| + |
PIM | down-regulates activity 
phosphorylation
|
H3C1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259409 |
Ser11 |
TKQTARKsTGGKAPR |
Homo sapiens |
|
| pmid |
sentence |
| 17643117 |
Pim1-dependent phosphorylation of histone h3 at serine 10 is required for myc-dependent transcriptional activation and oncogenic transformation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM | down-regulates
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259418 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
|
| pmid |
sentence |
| 10837473 |
Similar to pim1, pim2 phosphorylates bad, which antagonizes the pro-apoptotic function of bax |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
PIM | down-regulates activity
phosphorylation
|
BAD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259423 |
Ser118 |
GRELRRMsDEFVDSF |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259421 |
Ser75 |
EIRSRHSsYPAGTED |
Homo sapiens |
|
| pmid |
sentence |
| 16403219 |
All three Pim kinase family members predominantly phosphorylate Bad on Ser112 and in addition are capable of phosphorylating Bad on multiple sites associated with the inhibition of the pro-apoptotic function of Bad in HEK-293 cells. This would be consistent with the proposed function of Pim kinases in promoting cell proliferation and preventing cell death. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259422 |
Ser99 |
PFRGRSRsAPPNLWA |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16403219 |
Pim kinases phosphorylate multiple sites on Bad and promote 14-3-3 binding and dissociation from Bcl-XL. pim kinases are constitutively active when expressed in HEK-293 cells and are able to phosphorylate the Bcl-2 family member Bad on three residues, Ser112, Ser136 and Ser155 in vitro and in cells. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
PIM | up-regulates 
phosphorylation
|
MDM2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259433 |
Ser166 |
SSRRRAIsETEENSD |
Homo sapiens |
Lymphoma Cell |
| pmid |
sentence |
| 18467333 |
Additionally, the pim kinases phosphorylate mdm2 in vitro and in cultured cells at ser166 and ser186, two previously identified targets of other signaling pathways, including akt. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259434 |
Ser186 |
RQRKRHKsDSISLSF |
Homo sapiens |
Lymphoma Cell |
| pmid |
sentence |
| 18467333 |
Additionally, the pim kinases phosphorylate mdm2 in vitro and in cultured cells at ser166 and ser186, two previously identified targets of other signaling pathways, including akt. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
PIM | down-regulates
phosphorylation
|
FOXO3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259429 |
Ser253 |
APRRRAVsMDNSNKY |
Homo sapiens |
|
| pmid |
sentence |
| 18593906 |
Pim-mediated phosphorylation and inactivation of forkhead transcription factors, foxo1a and foxo3a, was involved in the transcriptional repression of the p27(kip1) gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3 in AML |
| + |
PIM | up-regulates
phosphorylation
|
RELA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259411 |
Ser276 |
SMQLRRPsDRELSEP |
Homo sapiens |
|
| pmid |
sentence |
| 19911008 |
In this study we show that phosphorylation of rela/p65 at ser276 prevents its degradation by ubiquitin-mediated proteolysis. importantly, we identify pim-1 as a further kinase responsible for the phosphorylation of rela/p65 at ser276. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
PIM | down-regulates
phosphorylation
|
MAP3K5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259410 |
Ser83 |
ATRGRGSsVGGGSRR |
Homo sapiens |
NCI-H1299 Cell |
| pmid |
sentence |
| 19749799 |
Pim1 phosphorylates and negatively regulates ask1-mediated apoptosispim1 phosphorylation of ask1 on ser83 inhibited ask1-mediated c-jun n-terminal kinase phosphorylation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM | down-regulates
phosphorylation
|
MARK3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259432 |
Ser96 |
KTQLNPTsLQKLFRE |
Homo sapiens |
|
| pmid |
sentence |
| 15319445 |
Here we show that the protein kinase cdc25 c-associated kinase 1 (c-tak1) is a binding partner and a substrate of pim-1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259431 |
Thr90 |
AIKIIDKtQLNPTSL |
Homo sapiens |
|
| pmid |
sentence |
| 15319445 |
Here we show that the protein kinase cdc25 c-associated kinase 1 (c-tak1) is a binding partner and a substrate of pim-1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259430 |
Thr95 |
DKTQLNPtSLQKLFR |
Homo sapiens |
|
| pmid |
sentence |
| 15319445 |
Here we show that the protein kinase cdc25 c-associated kinase 1 (c-tak1) is a binding partner and a substrate of pim-1. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
PIM | up-regulates quantity by stabilization
phosphorylation
|
CDKN1A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259424 |
Thr145 |
QGRKRRQtSMTDFYH |
Homo sapiens |
|
| pmid |
sentence |
| 20307683 |
Pim-2 phosphorylation of p21(cip1/waf1) enhances its stability and inhibits cell proliferation in hct116 cellshere we demonstrate that like pim-1, pim-2 also phosphorylates the cell cycle inhibitor p21(cip1/waf1) (p21) on thr145 in vitro and in vivo |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
PIM | down-regulates
phosphorylation
|
CDKN1B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259426 |
Thr157 |
GIRKRPAtDDSSTQN |
Homo sapiens |
|
| pmid |
sentence |
| 18593906 |
We show, herein, that all the pim family members (pim1, pim2, and pim3) bind to and directly phosphorylate the cyclin-dependent kinase inhibitor p27(kip1) at threonine-157 and threonine-198 residues in cells and in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
