| + |
PPM1A | up-regulates activity 
dephosphorylation
|
PI3K |
0.322 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252724 |
Ser608 |
ENTEDQYsLVEDDED |
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 15016818 |
Protein phosphatase-2C alpha as a positive regulator of insulin sensitivity through direct activation of phosphatidylinositol 3-kinase in 3T3-L1 adipocytes|PP2C_ dephosphorylates the p85 subunit of PI3K, and dephosphorylation of the p85 subunit of PI3K at Ser608 increases its activity |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
INSR | up-regulates activity
phosphorylation
|
PI3K |
0.613 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252692 |
Tyr368 |
STKMHGDyTLTLRKG |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 8385099 |
The alpha-type 85-kDa subunit of phosphatidylinositol 3-kinase is phosphorylated at tyrosines 368, 580, and 607 by the insulin receptor. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252691 |
Tyr580 |
LRKTRDQyLMWLTQK |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 8385099 |
The alpha-type 85-kDa subunit of phosphatidylinositol 3-kinase is phosphorylated at tyrosines 368, 580, and 607 by the insulin receptor. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252693 |
Tyr607 |
NENTEDQySLVEDDE |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 8385099 |
The alpha-type 85-kDa subunit of phosphatidylinositol 3-kinase is phosphorylated at tyrosines 368, 580, and 607 by the insulin receptor. |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | FAP: Insulin-mediated adipogenesis, Leptin Signaling, mTOR in cancer |
| + |
LCK | down-regulates activity 
phosphorylation
|
PI3K |
0.593 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252699 |
Tyr688 |
FAEPYNLySSLKELV |
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 9461588 |
The regulatory p85 subunit of phosphatidylinositol 3-kinase is phosphorylated on tyrosine residues. We report that this phosphorylation event is readily catalyzed by the Abl and Lck protein-tyrosine kinases in vitro, by Bcr-Abl or a catalytically activated Lck-Y505F in co-transfected COS cells. we have mapped a major phosphorylation site to Tyr-688 in the C-terminal SH2 domain of p85. Tyrosine phosphorylation of p85 in vitro or in vivo was not associated with detectable change in the enzymatic activity of the phosphatidylinositol 3-kinase heterodimer, but correlated with a strong reduction in the binding of some, but not all, phosphoproteins to the SH2 domains of p85. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | T cell activation |
| + |
PIK3CA | form complex 
binding
|
PI3K |
0.934 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255299 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805105 |
Phosphoinositol 3- kinase alpha (PI3Kα) is a heterodimeric enzyme formed by a catalytic subunit (p110α, encoded by PIK3CA) and one of several regulatory subunits (a major one being p85α, encoded by PI3KR1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | mTOR in cancer |
| + |
PI3K | up-regulates activity
binding
|
PIK3CD |
0.616 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252720 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 14665640 |
Signal transduction pathways triggered by Tie2 have been extensively examined. Tyr-1101of Tie2 directly associates in a phosphotyrosine (pTyr)-dependent manner with the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase, which in turn activate PI 3-kinase, leading to cell motility and survival |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
TNF | up-regulates activity 
|
PI3K |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252733 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Thyroid Hormone Metabolism |
| + |
GSK1059615 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252667 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI-103 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252651 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
A6/b4 integrin | up-regulates activity
binding
|
PI3K |
0.421 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259033 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9428518 |
Stable expression of alpha6beta4 increased carcinoma invasion in a pi3k-dependent manner, and transient expression of a constitutively active pi3k increased invasion in the absence of alpha6beta4. Ligation of alpha6beta4 stimulated significantly more pi3k activity than ligation of beta1 integrins, establishing specificity among integrins for pi3k activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Integrin Signaling |
| + |
PI3K | up-regulates quantity
|
superoxide |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255011 |
|
|
|
|
| pmid |
sentence |
| 23994464 |
The PI3Kγ pathway (but not PLCβ2/3) is required for chemotaxis of the cells while both pathways are required for GPCR-induced superoxide release |
|
| Publications: |
1 |
| + |
IRS1 | up-regulates activity
binding
|
PI3K |
0.765 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252695 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20966354 |
Irs proteins are capable of both regulating and activating pi3k, depending on the cell of origin. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252694 |
|
|
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). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256170 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20966354 |
Irs proteins are capable of both regulating and activating pi3k, depending on the cell of origin. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens, Rattus Norvegicus |
| Tissue: |
Skeletal Muscle, Lung Cancer Cell |
| Pathways: | Leptin Signaling, mTOR in cancer |
| + |
GNGT1 | up-regulates
binding
|
PI3K |
0.417 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252686 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17419683 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252687 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 16537363 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
