3 in an akt-dependent manner is shown here to be the yes-associated protein (yap), which is phosphorylated by akt at serine 127, leading to binding to 14-3-3. Akt promotes yap localization to the cytoplasm, resulting in loss from the nucleus where it functions as a coactivator of transcription factors including p73. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens, Chlorocebus Aethiops |
| Pathways: | Hippo Signaling |
| + |
14-3-3 | down-regulates
binding
|
FOXO3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183608 |
|
|
Homo sapiens |
Breast Cancer Cell, Prostate Gland Cancer Cell, Leukemia Cell, Glioblastoma Cell |
| pmid |
sentence |
| 19188143 |
In this study, we demonstrate that akt also regulates the activity of fkhrl1, a member of the forkhead family of transcription factors. In the presence of survival factors, akt phosphorylates fkhrl1, leading to fkhrl1's association with 14-3-3 proteins and fkhrl1's retention in the cytoplasm. Akt-dependent phosphorylation of foxo3a (thr32, ser253, and ser315 for human foxo3) enhances foxo3a/14?3?3 Interaction and promotes foxo3a nuclear export to the cytoplasm, resulting in the repression of foxo3a transcriptional function |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-15849 |
|
|
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 1010227 |
Progressive increase in akt activation during prostate cancer progression led to increase phosphorylation of foxo3a and binding with 14-3-3, which potentially affected its transcriptional activity in age-specific manner. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
binding
|
NEFL |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269953 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23230147 |
These results suggest the important role of 14-3-3 in the dynamic regulation of NF-L assembly, and in the capacity to prevent the formation of NF-L aggregates. all seven isoforms specifically interacted with NF-L, but not NF-M or NF-H. specific interaction of 14-3-3 proteins with phosphorylated NF-L subunits also indicated the role of 14-3-3 and NF-L phosphorylation in the disassembly of neurofilaments. What is more, binding of 14-3-3 to phosphorylated NF-L subunits may prevent the dephosphorylation of these subunits by phosphatases, maintaining the hyperphosphorylation state of the subunits, which facilitates the disassembly of neurofilaments. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
binding
|
TNK1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273869 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 34504101 |
We also discover a MARK-mediated phosphorylation on TNK1 at S502 that promotes an interaction between TNK1 and 14-3-3, which sequesters TNK1 and inhibits its kinase activity.Phosphorylation of TNK1 at S502 within the proline rich domain is required for TNK1 binding to 14-3-3.MARKs mediate phosphorylation at S502 and 14-3-3 binding to TNK1, which restrains the movement of TNK1 into heavy membrane-associated clusters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
binding
|
RGS18 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273787 |
|
|
Homo sapiens |
Blood Platelet |
| pmid |
sentence |
| 24244663 |
Cyclic AMP- and cyclic GMP-dependent kinases (PKA, PKG) inhibit the interaction of RGS18 and 14-3-3 by phosphorylating S216. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
KHSRP |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-151212 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17177604 |
Akt phosphorylates ksrp at a unique serine residue, creating a functional binding site for the molecular chaperone 14-3-3. As a consequence, akt activation impairs ksrp ability to interact with the exoribonucleolytic complex exosome and, in turn, to promote rapid mrna decay. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | up-regulates 
binding
|
GRB10 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-134198 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15722337 |
The interaction of phosphorylated grb10 with 14-3-3 may lead to the translocation of grb10 back to the cytosol |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | up-regulates quantity by stabilization
binding
|
GPSM3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264866 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 22843681 |
Mutation of serine 35 completely abrogates the 14-3-3 interaction (e.g. Fig. 2, B–F), suggesting that phosphorylation of serine 35 is obligatory for 14-3-3 binding|The GPSM3/14-3-3 interaction is seen to stabilize GPSM3 from degradation and also support the nuclear exclusion of both proteins. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
binding
|
EDC3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262630 |
|
|
Cricetulus griseus |
CHO Cell |
| pmid |
sentence |
| 20051463 |
14-3-3 binding to EDC3 resulted in a significant decrease in the binding of several key mRNA regulatory factors such as PABP and Y-box-binding protein 1 to EDC3. |
|
| Publications: |
1 |
Organism: |
Cricetulus Griseus |
| + |
14-3-3 | down-regulates
binding
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-44855 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8929531 |
14-3-3 blocks bad activity by promoting ser-155 phosphorylation, which induces the dissociation of bad and bcl-xl. in the presence of survival factor il-3, cells phosphorylated bad on two serine residues embedded in 14-3-3 consensus binding sites. Only the nonphosphorylated bad heterodimerized with bcl-x(l) at membrane sites to promote cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-81106 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10949026 |
14-3-3 blocks bad activity by promoting ser-155 phosphorylation, which induces the dissociation of bad and bcl-xl. in the presence of survival factor il-3, cells phosphorylated bad on two serine residues embedded in 14-3-3 consensus binding sites. Only the nonphosphorylated bad heterodimerized with bcl-x(l) at membrane sites to promote cell death. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