PIM | down-regulates activity
phosphorylation
|
CDKN1B |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259425 |
Thr198 |
PGLRRRQt |
Homo sapiens |
|
| pmid |
sentence |
| 18593906 |
We show, herein, that all the pim family members (pim1, pim2, and pim3) bind to and directly phosphorylate the cyclin-dependent kinase inhibitor p27(kip1) at threonine-157 and threonine-198 residues in cells and in vitro.|Pim kinases promote cell cycle progression and tumorigenesis by down-regulating p27(Kip1) expression at both transcriptional and posttranslational levels. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
PIM | down-regulates activity
phosphorylation
|
FOXO3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259428 |
Thr32 |
QSRPRSCtWPLQRPE |
Homo sapiens |
|
| pmid |
sentence |
| 18593906 |
Pim1s expression induced the phosphorylation of foxo3a (fig. 5a and b) and inactivated its transcriptional activity (fig. 5c). A previous report showed that phosphorylation at t32, s253, and s315 residues in foxo3a induced 14-3-3 binding, nuclear export, and proteasomemediated degradation (42). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3 in AML |
| + |
PIM | down-regulates activity
phosphorylation
|
Histone H3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265365 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17643117 |
Pim1-dependent phosphorylation of histone h3 at serine 10 is required for myc-dependent transcriptional activation and oncogenic transformation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM | up-regulates
phosphorylation
|
RPS19 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259412 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 16266891 |
The pim-1/rps19 interaction was demonstrated both in vitro and in living cells and led to phosphorylation of rps19 in an in vitro kinase assay. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM | down-regulates
phosphorylation
|
FOXO |
0.402 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259427 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18593906 |
Pim-mediated phosphorylation and inactivation of forkhead transcription factors, foxo1a and foxo3a, was involved in the transcriptional repression of the p27(kip1) gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
| + |
STAT5A | up-regulates quantity by expression 
transcriptional regulation
|
PIM |
0.429 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255733 |
|
|
Homo sapiens |
MV4-11 Cell |
| pmid |
sentence |
| 29507660 |
FLT3-ITD is the most frequent tyrosine kinase mutation in acute myeloid leukemia (AML) associated with poor prognosis. We previously reported that activation of STAT5 confers resistance to PI3K/Akt inhibitors on the FLT3-ITD-positive AML cell line MV4-11 and 32D cells driven by FLT3-ITD (32D/ITD) but not by FLT3 mutated in the tyrosine kinase domain (32D/TKD). Here, we report the involvement of Pim kinases expressed through STAT5 activation in acquisition of this resistance. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
| + |
STAT5A | up-regulates quantity by expression
transcriptional regulation
|
PIM |
0.429 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259436 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15498859 |
Pim-1 is know to be up regulated by signal transducer and activator of transcription 5 (stat5) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
| + |
ERG | up-regulates quantity by expression
transcriptional regulation
|
PIM |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259408 |
|
|
Homo sapiens |
Prostate Epithelium Cell Line |
| pmid |
sentence |
| 22140532 |
ERG deregulation induces PIM1 over-expression and aneuploidy in prostate epithelial cells. The up-regulation of PIM1 induced by tERG over-expression significantly modified Cyclin B1 levels and increased the percentage of aneuploid cells in the RWPE-1 cell line after taxane-based treatment. Here we provide the first evidence for an ERG-mediated PIM1 up-regulation in prostate cells in vitro and in vivo, suggesting a direct effect of ERG transcriptional activity in the alteration of genetic stability. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SGI-1776 | down-regulates
chemical inhibition
|
PIM |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259435 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PRKACA | up-regulates activity
phosphorylation
|
PIM |
0.27 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259413 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 30017192 |
In this study, we found that PKCα stabilized and activated PIM-1L by phosphorylation at Ser65. The PIM-1L phosphorylation suppressed sotrastaurin-induced apoptosis. These findings suggest that PKCα promotes cell survival and proliferation by upregulating PIM-1L in acute myeloid leukemia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIM | down-regulates 
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255732 |
|
|
Homo sapiens |
Hematopoietic Cell |
| pmid |
sentence |
| 16146838 |
The results of 2 microarray experiments demonstrated that the aberrant activation of STAT proteins by Flt3-ITDs resulted in the up-regulation of several STAT5-responsive genes, such as Pim-1, Pim-2, and members of the SOCS (suppressor of cytokine signaling) protein family. These results are particularly interesting because recent data point to an important role of Pim kinases in the antiapoptosis of hematopoietic cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD in AML |
3.0
PIM