| + |
PRKCA | down-regulates activity 
phosphorylation
|
KIT |
0.51 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248898 |
Ser741 |
TKADKRRsVRIGSYI |
Sus scrofa |
Porcine Aortic Endothelial Cell |
| pmid |
sentence |
| 7539802 |
We present here the identification of the major phosphorylation sites for PKC in Kit/SCFR. Two serine residues in the kinase insert, Ser-741 and Ser-746, are PKC-dependent phosphorylation sites in vivo and account for all phosphorylation by PKC in vitro. | Two additional serine residues, Ser-821 close to the major tyrosine autophosphorylation site in the kinase domain and Ser-959 in the carboxyl terminus are SCF-stimulated PKC-dependent phosphorylation sites. | Furthermore, the kinase activity of Kit/SCFR(S741A/S746A) toward an exogenous substrate was increased, which was reflected as a decreased Km and an increased Vmax, in accordance with the negative regulatory role of PKC on Kit/SCFR signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248899 |
Ser746 |
RRSVRIGsYIERDVT |
Sus scrofa |
|
| pmid |
sentence |
| 7539802 |
We present here the identification of the major phosphorylation sites for PKC in Kit/SCFR. Two serine residues in the kinase insert, Ser-741 and Ser-746, are PKC-dependent phosphorylation sites in vivo and account for all phosphorylation by PKC in vitro. | Two additional serine residues, Ser-821 close to the major tyrosine autophosphorylation site in the kinase domain and Ser-959 in the carboxyl terminus are SCF-stimulated PKC-dependent phosphorylation sites. | Furthermore, the kinase activity of Kit/SCFR(S741A/S746A) toward an exogenous substrate was increased, which was reflected as a decreased Km and an increased Vmax, in accordance with the negative regulatory role of PKC on Kit/SCFR signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248897 |
Ser821 |
ARDIKNDsNYVVKGN |
Sus scrofa |
|
| pmid |
sentence |
| 7539802 |
We present here the identification of the major phosphorylation sites for PKC in Kit/SCFR. Two serine residues in the kinase insert, Ser-741 and Ser-746, are PKC-dependent phosphorylation sites in vivo and account for all phosphorylation by PKC in vitro. | Two additional serine residues, Ser-821 close to the major tyrosine autophosphorylation site in the kinase domain and Ser-959 in the carboxyl terminus are SCF-stimulated PKC-dependent phosphorylation sites. | Furthermore, the kinase activity of Kit/SCFR(S741A/S746A) toward an exogenous substrate was increased, which was reflected as a decreased Km and an increased Vmax, in accordance with the negative regulatory role of PKC on Kit/SCFR signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248900 |
Ser959 |
DHSVRINsVGSTASS |
Sus scrofa |
Porcine Aortic Endothelial Cell |
| pmid |
sentence |
| 7539802 |
We present here the identification of the major phosphorylation sites for PKC in Kit/SCFR. Two serine residues in the kinase insert, Ser-741 and Ser-746, are PKC-dependent phosphorylation sites in vivo and account for all phosphorylation by PKC in vitro. | Two additional serine residues, Ser-821 close to the major tyrosine autophosphorylation site in the kinase domain and Ser-959 in the carboxyl terminus are SCF-stimulated PKC-dependent phosphorylation sites. | Furthermore, the kinase activity of Kit/SCFR(S741A/S746A) toward an exogenous substrate was increased, which was reflected as a decreased Km and an increased Vmax, in accordance with the negative regulatory role of PKC on Kit/SCFR signaling. |
|
| Publications: |
4 |
Organism: |
Sus Scrofa |
| + |
PRKCA | down-regulates
phosphorylation
|
KIT |
0.51 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-28601 |
Ser741 |
TKADKRRsVRIGSYI |
Homo sapiens |
|
| pmid |
sentence |
| 7539802 |
Phosphorylation of kit/scfr by pkc-_ in vitro: identification of ser-741 and ser-746 as the major phosphorylation sites for pkc / pkc, which acts in an scf-stimulated feedback loop, that negatively controls kit/scfr kinase activity |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-28605 |
Ser746 |
RRSVRIGsYIERDVT |
Homo sapiens |
|
| pmid |
sentence |
| 7539802 |
Phosphorylation of kit/scfr by pkc-_ in vitro: identification of ser-741 and ser-746 as the major phosphorylation sites for pkc / pkc, which acts in an scf-stimulated feedback loop, that negatively controls kit/scfr kinase activity |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
KIT | down-regulates activity
phosphorylation
|
SLA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263140 |
Tyr120 |
SETKKGFySLSVRHR |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 24284075 |
Oncogenic c-Kit-D816V phosphorylates SLAP on residues Y120, Y258 and Y273. Mutation of the SLAP tyrosine phosphorylation sites rescues its activity |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263141 |
Tyr258 |
KKSISLMyGGSKRKS |
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 24284075 |
Oncogenic c-Kit-D816V phosphorylates SLAP on residues Y120, Y258 and Y273. Mutation of the SLAP tyrosine phosphorylation sites rescues its activity |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263142 |
Tyr273 |
SFFSSPPyFED |
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 24284075 |
Oncogenic c-Kit-D816V phosphorylates SLAP on residues Y120, Y258 and Y273. Mutation of the SLAP tyrosine phosphorylation sites rescues its activity |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops |
| + |
KIT | up-regulates activity 
phosphorylation
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102633 |
Tyr568 |
EEINGNNyVYIDPTQ |
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 12824176 |
Upon binding its ligand, stem cell factor (scf), c-kit forms an active dimer that autophosphorylates itself and activates a signaling cascade that induces cell growth./ Tyr-568 and tyr-570 are significantly phosphorylated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102637 |