EGFR | up-regulates
binding
|
PI3K |
0.779 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252672 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14967450 |
The egf-r coimmunoprecipitated with p85 alpha |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252671 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 26918608 |
P85alpha promotes nucleolin transcription and subsequently enhances EGFR mRNA stability and EGF-induced malignant cellular transformation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast Cancer Cell |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, Hepatocellular Tumor, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling |
| + |
HRAS | up-regulates activity
binding
|
PI3K |
0.844 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252689 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 8052307 |
In vivo, dominant negative ras mutant n17 inhibits growth factor induced production of 3' phosphorylated phosphoinositides in pc12 cells, and transfection of ras, but not raf, into cos cells results in a large elevation in the level of these lipids. Grb2 binds and activates sos, which then activates ras, and this activates p110 independently of p85. it was also described that ras interacts with pi3k in a direct manner. lysine residue 227 is essential for the interaction of ras with pi3k |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | ErbB receptors in cancer, Hepatocellular Tumor, Integrin Signaling, Non-small-cell lung cancer (NSCLC), PI3K/AKT Signaling, RTKs in cancer, T cell activation, VEGF Signaling |
| + |
CH5132799 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252648 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3R3 | up-regulates
binding
|
PI3K |
0.731 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252723 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9415396 |
The region between the src homology 2 (sh2) domains of p55pik bound to the nh2 terminus region of p110alpha |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
(2S)-N1-[5-(2-tert-butyl-4-thiazolyl)-4-methyl-2-thiazolyl]pyrrolidine-1,2-dicarboxamide | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252658 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GAB2 | up-regulates
binding
|
PI3K |
0.513 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252677 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24737791 |
The signaling mechanism utilizes an adaptor protein, shc, which binds to a phosphotyrosine residue on the il-2/15r?, Resulting in activation of grb2 and onto akt via the shc-grb2-gab2-pi3k-akt signaling pathway to increase cell proliferation and/or survival |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LY294002 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252647 |
|
|
Homo sapiens |
Myoblast |
| pmid |
sentence |
| 10896679 |
Here we show that inhibition of pi3-k activity by the pharmacological agent ly294002 affects early processes of myoblast differentiation including the transcriptional activation of myogenin. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Skeletal Muscle |
| + |
CD19 | up-regulates activity
binding
|
PI3K |
0.514 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252669 |
|
|
Mus musculus |
Myeloma Cell Line |
| pmid |
sentence |
| 10201980 |
Phosphorylation of CD19 Y484 and Y515, and linked activation of phosphatidylinositol 3-kinase, are required for B cell antigen receptor-mediated activation of Bruton's tyrosine kinase. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252670 |
|
|
Mus musculus |
B-lymphocyte |
| pmid |
sentence |
| 25673924 |
CD19 has an extracellular region containing two C2-type Ig-like domains and a cytoplasmic region of ~240 amino acids with 9 conserved tyrosine residues24. Lyn, a Src-family protein tyrosine kinase member, is the dominant kinase that phosphorylates CD19 upon stimulation. Once tyrosyl-phosphorylated, CD19 serves as a membrane-bound adaptor protein for Src homology 2-containing signaling molecules such as Lyn, Vav, and phosphatidylinositol 3-kinase, which further mediate downstream activation cascades. |
|
| Publications: |
2 |
Organism: |
Mus Musculus |
| Pathways: | B-cell activation, EBV infection |
| + |
NRAS | up-regulates activity
binding
|
PI3K |
0.673 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252700 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
Grb2 binds and activates sos, which then activates ras, and this activates p110 independently of p85./it was also described that ras interacts with pi3k in a direct manner./lysine residue 227 is essential for the interaction of ras with pi3k |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
| + |
wortmannin | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252666 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8162590 |
The microbial product wortmannin and some of its analogues have been shown to be potent inhibitors of phosphatidylinositol-3-kinase. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252663 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 7503989 |
Wortmannin inhibited the activity of partially purified pi3-kinase from calf thymus, as well as the pi3-kinase activity in anti-pi3-kinase p85 immunoprecipitates from rbl-2h3 cells, at a concentration as low as 1.0 nm and with ic50 values of 3.0 nm. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
PKI-402 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252654 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3R6 | down-regulates activity
binding
|
PI3K |
0.512 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275724 |
|
|
|
|
| pmid |
sentence |
| 25753393 |
P84 forms a negative regulatory complex with p110gamma to control PI3Kgamma signalling during cell migration|Our findings suggest that p84 binding to p110γ may represent a novel negative feedback signal that terminates PI3Kγ activity. |
