| + |
PIK3CA | up-regulates activity 
phosphorylation
|
PIK3R1 |
0.935 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276004 |
Ser608 |
ENTEDQYsLVEDDED |
in vitro |
|
| pmid |
sentence |
| 14729945 |
We find that p110 alpha phosphorylates p85 alpha Ser608 in vivo with significant stoichiometry. However, p110 beta is far less efficient at phosphorylating p85 alpha Ser608, identifying a potential difference in the mechanisms by which these two isoforms are regulated. The p85 alpha Ser608 phosphorylation was increased by treatment with insulin, platelet-derived growth factor, and the phosphatase inhibitor okadaic acid. The functional effects of this phosphorylation are highlighted by mutation of Ser608, which results in reduced lipid kinase activity and reduced association of the p110 alpha catalytic subunit with p85 alpha. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Glioblastoma Multiforme, MTOR Signaling, IGF and Myogenesis |
| + |
PIK3CA | up-regulates activity
phosphorylation
|
TPM1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263027 |
Ser61 |
EDELDKYsEALKDAQ |
in vitro |
|
| pmid |
sentence |
| 16094730 |
Here, we demonstrate a requirement for the protein kinase activity of PI(3)K in agonist-dependent beta-adrenergic receptor (betaAR) internalization. Using PI(3)K mutants with either protein or lipid phosphorylation activity, we identify the cytoskeletal protein non-muscle tropomyosin as a substrate of PI(3)K, which is phosphorylated in a wortmannin-sensitive manner on residue Ser 61. A constitutively dephosphorylated (S61A) tropomyosin mutant blocks agonist-dependent betaAR internalization, whereas a tropomyosin mutant that mimics constitutive phosphorylation (S61D) complements the PI(3)K mutant, with only lipid phosphorylation activity reversing the defective betaAR internalization. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
MAP4K4 | down-regulates activity 
phosphorylation
|
PIK3CA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277921 |
Thr1061 |
KMDWIFHtIKQHALN |
in vitro |
|
| pmid |
sentence |
| 38060450 |
MST1/2 and HGK inhibit catalytic activity of p110α through phosphorylation at T1061 |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
STK3 | down-regulates activity
phosphorylation
|
PIK3CA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277922 |
Thr1061 |
KMDWIFHtIKQHALN |
in vitro |
|
| pmid |
sentence |
| 38060450 |
MST1/2 and HGK inhibit catalytic activity of p110α through phosphorylation at T1061 |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
STK4 | down-regulates activity
phosphorylation
|
PIK3CA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277920 |
Thr1061 |
KMDWIFHtIKQHALN |
in vitro |
|
| pmid |
sentence |
| 38060450 |
MST1/2 and HGK inhibit catalytic activity of p110α through phosphorylation at T1061 |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
PIK3CA | up-regulates quantity
chemical modification
|
PIP3 |
0.8 |
| 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. |
|
| 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 |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Prostate Cancer |
| + |
PKI-587 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-205989 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3AP1 | up-regulates
binding
|
PIK3CA |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191664 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 22187458 |
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. Therefore, bcap is an essential activator of the pi3k pathway downstream of tlr signaling, providing a brake to limit potentially pathogenic excessive tlr responses. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PIK3CA |
0.908 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175204 |
|
|
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: | Colorectal Carcinoma, Glioblastoma Multiforme, Luminal Breast Cancer, Rhabdomyosarcoma |
| + |
GSK1059615 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-192771 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CH5132799 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-190943 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GNB1 | up-regulates
binding
|
PIK3CA |
0.549 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145119 |
|
|
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 |
| + |
GNG2 | up-regulates
binding
|
PIK3CA |
0.46 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154255 |
|
|
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-145122 |
|
|
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 |
| + |
PIK3R1 | up-regulates activity
binding
|
PIK3CA |
0.935 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242637 |
|
|
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 |
| Pathways: | Glioblastoma Multiforme, MTOR Signaling, IGF and Myogenesis |
| + |
XL147 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207854 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PI-103 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206163 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3R3 | up-regulates
binding
|
PIK3CA |
0.841 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-53597 |
|
|
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 |
| + |
PIK3CA | up-regulates 
|
MTOR |
0.533 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-180453 |
|
|
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: | Glioblastoma Multiforme, MTOR Signaling |
| + |
DAB2IP | down-regulates activity
binding
|
PIK3CA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254750 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27858941 |
