| + |
INPPL1 | down-regulates 
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-47537 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9111325 |
Sip specifically and markedly reduced the level of phosphatidylinositol (3,4,5) triphosphate [ptdins(3,4,5)p3] generated in oocytes in response to insulin |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates activity 
relocalization
|
AKT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236509 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23119004 |
Binding of IGF to IGF-1R activates PI3K to generate PIP3 which in turn recruits and activates proteins that contain a pleckstrin homology ph) domain, including AKT and PDK1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236490 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23633519 |
Akt is a serine-threonine protein kinase that plays important roles in cell growth, proliferation and apoptosis. It is activated after binding to phosphatidylinositol phosphates pips) with phosphate groups at positions 3,4 and 3,4,5 on the inositol ring. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Prostate Gland Cancer Cell |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, miRNA in AML, AMPK Signaling, B-cell activation, EGFR Signaling, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Non-small-cell lung cancer (NSCLC), Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling |
| + |
PTEN | down-regulates quantity
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-228145 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11875759 |
PTEN dephosphorylates PI3P, lowering its cellular levels and resulting in the down-regulation of AKT. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, B-cell activation, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, Malignant Melanoma, MTOR Signaling, Prostate Cancer, PI3K/AKT Signaling, Thyroid cancer |
| + |
PIP3 | up-regulates activity
relocalization, chemical activation
|
PDPK1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175253 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21798082 |
Pip3 acts in turn as a docking site for two kinases, phosphoinositide-dependent kinase 1 (PDK1) and AKT, and the subsequent phosphorylation of AKT at serine 308 by PDK1, leading to AKT activation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-243274 |
|
|
in vitro |
|
| pmid |
sentence |
| 9094314 |
We tested the kinase in the presence of several inositol phospholipids and found that only low micromolar concentrations of the D enantiomers of either phosphatidylinositol 3,4,5-triphosphate (PtdIns(3,4,5)P3) or PtdIns(3,4)P2 were effective in potently activating the kinase, which has been named PtdIns(3,4,5)P3-dependent protein kinase-1 (PDK1) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249628 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19951971 |
PIP3 recruits PDK1 and AKT to the plasma membrane, where PDK1 phosphorylates AKT on Thr308 in the activation loop of the kinase domain. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-58313 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 9637919 |
In response to PDGF, binding of ptdlns (3,4,5)p3 and/or ptdlns(3,4)p2 to the PH domain of PDK-1 causes its translocation to the plasma membrane where it co-localises with PKB, significantly contributing to the scale of PKB activation. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens, In Vitro, Chlorocebus Aethiops |
| Pathways: | Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, miRNA in AML, AMPK Signaling, B-cell activation, EGFR Signaling, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Non-small-cell lung cancer (NSCLC), Prostate Cancer, PI3K/AKT Signaling, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling |
| + |
PIK3CB | up-regulates quantity
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175241 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
The activation of pi3k results in the generation of the second messenger, phosphatidylinositol 3,4,5-triphosphate (pip3) from phosphatidylinositol 4,5-bisphosphate (pip2). In vivo, class i pi3ks primarily generate phosphatidylinositol-3,4,5-trisphosphate (pip3) from phosphatidylinositol- 4,5-bisphosphate (pi-4,5-p2) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, Insulin Signaling |
| + |
PI3K | up-regulates quantity
, chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252722 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21798082 |
Phosphorylated irs then acts as docking site to recruit and activate phosphatidylinositol-3-kinase (pi3k) which phosphorylates membrane phospholipids, generating phosphoinositide-3,4,5-triphosphate (pip3) from phosphoinositide-4,5-biphosphate. (pip2). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252712 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24647478 |
Stimulation of tyrosine kinase receptors initiates a signaling cascade that activates pi3k. Activated pi3k uses pip2 to generate pip3, 24647478 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252713 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12040186 |
The activated PI3K converts the plasma membrane lipid phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] to phosphatidylinositol-3,4,5-trisphosphate [PI(3,4,5)P3]. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, B-cell activation, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD signaling, Hepatocellular Tumor, mTOR in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, T cell activation, VEGF Signaling |