|
| Publications: |
1 |
| + |
IRS2 | up-regulates activity
binding
|
PI3K |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252696 |
|
|
Mus musculus |
Mammary Gland Tumor Cell |
| pmid |
sentence |
| 24811175 |
Insulin receptor substrate 1 (IRS-1) and IRS-2 are cytoplasmic adaptor proteins that mediate the activation of signaling pathways in response to ligand stimulation of upstream cell surface receptors. Despite sharing a high level of homology and the ability to activate PI3K, only Irs-2 positively regulates aerobic glycolysis in mammary tumor cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
PI3K | up-regulates activity
|
AKT |
0.794 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252703 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19573809 |
However, here we show through phosphoprotein profiling and functional genomic studies that many PIK3CA mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation and a diminished reliance on AKT for anchorage-independent growth |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252715 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12167717 |
PKB induction requires phosphorylation of two critical residues, threonine 308 in the activation loop and serine 473 near the carboxyl terminus. Membrane localization of PKB was found to be a primary determinant of serine 473 phosphorylation. PI3K activity was equally important for promoting phosphorylation of serine 473, |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast Cancer Cell |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, BCR-ABL in AML, FLT3 in AML, KIT in AML, B-cell activation, COVID-19 Causal Network, EBV infection, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Inflammosome Activation, Integrin Signaling, Leptin Signaling, mTOR in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, SARS-CoV INFLAMMATORY RESPONSE, T cell activation, Thyroid Hormone Metabolism, VEGF Signaling, WNT/FLT3 |
| + |
ZSTK-474 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252646 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK2126458 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252645 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI3K | up-regulates activity
phosphorylation
|
AKT |
0.794 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254950 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15526160 |
C-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, BCR-ABL in AML, FLT3 in AML, KIT in AML, B-cell activation, COVID-19 Causal Network, EBV infection, ErbB receptors in cancer, FAP: Insulin-mediated adipogenesis, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Inflammosome Activation, Integrin Signaling, Leptin Signaling, mTOR in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, SARS-CoV INFLAMMATORY RESPONSE, T cell activation, Thyroid Hormone Metabolism, VEGF Signaling, WNT/FLT3 |
| + |
PI3K | up-regulates
|
MTOR |
0.575 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252705 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18721898 |
Phosphoinositide 3-kinase (pi3k)-dependent activation of the rheb-mtor pathway triggers the simultaneous local synthesis of tc10 and par3. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, KIT in AML, FLT3-ITD in AML, FLT3-ITD signaling, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA) |
| + |
PI3K | up-regulates
|
Chemotaxis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255012 |
|
|
|
|
| pmid |
sentence |
| 23994464 |
The PI3Kγ pathway (but not PLCβ2/3) is required for chemotaxis of the cells while both pathways are required for GPCR-induced superoxide release |
|
| Publications: |
1 |
| + |
CUDC-907 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252661 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GNB/GNG | up-regulates
|
PI3K |
0.481 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255010 |
|
|
|
|
| pmid |
sentence |
| 23994464 |
Similar to PLCβ activation, PI3K-activation by neutrophil GPCRs also occurs primarily through Gβγ subunits, through the unique PI3Kγ isoform which is directly activated by Gβγ dimers |
|
| Publications: |
1 |
| + |
pictrelisib | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252664 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21876152 |
Currently, several pi3k inhibitors, including gdc0941 (genentech) and bez235 (novartis pharmaceuticals), have entered phase i clinical trials, and in addition, isoform-specific compounds are being developed |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast |
| + |
PI3K | up-regulates
|
Survival |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252706 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 14665640 |
Signal transduction pathways triggered by Tie2 have been extensively examined. Tyr-1101of Tie2 directly associates in a phosphotyrosine (pTyr)-dependent manner with the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase, which in turn activate PI 3-kinase, leading to cell motility and survival |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255576 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 19436055 |
Low pM concentrations of GM-CSF mediate βc Ser585 phosphorylation, leading to 14-3-3 binding, PI-3 kinase activation, and hemopoietic cell survival, whereas at concentrations of 10 pM or more, GM-CSF mediates βc Tyr577 phosphorylation, Shc recruitment, and PI-3 kinase activation, thereby promoting both survival and proliferation. |
|
| Publications: |
2 |
Organism: |
Chlorocebus Aethiops, Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | ErbB receptors in cancer, Hepatocellular Tumor, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer |
| + |
PI3K | down-regulates activity 
|
IRS1 |
0.765 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252717 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11160134 |