Tyr570 |
INGNNYVyIDPTQLP |
Homo sapiens |
|
| pmid |
sentence |
| 12824176 |
Upon binding its ligand, stem cell factor (scf), c-kit forms an active dimer that autophosphorylates itself and activates a signaling cascade that induces cell growth./ Tyr-568 and tyr-570 are significantly phosphorylated |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-102641 |
Tyr823 |
DIKNDSNyVVKGNAR |
Homo sapiens |
|
| pmid |
sentence |
| 12824176 |
Upon binding its ligand, stem cell factor (scf), c-kit forms an active dimer that autophosphorylates itself and activates a signaling cascade that induces cell growth. / tyr-823 is the last tyrosine residue to be autophosphorylated |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML, Malignant Melanoma |
| + |
KIT | up-regulates activity
phosphorylation
|
STAT1 |
0.714 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251365 |
Tyr701 |
DGPKGTGyIKTELIS |
in vitro |
|
| pmid |
sentence |
| 21135090 |
KIT is responsible for the permanent phosphorylation of all three STAT proteins. STAT1, -3, and -5 were phosphorylated on their activation-specific Tyr701, Tyr704, and Tyr694, respectively, following KIT stimulation. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
PTPRG | down-regulates activity
dephosphorylation
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254709 |
Tyr703 |
DHAEAALyKNLLHSK |
in vitro |
|
| pmid |
sentence |
| 25624455 |
PTPRG activation by the P1-WD peptide affected the tyrosine phosphorylation of several signaling molecules. Data analysis identified 31 molecules whose phosphorylation was modified in a statistically significant manner (Table I). inhibition of ABL1, BMX, BTK, DAB1, ITGB1, JAK2, KDR, KIT, LIMK1, MET, PDGFRB, SHC1, and VCL correlates with tyrosine dephosphorylation. In contrast, SRC inhibition correlates with hyperphosphorylation of the inhibitory Tyr530 residue and with dephosphorylation of the activatory Tyr419. Moreover, CDK2 and CTTN inhibition correlates with a hyperphosphorylation of the inhibitory Tyr15 and Tyr470, respectively. In contrast, a subgroup of 13 proteins, including BLNK, DOK2, ERBB2, GRIN2B, INSR, PDGFRA, PRKCD, PXN, STAT1, STAT2, STAT3, STAT5A, and ZAP70, appears to be activated by PTPRG activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254710 |
Tyr730 |
DMKPGVSyVVPTKAD |
in vitro |
|
| pmid |
sentence |
| 25624455 |
PTPRG activation by the P1-WD peptide affected the tyrosine phosphorylation of several signaling molecules. Data analysis identified 31 molecules whose phosphorylation was modified in a statistically significant manner (Table I). inhibition of ABL1, BMX, BTK, DAB1, ITGB1, JAK2, KDR, KIT, LIMK1, MET, PDGFRB, SHC1, and VCL correlates with tyrosine dephosphorylation. In contrast, SRC inhibition correlates with hyperphosphorylation of the inhibitory Tyr530 residue and with dephosphorylation of the activatory Tyr419. Moreover, CDK2 and CTTN inhibition correlates with a hyperphosphorylation of the inhibitory Tyr15 and Tyr470, respectively. In contrast, a subgroup of 13 proteins, including BLNK, DOK2, ERBB2, GRIN2B, INSR, PDGFRA, PRKCD, PXN, STAT1, STAT2, STAT3, STAT5A, and ZAP70, appears to be activated by PTPRG activity. |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
KIT | up-regulates
phosphorylation
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68643 |
Tyr703 |
DHAEAALyKNLLHSK |
Homo sapiens |
|
| pmid |
sentence |
| 10377264 |
Identification of tyr-703 and tyr-936 as autophosphorylation sites in c-kit/scfr |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68647 |
Tyr936 |
SESTNHIySNLANCS |
Homo sapiens |
|
| pmid |
sentence |
| 10377264 |
Identification of tyr-703 and tyr-936 as autophosphorylation sites in c-kit/scfr |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML, Malignant Melanoma |
| + |
SRC | up-regulates activity
phosphorylation
|
KIT |
0.395 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-103999 |
Tyr900 |
EHAPAEMyDIMKTCW |
Homo sapiens |
|
| pmid |
sentence |
| 12878163 |
C-src phosphorylates tyr900 in the second part of the kinase domain of c-kit. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOHLH2 | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.332 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266206 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 22328502 |
Our results suggest that SOHLH1 and SOHLH2 directly stimulate Kit transcription in postnatal spermatogonia, thus activating the signaling involved in spermatogonia differentiation and spermatogenetic progression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CBLB | down-regulates activity
ubiquitination
|
KIT |
0.333 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260105 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15315962 |
KIT binds to and induces the phosphorylation of Cbl proteins, which in turn act as E3 ligases, mediating the ubiquitination and degradation of KIT and themselves. Tyrosine kinase binding and RING finger domains of Cbl are essential for Cbl-mediated ubiquitination and degradation of KIT. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
DAB2IP | down-regulates quantity by repression 
transcriptional regulation
|
KIT |
0.278 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254769 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27858941 |
DAB2IP suppresses transcription of stem cell factor receptor CD117, by interacting with GATA-1 on a silencer element on its gene |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
dovitinib; bis(lactic acid) | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191421 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SLA | down-regulates quantity by destabilization
ubiquitination
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263143 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 24284075 |