| + |
PIK3CG | up-regulates
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175244 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
The activation of pi3k results in the generation of the second messenger, phosphatidylinositol 3,4,5-triphosphate (pip3) from phosphatidylinositol 4,5-bisphosphate (pip2). In vivo, class i pi3ks primarily generate phosphatidylinositol-3,4,5-trisphosphate (pip3) from phosphatidylinositol- 4,5-bisphosphate (pi-4,5-p2) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-147954 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16847462 |
The activation of pi3k results in the generation of the second messenger, phosphatidylinositol 3,4,5-triphosphate (pip3) from phosphatidylinositol 4,5-bisphosphate (pip2). In vivo, class i pi3ks primarily generate phosphatidylinositol-3,4,5-trisphosphate (pip3) from phosphatidylinositol- 4,5-bisphosphate (pi-4,5-p2) |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates activity
relocalization
|
AKT1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252642 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23119004 |
Binding of igf to igf-ir activates pi3k to generate pip3 which in turn recruits and activates proteins that contain a pleckstrin homology ph) domain, including akt and pdk1. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252641 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23633519 |
Akt is a serine-threonine protein kinase that plays important roles in cell growth, proliferation and apoptosis. It is activated after binding to phosphatidylinositol phosphates pips) with phosphate groups at positions 3,4 and 3,4,5 on the inositol ring. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236349 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21798082 |
Pip3 acts in turn as a docking site for two kinases, phosphoinositidedependent kinase 1 pdk1) and akt, and the subsequent phosphorylation of akt at serine 308 by pdk1, leading to akt activation. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, FLT3-ITD signaling, Glioblastoma Multiforme |
| + |
PIP3 | up-regulates
chemical activation
|
WIPI2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177226 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22082875 |
We identified the human wipi protein family and found that wipi-1 specifically binds ptdins(3)p, accumulates at the phagophore and becomes a membrane protein of generated autophagosomes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
INPP5D | down-regulates quantity
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252428 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12421919 |
Two inositol phosphatases implicated in the degradation of PI(3, 4, 5)P3, namely the 5_ phosphatase Src homology 2 domain containing inositol polyphosphate phosphatase (SHIP) and the 3_ phosphatase and tensin homolog deleted on chromosome ten |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, B-cell activation |
| + |
PIP3 | up-regulates
relocalization
|
AKT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254982 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 8645147 |
Activated hyperphosphorylated Akt-1 bound to Ptd Ins(3,4,5)P3 -containing vesicles in a similar manner to the inactive dephosphorylated enzyme |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, miRNA in AML, AMPK Signaling, B-cell activation, EGFR Signaling, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD signaling, Glioblastoma Multiforme, Hepatocellular Tumor, Insulin Signaling, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Non-small-cell lung cancer (NSCLC), Prostate Cancer, Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, Thyroid cancer, T cell activation, VEGF Signaling |
| + |
PIP3 | up-regulates activity
chemical activation
|
mTORC2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252430 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26293922 |
PtdIns(3,4,5)P3, but not other PtdInsPn species, interacts with SIN1-PH to release its inhibition on the mTOR kinase domain, thereby triggering mTORC2 activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, mTOR in cancer, MTOR Signaling, PI3K/AKT Signaling |
| + |
PIK3C2A | up-regulates
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199367 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23119004 |
Pi3ks phosphorylate the d3 position of membrane phosphatidylinositides to generate phosphatidylinositol 3,4,5-triphosphate (pip3). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates
chemical activation
|
PLEKHG1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-169179 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21041639 |
Phosphatidylinositol-3,4,5-trisphosphate (pip3), the product of pi3k activity and a key signaling molecule, acts by recruiting pleckstrin-homology (ph) domain-containing proteins to cell membranes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | up-regulates quantity
chemical modification
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-147948 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24367090 |