Ly294002 or wortmannin were used to determine whether pi 3-kinasedependent pathways mediate ser307 phosphorylation during insulin/igf-1 or TNF-alpha Stimulation. As expected, the pi-3 kinase inhibitors ly294002 or wortmannin inhibited activation of pkb/akt in insulin or igf-1 stimulated 3t3-l1 preadipocytes, but were without effect on erk1/2. these results suggest that elements of the pi 3-kinase cascade mediate insulin/igf-1stimulated phosphorylation of ser307 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Leptin Signaling, mTOR in cancer |
| + |
ITGB4 | up-regulates
binding
|
PI3K |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252697 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9428518 |
Stable expression of alpha6beta4 increased carcinoma invasion in a pi3k-dependent manner, and transient expression of a constitutively active pi3k increased invasion in the absence of alpha6beta4. Ligation of alpha6beta4 stimulated significantly more pi3k activity than ligation of beta1 integrins, establishing specificity among integrins for pi3k activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Integrin Signaling |
| + |
D-106669 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252649 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates
binding
|
PI3K |
0.35 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252730 |
|
|
Homo sapiens |
Respiratory Smooth Muscle |
| pmid |
sentence |
| 9435577 |
These studies revealed that PI 3-kinase is associated in vivo with both TGF-_ receptor subtypes and that TGF-_1 stimulation enhances PI 3-kinase activity associated with type I TGF-_ receptor in hASM cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), Thyroid Hormone Metabolism |
| + |
PIK-75 Hydrochloride | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252652 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI3K | up-regulates activity
|
AKT1 |
0.794 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252708 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 9346240 |
Growth factors can promote cell survival by activating the phosphatidylinositide-3'-OH kinase and its downstream target, the serine-threonine kinase Akt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252711 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16293724 |
We show that PGE2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein;G protein)-coupled receptor, EP2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase Akt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252704 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19573809 |
However, here we show through phosphoprotein profiling and functional genomic studies that many PIK3CA mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation and a diminished reliance on AKT for anchorage-independent growth |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252710 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12167717 |
PKB induction requires phosphorylation of two critical residues, threonine 308 in the activation loop and serine 473 near the carboxyl terminus. Membrane localization of PKB was found to be a primary determinant of serine 473 phosphorylation. PI3K activity was equally important for promoting phosphorylation of serine 473, |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Tissue: |
Colonic Cancer Cell, Breast Cancer Cell |
| Pathways: | FLT3-ITD signaling |
| + |
ErbB receptor family | up-regulates activity
binding
|
PI3K |
0.779 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256168 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17306385 |
Another phospholipid modifying signaling pathway activated by RTKs is the PI3K pathway. This heterodimeric enzyme comprises two subunits, the p85 regulatory subunit harboring two SH2 domains, and the p110 catalytic subunit. PI3K activation may be achieved by binding of its p85 regulatory subunit to an activated receptor. Alternatively, RTK signaling may activate the small G protein Ras, which in turn recruits PI3K to the plasma membrane and induces a stimulatory conformational change in the lipid kinase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | ErbB receptors in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), RTKs in cancer |
| + |
IFNAR1 | up-regulates activity
phosphorylation
|
PI3K |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260435 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21631354 |
These results indicate that NF-κB activation by IFN via the PI3K pathway is distinct from the ISRE-driven mechanism in regulating gene expression. Activation of PI3K/AKT by IFN has also been described through the insulin receptor substrate 1 (Uddin and others 1997) and through the direct interaction of PI3K with IFNAR1, which also leads to induction of NF-κB activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HECW2 | up-regulates activity
binding
|
PI3K |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269458 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 27119228 |
NEDL2 acts as a scaffold protein to promote GDNF-stimulated Akt activation. biochemical analysis indicated that NEDL2 appears to act like a scaffold protein to recruit SHC, Grb2, PI3K (p110 and p85), PDK1 and Akt together to promote the signaling transduction. NEDL2 binds p85, p110 and Akt with different domains |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI3K | up-regulates
|
AKT2 |
0.646 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252716 |
|
|
Homo sapiens |
Colonic Cancer Cell |
| pmid |
sentence |
| 16293724 |
We show that pge2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein (g protein)coupled receptor, ep2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase akt by free g protein bg subunits and the direct association of the g protein as subunit with the regulator of g protein signaling (rgs) domain of axin. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GRB10 | up-regulates activity