DAB2IP inhibits the PI3K–AKT axis by directly interacting with both proteins, reducing phosphorylation and activation of AKT. The GAP activity of DAB2IP can further enforce inhibition of the PI3K–AKT axis by reducing Ras-dependent activation of PI3K p110α subunit. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | up-regulates activity
phosphorylation
|
AKT |
0.813 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244429 |
|
|
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: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, Luminal Breast Cancer, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Prostate Cancer, Rhabdomyosarcoma |
| + |
TRAF6 | up-regulates activity
ubiquitination
|
PIK3CA |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278727 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29729098 |
In contrast to NEDD4L, overexpression of TRAF6 increases the stability of PIK3CA protein and promotes PI3K activation.|TRAF6 ubiquitinates PIK3CA in vivo. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NRAS | up-regulates activity
binding
|
PIK3CA |
0.839 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175222 |
|
|
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: | Malignant Melanoma |
| + |
HRAS | up-regulates activity
binding
|
PIK3CA |
0.923 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236443 |
|
|
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: | EGFR Signaling, Glioblastoma Multiforme |
| + |
PIK3CA | up-regulates activity
|
AKT1 |
0.813 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235914 |
|
|
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-236353 |
|
|
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, |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236428 |
|
|
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-252634 |
|
|
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 |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Tissue: |
Colonic Cancer Cell, Breast Cancer Cell |
| Pathways: | Glioblastoma Multiforme, IGF and Myogenesis |
| + |
IRS2 | up-regulates activity
binding
|
PIK3CA |
0.675 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251492 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22810696 |
These results strongly suggest that the IGF2–IGF1R–IRS2 axis signals to PI3K in CRC and imply that therapeutic targeting of the pathway could act to block PI3K activity in this subset of patients. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Colorectal Carcinoma |
| + |
PIK-90 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206223 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CUDC-907 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191212 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| 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
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-204490 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
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
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-192604 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | up-regulates
|
AKT2 |
0.661 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141814 |
|
|
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 |
| + |
GNG3 | up-regulates
binding
|
PIK3CA |
0.363 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145125 |
|
|
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 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154258 |
|
|
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 |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | up-regulates activity
phosphorylation
|
BTK |
0.497 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249610 |
|
|
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 |
| + |
PIK3CA | up-regulates
|
RAC1 |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175238 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
Pi3k can also activate rac, and this activation is involved in cytoskeleton reorganization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | form complex 
binding
|
PI3K |
0.935 |
| 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 |
| + |
PP121 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206292 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XL765 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207872 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PIK3CA | up-regulates activity
|
AKT |
0.813 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236436 |
|
|
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 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Breast Cancer Cell |
| Pathways: | AMPK Signaling, EGFR Signaling, Glioblastoma Multiforme, Luminal Breast Cancer, mTOR in cancer, Malignant Melanoma, MTOR Signaling, Prostate Cancer, Rhabdomyosarcoma |
| + |
PIK3CA | down-regulates activity 
|
IRS1 |
0.713 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-104911 |
|
|
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: | AMPK Signaling, Luminal Breast Cancer, mTOR in cancer, MTOR Signaling, IGF and Myogenesis |
| + |
TNF | up-regulates activity
|
PIK3CA |
0.276 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-70616 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | MTOR Signaling |
| + |
AFAP1L2 | up-regulates activity
binding
|
PIK3CA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263193 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 19060924 |
RET/PTC induced robust tyrosine phosphorylation of XB130, which promoted its subsequent association with the p85alpha subunit of phosphatidylinositol 3-kinase (PI 3-kinase). We identified tyrosine 54 of XB130 as the major target of RET/PTC-mediated phosphorylation and a critical binding site for the SH2 domains of p85alpha. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GSK2126458 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-192892 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERBB4 | up-regulates