Insulin activation of phosphoinositide 3-kinase (pi3k) signaling regulates glucose homeostasis through the production of phosphatidylinositol 3,4,5-trisphosphate (pip3). The dual-specificity phosphatase and tensin homolog deleted on chromosome 10 (pten) blocks pi3k signaling by dephosphorylating pip3, and is inhibited through its interaction with phosphatidylinositol 3,4,5-trisphosphate-dependent rac exchanger 2 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65409 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24647478 |
Stimulation of tyrosine kinase receptors initiates a signaling cascade that activates pi3k. Activated pi3k uses pip2 to generate pip3, which recruit akt to the plasma membrane through its pleckstrin homology (ph) domain, permitting its activation by pdks. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Prostate Cancer |
| + |
PIP3 | up-regulates
chemical activation
|
ZFYVE1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180527 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18725538 |
Dfcp1 contains two fyve domains (thus explaining its pi(3)p binding) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates
chemical activation
|
WIPI1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-177169 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22082875 |
We identified the human wipi protein family and found that wipi-1 specifically binds ptdins(3)p, accumulates at the phagophore and becomes a membrane protein of generated autophagosomes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates activity
chemical activation
|
WDR45B |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268476 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 28561066 |
All WIPI members fold into seven-bladed β-propeller proteins that bind PtdIns3P and co-localize at nascent autophagosomes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates
chemical activation
|
AKT3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175250 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
When active, pi3k converts phosphatidylinositol (4,5)-bisphosphate (pip2) into phosphatidylinositol (3,4,5)-trisphosphate (pip3). Pip3, in turn, binds the pleckstrin homology (ph) domain of akt/pkb, stimulating its kinase activity, resulting in the phosphorylation of a host of other proteins that affect cell growth, cell cycle entry, and cell survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates quantity
binding
|
RPS6KC1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273743 |
|
|
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 12077123 |
We have shown here that a newly identified protein, RPK118, can bind to and co-localize with SPHK1 in COS7-cells. As shown in Fig.8, RPK118 exhibited specific binding to PtdIns (3)P compared with other phosphoinositides. RPK118 Interacts Specifically with Phosphatidylinositol 3-Phosphate (PtdIns (3)P) through Its PX Domain. In vitro protein kinase assay showing that RPK118 has no protein kinase activity. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
PIP3 | up-regulates activity
chemical activation
|
MAPKAP1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252429 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26293922 |
PtdIns(3,4,5)P3, but not other PtdInsPn species, interacts with SIN1-PH to release its inhibition on the mTOR kinase domain, thereby triggering mTORC2 activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3R1 | up-regulates quantity 
|
PIP3 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175678 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 21798082 |
Phosphorylated irs then acts as docking site to recruit and activate phosphatidylinositol-3-kinase (pi3k) which phosphorylates membrane phospholipids, generating phosphoinositide-3,4,5-triphosphate (pip3) from phosphoinositide-4,5-biphosphate. (pip2). |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Glioblastoma Multiforme, MTOR Signaling, T cell activation |
| + |
PIP3 | up-regulates activity
chemical activation
|
AKT2 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175247 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
When active, pi3k converts phosphatidylinositol (4,5)-bisphosphate (pip2) into phosphatidylinositol (3,4,5)-trisphosphate (pip3). Pip3, in turn, binds the pleckstrin homology (ph) domain of akt/pkb, stimulating its kinase activity, resulting in the phosphorylation of a host of other proteins that affect cell growth, cell cycle entry, and cell survival. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates activity
chemical activation
|
WDR45 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268475 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 28561066 |
All WIPI members fold into seven-bladed β-propeller proteins that bind PtdIns3P and co-localize at nascent autophagosomes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIP3 | up-regulates quantity
relocalization
|
ZFYVE26 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265537 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 20208530 |
We show that PtdIns(3)P localizes to the midbody during cytokinesis and recruits a centrosomal protein, FYVE-CENT (ZFYVE26), and its binding partner TTC19, which in turn interacts with CHMP4B, an endosomal sorting complex required for transport (ESCRT)-III subunit implicated in the abscission step of cytokinesis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
PIP3