binding
|
PI3K |
0.335 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255946 |
|
|
Mus musculus |
BA/F3 Cell |
| pmid |
sentence |
| 23246379 |
Grb10 transduces signal from FLT3 by direct interaction with p85 and Ba/F3-FLT3-ITD cells expressing Grb10 exhibits higher STAT5 activation |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD signaling |
| + |
GNB3 | up-regulates
binding
|
PI3K |
0.392 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252680 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14668344 |
Expression of the g__ sequestrant, _-transducin, inhibits both ras activation and membrane translocation of _-arrestin1, suggesting that g__ dimers from g_i2 and g_q activate different effectors to coordinately regulate the pi 3-kinase/akt pathway. , these data indicate that _-thrombin stimulates rapid pi 3-kinase activity and akt phosphorylation by the g__ dimers released from a ptx-sensitive g protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GNB1 | up-regulates
binding
|
PI3K |
0.52 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252679 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 16537363 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LAT | up-regulates activity
binding
|
PI3K |
0.407 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252734 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11368773 |
By substituting these tyrosine residues in LAT with phenylalanine and by utilizing phosphorylated peptides derived from these sites, we mapped the tyrosine residues in LAT required for the direct interaction and activation of Vav, p85/p110alpha and phospholipase Cgamma1 (PLCgamma1). Our results indicate that Tyr(226) and Tyr(191) are required for Vav binding, whereas Tyr(171) and Tyr(132) are necessary for association and activation of phosphoinositide 3-kinase activity and PLCgamma1 respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | B-cell activation, T cell activation |
| + |
PI3K | up-regulates quantity
chemical modification,
|
PIP3 |
0.8 |
| 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]. |
|
| 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-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). |
|
| 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 |
| + |
RTKs | up-regulates activity
binding
|
PI3K |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256166 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17306385 |
Another phospholipid modifying signaling pathway activated by RTKs is the PI3K pathway. This heterodimeric enzyme comprises two subunits, the p85 regulatory subunit harboring two SH2 domains, and the p110 catalytic subunit. PI3K activation may be achieved by binding of its p85 regulatory subunit to an activated receptor. Alternatively, RTK signaling may activate the small G protein Ras, which in turn recruits PI3K to the plasma membrane and induces a stimulatory conformational change in the lipid kinase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Integrin Signaling, PI3K/AKT Signaling, RTKs in cancer |
| + |
TGFB1 | up-regulates activity
binding
|
PI3K |
0.266 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252729 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19114990 |
While association of the TGF_RI receptor with p85 requires TGF-_ stimulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Thyroid Hormone Metabolism |
| + |
PI3K | up-regulates
|
RAC1 |
0.536 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252707 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
Pi3k can also activate rac, and this activation is involved in cytoskeleton reorganization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML, WNT/FLT3 |
| + |
GAB1 | up-regulates
binding
|
PI3K |
0.502 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252676 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11043767 |
We have shown that gab1 colocalizes pi3k with sh2 domain-containing inositol phosphatase (ship) and shp2, two enzymes that regulate pi3k-dependent signaling. The src homology 2 (sh2) domain of the phosphatidylinositol 3-kinase (pi3k) regulatory subunit binds gab1 in a phosphorylation-independent manner. Moreover, the regulatory subunit of pi3k can mediate the association of gab1 and receptor protein-tyrosine kinases including the insulin, egf, and ngf receptors, all of which phosphorylate gab1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, PI3K/AKT Signaling |
| + |
PIK3AP1 | up-regulates
binding
|
PI3K |
0.514 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252701 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 22187458 |
Bcap is constitutively phosphorylated and associated with the p85 subunit of pi3k in macrophages. Tlr signaling causes the phosphorylation of the small amount of bcap that is associated with membranes in the resting state or the translocation of phosphorylated bcap from the cytoplasm to the membrane. This accumulation of tyrosine-phosphorylated bcap at the membrane with its associated pi3k would then allow for the catalysis of ptd ins p2 to ptd ins p3 and downstream pi3k-dependent signals. Bcap is an essential activator of the pi3k pathway downstream of tlr signaling |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3R1 | form complex
binding
|
PI3K |
0.934 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255300 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19805105 |
Phosphoinositol 3- kinase alpha (PI3Kα) is a heterodimeric enzyme formed by a catalytic subunit (p110α, encoded by PIK3CA) and one of several regulatory subunits (a major one being p85α, encoded by PI3KR1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | T cell activation |
| + |
Amyloid_fibril_formation | down-regulates
|
PI3K |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255492 |
|
|
|
|
| pmid |
sentence |