FOXO |
0.702 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252818 |
|
|
Homo sapiens |
Breast Cancer Cell, Prostate Gland Cancer Cell, Leukemia Cell, Glioblastoma Cell |
| pmid |
sentence |
| 19188143 |
In this study, we demonstrate that akt also regulates the activity of fkhrl1, a member of the forkhead family of transcription factors. In the presence of survival factors, akt phosphorylates fkhrl1, leading to fkhrl1's association with 14-3-3 proteins and fkhrl1's retention in the cytoplasm. Akt-dependent phosphorylation of foxo3a (thr32, ser253, and ser315 for human foxo3) enhances foxo3a/14?3?3 Interaction and promotes foxo3a nuclear export to the cytoplasm, resulting in the repression of foxo3a transcriptional function |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252819 |
|
|
Homo sapiens |
Prostate Gland Cancer Cell |
| pmid |
sentence |
| 1010227 |
Progressive increase in akt activation during prostate cancer progression led to increase phosphorylation of foxo3a and binding with 14-3-3, which potentially affected its transcriptional activity in age-specific manner. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
relocalization
|
MLXIPL |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255667 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 26984404 |
AMP inhibits the nuclear localization of ChREBP through an allosteric activation of ChREBP/14-3-3 interactions |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
14-3-3 | down-regulates
binding
|
BCL2L11 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141577 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16282323 |
Cytokine stimulation promotes bim(el) binding to 14-3-3 proteins. Akt could directly phosphorylate a gst-bim(el) fusion protein and identified the akt phosphorylation site in the bim(el) domain as ser(87). we propose that ser87 of bimel is an important regulatory site that is targeted byakt to attenuate thepro-apoptotic function of bim el, thereby promoting cell survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
mTORC1 |
0.511 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217565 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20006481 |
Akt can phosphorylate pras40, a raptor binding protein that also acts as an inhibitor of torc1. Akt-mediated phosphorylation of pras40 again promotes 14-3-3 binding, in this case leading to relief from pras40-mediated inhibition. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates activity
binding
|
CABLES1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276758 |
|
|
in vitro |
|
| pmid |
sentence |
| 25361894 |
Here, we report that Cables1 levels are controlled by a phosphorylation and 14-3-3-dependent mechanism. Mutagenic analyses identified two residues, T44 and T150, that are specifically critical for 14-3-3 binding and that serve as substrates for phosphorylation by the cell survival kinase Akt, which by binding directly to Cables1 recruits 14-3-3 to the complex.Ectopic expression of activated Akt (AKT1) prevented Cables1-induced apoptosis. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
14-3-3 | up-regulates activity
binding
|
HJURP |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262624 |
|
|
in vitro |
|
| pmid |
sentence |
| 17256767 |
These data define a new protein complex in mammalian cells where 14‐3‐3 associates with FAKTS through phosphorylated S479. Our research identifies a widely expressed eukaryotic protein FAKTS, as a new Akt/PKB substrate localized in the nucleus. Akt/PKB promotes FAKTS association with 14‐3‐3, placing FAKTS under the control of 14‐3‐3 proteins. FAKTS may play an important role in transmitting Akt/PKB‐mediated signals in the complex network of intracellular signal transduction. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
14-3-3 | down-regulates
binding
|
HDAC5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-89444 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12058061 |
In the cytoplasm, 14-3-3 proteins bind the phosphorylated hdac5 and retain it in the cytosol. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Skeletal Muscle |
| + |
14-3-3 | down-regulates
binding
|
AKT1S1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-162003 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20006481 |
Akt can phosphorylate pras40, a raptor binding protein that also acts as an inhibitor of torc1. Akt-mediated phosphorylation of pras40 again promotes 14-3-3 binding, in this case leading to relief from pras40-mediated inhibition. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
RASSF1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175121 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21776416 |
Basal inactivation of rassf1a is achieved by rassf1a self association and via 14-3-3 interactions (to isoforms s and e) at serine 175/178/179 of rassf1a. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hippo Signaling |
| + |
14-3-3 | down-regulates
binding
|
MAP3K5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-69408 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 10411906 |
14-3-3 may suppress ask1-induced cell death by directly inhibiting the catalytic activity of ask1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
14-3-3 | down-regulates
binding
|
WWTR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-169716 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21084559 |
Phosphorylation of yap ser127 and of the corresponding sites in yki and taz generates a protein-binding motif for the 14-3-3 family proteins, which, upon binding by a 14-3-3 protein, leads to their cytoplasmic retention. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hippo Signaling |
3.0
14-3-3