| + |
PPP2CB |
dephosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248588 |
Ser432 |
SAYGGLTsPGLSYSL |
Homo sapiens |
HT-29 Cell |
| pmid |
sentence |
| 16554440 |
K8 Ser431-P is a physiologic substrate to PP2A during hyposmotic conditions and possibly other biologic contexts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK3 |
phosphorylation
|
KRT8 |
0.429 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249468 |
Ser432 |
SAYGGLTsPGLSYSL |
|
|
| pmid |
sentence |
| 16554440 |
Also, several probable in vivo K8 kinases have been identified including Erk1/2 for K8 Ser431 (Ku and Omary, 1997), and p38 and Jun kinases for K8 Ser73 (Ku et al., 2002a; He et al., 2002). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196141 |
Ser432 |
SAYGGLTsPGLSYSL |
Homo sapiens |
|
| pmid |
sentence |
| 22344252 |
Our data suggested a close relationship between k8(s431) phosphorylation and keratin reorganization in epithelial tumor cells. |
|
| Publications: |
2 |
Organism: |
, Homo Sapiens |
| + |
MAPK1 |
phosphorylation
|
KRT8 |
0.389 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249411 |
Ser432 |
SAYGGLTsPGLSYSL |
|
|
| pmid |
sentence |
| 16554440 |
Also, several probable in vivo K8 kinases have been identified including Erk1/2 for K8 Ser431 (Ku and Omary, 1997), and p38 and Jun kinases for K8 Ser73 (Ku et al., 2002a; He et al., 2002). |
|
| Publications: |
1 |
| + |
CDK1 | up-regulates 
phosphorylation
|
KRT8 |
0.25 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56054 |
Ser432 |
SAYGGLTsPGLSYSL |
Homo sapiens |
|
| pmid |
sentence |
| 9524113 |
With regard to k8 phosphorylation at ser-431, it increases dramatically upon stimulation of cells with epidermal growth factor (egf) or after mitotic arrest and is the major k8 phosphorylated residue after incubating k8 immunoprecipitates with mitogen-activated protein or cdc2 kinases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTP4A3 | down-regulates activity 
dephosphorylation
|
KRT8 |
0.276 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248341 |
Ser432 |
SAYGGLTsPGLSYSL |
Homo sapiens |
Colonic Cancer Cell |
| pmid |
sentence |
| 19115206 |
the cytoskeletal intermediate filament keratin 8 (KRT8) was identified as a physiological PRL-3-interacting protein. Indeed, treatment with the PRL-3 inhibitor effectively suppressed the phosphorylation of KRT8 at S73 and S431 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248340 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
Colonic Cancer Cell |
| pmid |
sentence |
| 19115206 |
the cytoskeletal intermediate filament keratin 8 (KRT8) was identified as a physiological PRL-3-interacting protein. Indeed, treatment with the PRL-3 inhibitor effectively suppressed the phosphorylation of KRT8 at S73 and S431|The site-specific phosphorylation of keratins induces the disassembly of these filaments, and the balance between their phosphorylation and dephosphorylation controls the continuous exchange of intermediate filament subunits between a soluble pool and polymerized filaments |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PPP2CA |
dephosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248623 |
Ser432 |
SAYGGLTsPGLSYSL |
Homo sapiens |
HT-29 Cell |
| pmid |
sentence |
| 16554440 |
K8 Ser431-P is a physiologic substrate to PP2A during hyposmotic conditions and possibly other biologic contexts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK14 | up-regulates
phosphorylation
|
KRT8 |
0.574 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114079 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Keratin 8 (k8) serine 73 occurs within a relatively conserved type ii keratin motif ((68)nqsllspl) and becomes phosphorylated in cultured cells and organs during mitosis, cell stress, and apoptosis. Here we show that ser-73 is exclusively phosphorylated in vitro by p38 mitogen-activated protein kinase.The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK11 | up-regulates
phosphorylation
|
KRT8 |
0.402 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114063 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Keratin 8 (k8) serine 73 occurs within a relatively conserved type ii keratin motif . Here we show that ser-73 is exclusively phosphorylated in vitro by p38 mitogen-activated protein kinase. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK8 | up-regulates
phosphorylation
|
KRT8 |
0.383 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114083 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Kinase assays showed that c-jun n-terminal kinase (jnk) was also activated with activation kinetics corresponding to that of k8 phosphorylation. Furthermore, k8 was also phosphorylated on ser-73 by jnk in vitro. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113645 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11781324 |
Kinase assays showed that c-jun n-terminal kinase (jnk) was also activated with activation kinetics corresponding to that of k8 phosphorylation. Furthermore, k8 was also phosphorylated on ser-73 by jnk in vitro. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAPK12 | up-regulates
phosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114067 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Keratin 8 (k8) serine 73 occurs within a relatively conserved type ii keratin motif . Here we show that ser-73 is exclusively phosphorylated in vitro by p38 mitogen-activated protein kinase. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK13 | up-regulates
phosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-114075 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Keratin 8 (k8) serine 73 occurs within a relatively conserved type ii keratin motif . Here we show that ser-73 is exclusively phosphorylated in vitro by p38 mitogen-activated protein kinase. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKCD | up-regulates
phosphorylation
|
KRT8 |
0.329 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260887 |
Ser74 |
TVNQSLLsPLVLEVD |
Homo sapiens |
|
| pmid |
sentence |
| 15972820 |
The present study showed that shear stress, but not stretch, activates PKC delta and phosphorylates K8 Ser-73, which then mediates the disassembly/reorganization of keratin IF in AEC. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTPN1 | down-regulates activity
dephosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265495 |
Tyr267 |
IAEVKAQyEDIANRS |
Homo sapiens |
HT-29 Cell |
| pmid |
sentence |
| 24003221 |
Keratin 8 phospho-Tyr-267 is dephosphorylated by PTP1B and promotes insolubility and filament organization, as does the paralogous GFAP tyrosine. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
p38 | up-regulates
phosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270125 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11788583 |
Keratin 8 (k8) serine 73 occurs within a relatively conserved type ii keratin motif . Here we show that ser-73 is exclusively phosphorylated in vitro by p38 mitogen-activated protein kinase. The ser-73 --> ala-associated filament reorganization defect is rescued by a ser-73 --> asp mutation. Also, disease-causing keratin mutations can modulate keratin phosphorylation and organization, which may affect disease pathogenesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERK1/2 |
phosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270135 |
|
|
|
|
| pmid |
sentence |
| 16554440 |
Also, several probable in vivo K8 kinases have been identified including Erk1/2 for K8 Ser431 (Ku and Omary, 1997), and p38 and Jun kinases for K8 Ser73 (Ku et al., 2002a; He et al., 2002). |
|
| Publications: |
1 |
| + |
Gbeta |
phosphorylation
|
KRT8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270003 |
|
|
|
|
| pmid |
sentence |
| 16554440 |
Also, several probable in vivo K8 kinases have been identified including Erk1/2 for K8 Ser431 (Ku and Omary, 1997), and p38 and Jun kinases for K8 Ser73 (Ku et al., 2002a; He et al., 2002). |
|
| Publications: |
1 |
3.0
KRT8
- 
- 