| 26721223 |
Excessive accumulation of Aβ protein in the AD brain may lead to a decrease in the levels of phosphatidylinositol-3 kinase (PI3K) and the serine/threonine protein kinase B (Akt) activity. |
|
| Publications: |
1 |
| + |
KIT | up-regulates activity
phosphorylation, , binding
|
PI3K |
0.717 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254949 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 15526160 |
Activation of PI3-kinase by c-Kit has been linked to mitogenesis, differentiation, survival, adhesion, secretion and actin cytoskeletal reorganization. In c-Kit, Y721 has been found to directly interact with PI3-kinase |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255949 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 7509796 |
Tyrosine residue 719 of the c-kit receptor is essential for binding of the P85 subunit of phosphatidylinositol (PI) 3-kinase and for c-kit-associated PI 3-kinase activity in COS-1 cells |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256121 |
|
|
Mus musculus |
Bone Marrow |
| pmid |
sentence |
| 18179858 |
KIT mutations within the carboxy-terminal region of the cytoplasmic tyrosine kinase domain (TK2), such as KITD816V, stabilize the KIT activation loop conformation in its active form.Previous studies have demonstrated hyperactivation of p85α regulatory subunit of class IA phosphatidylinositol-3-kinase (PI3K) in cell lines expressing the activation loop mutant of KIT. Although p85α is hyperphosphorylated and constitutively bound to KITD814V in cell-line models. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens, Chlorocebus Aethiops, Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
| + |
PI3K | up-regulates activity
phosphorylation
|
BTK |
0.478 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252709 |
|
|
Mus musculus |
Myeloma Cell Line |
| pmid |
sentence |
| 10201980 |
Activation of Btk occurs by transphosphorylation of tyrosine 551 in the catalytic domain, resulting in a dramatic increase in the catalytic activity of the kinase (11, 12, 13). This allows for autophosphorylation at tyrosine 223 in the SH3 domain (14). Both Lyn and Syk have been demonstrated to be involved in BCR-mediated Btk activation (11), but processes that drive colocalization of these kinases are ill-defined. Recently, it was suggested that phosphatidylinositol 3-kinase (PI3-K) is also involved in Btk activation |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | B-cell activation |
| + |
IGF1R | up-regulates
binding
|
PI3K |
0.696 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252690 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18595745 |
Igf-1 activated both the pi3k and the extracellular signal-regulated kinase [?] (erk [?]) Pathways as evidenced by phosphorylation of either akt or erk1 [?]/2 (respectively) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, Hepatocellular Tumor, Non-small-cell lung cancer (NSCLC) |
| + |
FLT3 | up-regulates activity
|
PI3K |
0.552 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260083 |
|
|
Mus musculus |
BA/F3 Cell |
| pmid |
sentence |
| 23246379 |
Grb10 transduces signal from FLT3 by direct interaction with p85 and Ba/F3-FLT3-ITD cells expressing Grb10 exhibits higher STAT5 activation. These results suggest that Grb10 binds to both normal and oncogenic FLT3 and induces PI3K-Akt and STAT5 signaling pathways resulting in an enhanced proliferation, survival and colony formation of hematopoietic cells. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, FLT3 in AML, FLT3-ITD in AML, FLT3-ITD signaling, WNT/FLT3 |
| + |
TGFBR2 | up-regulates activity
binding
|
PI3K |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252731 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19114990 |
In immunoprecipitation esperiments, the TGF _ RII receptor was found to be constitutively associated with p85, the regulatory subunity of PI3K |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA) |
| + |
GNG3 | up-regulates
binding
|
PI3K |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252685 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17419683 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252684 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16537363 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
GNG2 | up-regulates
binding
|
PI3K |
0.442 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252682 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17419683 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252683 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 16537363 |
Gbetagamma subunits released from gi can activate pi3k (phosphoinositide 3-kinase), and can be therefore implicated in smo-dependent activation of akt. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
IC-87114 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252662 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GNG12 | up-regulates
binding
|
PI3K |
0.39 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252681 |
|
|
Homo sapiens |
Colonic Cancer Cell |
| pmid |
sentence |
| 16293724 |
We show that pge2 stimulates colon cancer cell growth through its heterotrimeric guanine nucleotide-binding protein (g protein)coupled receptor, ep2, by a signaling route that involves the activation of phosphoinositide 3-kinase and the protein kinase akt by free g protein bg subunits and the direct association of the g protein as subunit with the regulator of g protein signaling (rgs) domain of axin. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK-90 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252653 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BKM120 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252656 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CSF2RA/CSF2RB | up-regulates activity
binding
|
PI3K |
0.457 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255585 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19436055 |
