| + |
CSNK2A2 | up-regulates activity 
phosphorylation
|
IL16 |
0.331 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251009 |
Ser743 |
MPLQPNAsLNEEEGT |
in vitro |
|
| pmid |
sentence |
| 12450396 |
We now show that N-terminal to the NLS domain of pro-IL-16 are protein kinase CK2 substrate and cdc2 kinase substrate sites which, along with the NLS, constitute a dual phosphorylation-regulated CcN motif which regulates nuclear localization of pro-IL-16. In addition, we demonstrate that mutation of either site is associated with impairment of the N-terminal domain's ability to induce G(0)/G(1) cell cycle arrest. | Thus, we confirm that the N-terminal (42SLNEE46) sequence of pro-IL-16 is in fact a site for protein kinase CK2 phosphorylation. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
CSNK2A1 | up-regulates activity
phosphorylation
|
IL16 |
0.331 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250905 |
Ser743 |
MPLQPNAsLNEEEGT |
in vitro |
|
| pmid |
sentence |
| 12450396 |
We now show that N-terminal to the NLS domain of pro-IL-16 are protein kinase CK2 substrate and cdc2 kinase substrate sites which, along with the NLS, constitute a dual phosphorylation-regulated CcN motif which regulates nuclear localization of pro-IL-16. In addition, we demonstrate that mutation of either site is associated with impairment of the N-terminal domain's ability to induce G(0)/G(1) cell cycle arrest. | Thus, we confirm that the N-terminal (42SLNEE46) sequence of pro-IL-16 is in fact a site for protein kinase CK2 phosphorylation. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
MAPK1 | up-regulates
phosphorylation
|
IL16 |
0.269 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121852 |
Ser845 |
SIRQRISsFETFGSS |
Homo sapiens |
|
| pmid |
sentence |
| 14768064 |
The precursor form of the cytokine il-16 (proil-16) was shown to be phosphorylated on ser144 . the phosphorylation of proil-16 is dependent on activation of the kinases erk1/2. Il-16 is secreted by mitogen-activated t cells, and the biochemical link between proil-16 and erk1/2, revealed by studies with pap-1, prompted analysis of the role of map kinases in this response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 | up-regulates
phosphorylation
|
IL16 |
0.269 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121856 |
Ser845 |
SIRQRISsFETFGSS |
Homo sapiens |
|
| pmid |
sentence |
| 14768064 |
The precursor form of the cytokine il-16 (proil-16) was shown to be phosphorylated on ser144 in antigen receptor-, sdf1alpha- and il-2-activated t cells. Genetic and pharmacological-inhibitor experiments showed that the phosphorylation of proil-16 is dependent on activation of the kinases erk1/2. Il-16 is secreted by mitogen-activated t cells, and the biochemical link between proil-16 and erk1/2, revealed by studies with pap-1, prompted analysis of the role of map kinases in this response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERK1/2 | up-regulates
phosphorylation
|
IL16 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270168 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 14768064 |
The precursor form of the cytokine il-16 (proil-16) was shown to be phosphorylated on ser144 in antigen receptor-, sdf1alpha- and il-2-activated t cells. Genetic and pharmacological-inhibitor experiments showed that the phosphorylation of proil-16 is dependent on activation of the kinases erk1/2. Il-16 is secreted by mitogen-activated t cells, and the biochemical link between proil-16 and erk1/2, revealed by studies with pap-1, prompted analysis of the role of map kinases in this response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Gbeta | up-regulates
phosphorylation
|
IL16 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270056 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 14768064 |
The precursor form of the cytokine il-16 (proil-16) was shown to be phosphorylated on ser144 in antigen receptor-, sdf1alpha- and il-2-activated t cells. Genetic and pharmacological-inhibitor experiments showed that the phosphorylation of proil-16 is dependent on activation of the kinases erk1/2. Il-16 is secreted by mitogen-activated t cells, and the biochemical link between proil-16 and erk1/2, revealed by studies with pap-1, prompted analysis of the role of map kinases in this response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
IL16
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