binding
|
PIK3CA |
0.598 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146879 |
|
|
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 |
| + |
wortmannin | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-36557 |
|
|
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-26677 |
|
|
Homo sapiens |
|
| 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 |
| + |
BKM120 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-190383 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GNGT1 | up-regulates
binding
|
PIK3CA |
0.412 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-154261 |
|
|
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-145128 |
|
|
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 |
| + |
torkinib | down-regulates activity
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258269 |
|
|
in vitro |
|
| pmid |
sentence |
| 22037378 |
Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. | The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
HRAS | up-regulates
binding
|
PIK3CA |
0.923 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-35878 |
|
|
Homo sapiens |
|
| 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: |
Homo Sapiens |
| Pathways: | EGFR Signaling, Glioblastoma Multiforme |
| + |
PIK3CA | up-regulates
|
Survival |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242649 |
|
|
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 |
| Pathways: | Colorectal Carcinoma, Glioblastoma Multiforme, Luminal Breast Cancer, Malignant Melanoma, Prostate Cancer, Rhabdomyosarcoma |
| + |
pictrelisib | down-regulates activity
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258113 |
|
|
in vitro |
|
| pmid |
sentence |
| 22037378 |
Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. | The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
ITGB4 | up-regulates
binding
|
PIK3CA |
0.396 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-54530 |
|
|
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 |
| + |
dactolisib | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175706 |
|
|
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 21803746 |
The dual pi3k and mtorc1/2 inhibitor bez235 was highly specific |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
pictrelisib | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-176292 |
|
|
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 |
| + |
PIK-75 Hydrochloride | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206211 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
D-106669 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191256 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IC-87114 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206184 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GAB1 | up-regulates
binding
|
PIK3CA |
0.432 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-83343 |
|
|
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: | EGFR Signaling, Rhabdomyosarcoma |
| + |
IRS1 | up-regulates activity
binding
|
PIK3CA |
0.713 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168985 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20966354 |
Irs proteins are capable of both regulating and activating pi3k, depending on the cell of origin. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | AMPK Signaling, Luminal Breast Cancer, mTOR in cancer, MTOR Signaling, IGF and Myogenesis |
| + |
ZSTK-474 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207935 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GAB2 | up-regulates
binding
|
PIK3CA |
0.448 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-204966 |
|
|
Homo sapiens |
T-lymphocyte, Leukemia Cell, Lymphoma Cell |
| 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 |
| + |
PI-103 | down-regulates activity
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258266 |
|
|
in vitro |
|
| pmid |
sentence |
| 22037378 |
Our data set represents the most detailed comprehensive assessment of the reactivity of known and clinical kinase inhibitors across the kinome published to date. | The data also show that for at least 15 of the 27 kinases that are the primary, intended targets for the compounds tested and that are represented in the assay panel, selective inhibitors, as assessed by both absolute selectivity across the kinome and selectivity relative to the primary target, are among the 72 tested here. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
PKI-402 | down-regulates
chemical inhibition
|
PIK3CA |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206250 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTEN | down-regulates activity
|
PIK3CA |
0.726 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-209856 |
|
|
Homo sapiens |
|
| 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: | Colorectal Carcinoma, Glioblastoma Multiforme, Luminal Breast Cancer, Malignant Melanoma, MTOR Signaling, Prostate Cancer |
| + |
ERBB3 | up-regulates
binding
|
PIK3CA |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-146861 |
|
|
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 |
| + |
GNG12 | up-regulates
binding
|
PIK3CA |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141795 |
|
|
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 |
| + |
GNB3 | up-regulates
binding
|
PIK3CA |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-120264 |
|
|
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 |
| + |
LAT | up-regulates activity
binding
|
PIK3CA |
0.393 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-246065 |
|
|
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 |
3.0
PIK3CA
- 
- 