As a consequence of Jak2 activation and tyrosine phosphorylation of the cytoplasmic tail of βc, Src homology 2 and phosphotyrosine binding domain proteins are recruited to the active receptor and initiate the major tyrosine phosphorylation-dependent signaling pathways, including the Jak/signal transducer and activator of transcription, Ras/mitogen-activated protein kinase, and phosphatidylinositol 3 (PI-3) kinase pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML |
| + |
ERBB3 | up-regulates
binding
|
PI3K |
0.714 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252673 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16729043 |
Pi3k is the sole binding partner to six tyrosines of erbb3 and one in erbb4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ESR1 | up-regulates
binding
|
PI3K |
0.658 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252675 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16169518 |
Recently, it has been known that er activates phosphatidylinositol-3-oh kinase (pi3k) through binding with the p85 regulatory subunit of pi3k. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KDR | up-regulates activity
binding
|
PI3K |
0.566 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261916 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11278468 |
These results demonstrate that activation of VEGFR-2 results in activation of PI3K and that activation of PI3K/S6kinase pathway, but not Ras/MAPK, is responsible for VEGFR-2-mediated cell growth. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | VEGF Signaling |
| + |
PP121 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252655 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI3K | up-regulates activity
phosphorylation
|
AKT1 |
0.794 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255106 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15829723 |
IGF-I binding to its receptor activates the kinase activity of the receptor, which then recruits the insulin response substrate-1, causing activation of phosphatidyl-inositol-3 kinase (PI3K) to phosphorylate Akt. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | FLT3-ITD signaling |
| + |
KRAS | up-regulates
binding
|
PI3K |
0.737 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252698 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
Grb2 binds and activates sos, which then activates ras, and this activates p110 independently of p85./it was also described that ras interacts with pi3k in a direct manner./lysine residue 227 is essential for the interaction of ras with pi3k phosphatidylinositol 3-kinase (pi3k) is one of the main effector pathways of ras, regulating cell growth, cell cycle entry, cell survival, cytoskeleton reorganization, and metabolism. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, COVID-19 Causal Network, FLT3-ITD signaling, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA) |
| + |
dactolisib | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252665 |
|
|
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21803746 |
The dual pi3k and mtorc1/2 inhibitor bez235 was highly specific |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR2 | up-regulates
binding
|
PI3K |
0.415 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252732 |
|
|
Homo sapiens |
Respiratory Smooth Muscle |
| pmid |
sentence |
| 9435577 |
These studies revealed that PI 3-kinase is associated in vivo with both TGF-_ receptor subtypes and that TGF-_1 stimulation enhances PI 3-kinase activity associated with type I TGF-_ receptor in hASM cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA) |
| + |
PIK3IP1 | down-regulates activity
binding
|
PI3K |
0.282 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260073 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24316979 |
We demonstrate that CUX1 deficiency activates phosphoinositide 3-kinase (PI3K) signaling through direct transcriptional downregulation of the PI3K inhibitor PIK3IP1 (phosphoinositide-3-kinase interacting protein 1), leading to increased tumor growth and susceptibility to PI3K-AKT inhibition. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
IFNAR | up-regulates activity
binding
|
PI3K |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260436 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21631354 |
These results indicate that NF-κB activation by IFN via the PI3K pathway is distinct from the ISRE-driven mechanism in regulating gene expression. Activation of PI3K/AKT by IFN has also been described through the insulin receptor substrate 1 (Uddin and others 1997) and through the direct interaction of PI3K with IFNAR1, which also leads to induction of NF-κB activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
XL147 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252659 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTPRJ | down-regulates
dephosphorylation
|
PI3K |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252727 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18348712 |
As reduction of pi3k activity by cd148 or shp-1 [32] is not large (2540%), it is likely that these ptps may function as modulators of the pi3k pathway rather than suppressors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD in AML |
| + |
TEK | up-regulates activity
binding
|
PI3K |
0.495 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252728 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 14665640 |
Signal transduction pathways triggered by Tie2 have been extensively examined. Tyr-1101of Tie2 directly associates in a phosphotyrosine (pTyr)-dependent manner with the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase, which in turn activate PI 3-kinase, leading to cell motility and survival |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
LMP1 | up-regulates activity
|
PI3K |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267618 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26428373 |
Activation of the PI3-K/AKT pathway was first linked to LMP1 in the year 2003. Although it is still unclear whether this interaction is direct, expression of LMP1 CTAR1 caused (i) an enrichment of the PI3-K substrate phosphatidylinositol-3,4,5-trisphosphate (PIP3) in the plasma membrane and (ii) the phosphorylation and activation of AKT kinase, also known as protein kinase B, at serine 473. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection |
| + |
GNAS | up-regulates
binding
|
PI3K |
0.364 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252678 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22179044 |
Notably, the fzd7 receptor complex was associated with g_?(s) and pi(3)k and these components were required for wnt7a to activate the akt/mtor growth pathway in myotubes. These data led us to hypothesize that g_?s Mediates the activation of pi3kinase following wnt7a binding to fzd7. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Skeletal Muscle, Myotube |
| Pathways: | Thyroid Hormone Metabolism, WNT/FLT3 |
| + |
PI3K | up-regulates activity
binding
|
PIK3CB |
0.633 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252719 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 14665640 |
Signal transduction pathways triggered by Tie2 have been extensively examined. Tyr-1101of Tie2 directly associates in a phosphotyrosine (pTyr)-dependent manner with the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase, which in turn activate PI 3-kinase, leading to cell motility and survival |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
1-[4-[[2-(2-amino-5-pyrimidinyl)-7-methyl-4-(4-morpholinyl)-6-thieno[3,2-d]pyrimidinyl]methyl]-1-piperazinyl]-2-hydroxy-1-propanone | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252657 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTK2 | up-regulates
binding
|
PI3K |
0.561 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252726 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9416004 |
Pi3-kinase has also been shown to bind fak in a cell cell adhesion-dipendent manner at the major autophosphorylation site y397. This association could live to activation of pi3-kinase and its downstream effectors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Integrin Signaling, VEGF Signaling |
| + |
PKI-587 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252650 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XL765 | down-regulates
chemical inhibition
|
PI3K |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252660 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTEN | down-regulates activity
|
PI3K |
0.722 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252725 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 18794881 |
The pten tumour suppressor is a lipid and protein phosphatase that inhibits phosphoinositide 3-kinase (pi3k)-dependent by dephosphorylating phosphatidylinositol 3,4,5-trisphosphate (ptdinsp(3)). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, Onco-fusion proteins in AML, B-cell activation, Hepatocellular Tumor, PI3K/AKT Signaling |
| + |
CBL | down-regulates
ubiquitination
|
PI3K |
0.598 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252668 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 11526404 |
Cbl-b, a ring-type e3 ubiquitin protein ligase, is implicated in setting the threshold of t lymphocyte activation. The p85 regulatory subunit of phosphatidylinositol 3 kinase (pi3k) was identified as a substrate for cbl-b. We have shown that cbl-b negatively regulated p85 in a proteolysis-independent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, KIT in AML |
| + |
ERBB4 | up-regulates
binding
|
PI3K |
0.557 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252674 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16729043 |
Pi3k is the sole binding partner to six tyrosines of erbb3 and one in erbb4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI3K | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255577 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 19436055 |
Low pM concentrations of GM-CSF mediate βc Ser585 phosphorylation, leading to 14-3-3 binding, PI-3 kinase activation, and hemopoietic cell survival, whereas at concentrations of 10 pM or more, GM-CSF mediates βc Tyr577 phosphorylation, Shc recruitment, and PI-3 kinase activation, thereby promoting both survival and proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | Acute Myeloid Leukemia, ASXL1 in AML, BCR-ABL in AML, FLT3 in AML, Onco-fusion proteins in AML, KIT in AML, B-cell activation, COVID-19 Causal Network, EBV infection, ErbB receptors in cancer, FLT3-ITD in AML, FLT3-ITD signaling, Hepatocellular Tumor, Integrin Signaling, Leptin Signaling, mTOR in cancer, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), PI3K/AKT Signaling, RTKs in cancer, VEGF Signaling, WNT/FLT3 |
| + |
PI3K | up-regulates activity
binding
|
PIK3CG |
0.597 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252721 |
|
|
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 14665640 |
Signal transduction pathways triggered by Tie2 have been extensively examined. Tyr-1101of Tie2 directly associates in a phosphotyrosine (pTyr)-dependent manner with the p85 regulatory subunit of phosphatidylinositol (PI) 3-kinase, which in turn activate PI 3-kinase, leading to cell motility and survival |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
PI3K | down-regulates activity
phosphorylation
|
BAD |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254951 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 15526160 |
C-Kit promotes survival via PI3-kinase-dependent activation of Akt and phosphorylation of Bad, a pro-apoptotic molecule, at S136 in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, FLT3-ITD in AML, FLT3-ITD signaling, VEGF Signaling |
4.0
PI3K
CPX-2384