In this report, we show that SLAP associates with both wild-type and oncogenic c-Kit (c-Kit-D816V). The association involves the SLAP SH2 domain and receptor phosphotyrosine residues different from those mediating Src interaction. Association of SLAP triggers c-Kit ubiquitylation which, in turn, is followed by receptor degradation |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
N-(1,3-benzodioxol-5-ylmethyl)-4-(4-benzofuro[3,2-d]pyrimidinyl)-1-piperazinecarbothioamide | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-189525 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GATA1 | down-regulates quantity by repression
transcriptional regulation
|
KIT |
0.406 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254771 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27858941 |
DAB2IP suppresses transcription of stem cell factor receptor CD117, by interacting with GATA-1 on a silencer element on its gene |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOHLH1 | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.355 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266205 |
|
|
|
HEK-293T Cell |
| pmid |
sentence |
| 22328502 |
Our results suggest that SOHLH1 and SOHLH2 directly stimulate Kit transcription in postnatal spermatogonia, thus activating the signaling involved in spermatogonia differentiation and spermatogenetic progression. |
|
| Publications: |
1 |
| + |
PTPN6 | down-regulates
binding
|
KIT |
0.557 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56104 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9528781 |
Shp-1 binds and negatively modulates the c-kit receptor by interaction with tyrosine 569 in the c-kit juxtamembrane domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
KIT | up-regulates activity
binding
|
GRB7 |
0.566 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248291 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 10377264 |
We furthermore demonstrate that the adapter protein Grb2 is a specific binding partner for both phosphorylated Tyr-703 and phosphorylated Tyr-936, whereas the adapter protein Grb7 binds selectively to phosphorylated Tyr-936. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KIT | up-regulates
phosphorylation
|
SRC_kinase_family |
0.576 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254995 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15526160 |
Binding of SCF to c-Kit leads to a rapid increase in SFK kinase activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
nilotinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258257 |
|
|
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 |
| + |
vatalanib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207648 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
masitinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-194257 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KITLG | up-regulates
binding
|
KIT |
0.933 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-21193 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1698556 |
We have also provided biological and physical evidence that scf is a ligand for the c-kit receptor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma |
| + |
regorafenib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206415 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
imatinib methanesulfonate | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-193393 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
3-(4-quinolinylmethylamino)-N-[4-(trifluoromethoxy)phenyl]-2-thiophenecarboxamide | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195675 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Ast-487 | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258070 |
|
|
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. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259694 |
|
|
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: |
2 |
Organism: |
In Vitro |
| + |
STAP1 | up-regulates activity
binding
|
KIT |
0.484 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261822 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10679268 |
STAP-1 was tyrosine-phosphorylated by activated c-kit. An in vitro binding assay suggested that the STAP-1 SH2 domain interacted with several tyrosine-phosphorylated proteins including c-kit and STAT5. These suggest that STAP-1 functions as an adaptor molecule downstream of c-kit in hematopoietic stem cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
axitinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171866 |
|
|
Homo sapiens |
Breast Cancer Cell |
| pmid |
sentence |
| 21297102 |
The inhibitory effect of four tkis (axitinib, imatinib, masitinib, and vatalanib) for proliferation and phosphorylation of c-kit receptor as well as the expression and function of abcb1 were investigated in three cmct cell lines (hrmc, vimc1, and cmmc1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
midostaurin | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258248 |
|
|
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 |
| Pathways: | Acute Myeloid Leukemia |
| + |
cabozantinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262243 |
|
|
Homo sapiens |
Medullary Thyroid Carcinoma Cell |
| pmid |
sentence |
| 26536165 |
Cabozantinib (XL184) is a small-molecule kinase inhibitor with potent activity toward MET and VEGF receptor 2 (VEGFR2), as well as a number of other receptor tyrosine kinases that have also been implicated in tumor pathobiology, including RET, KIT, AXL, and FLT3. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
tandutinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258297 |
|
|
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 |
| + |
KIT | up-regulates activity
binding, phosphorylation,
|
PI3K |
0.709 |
| 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. |
|
| 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 |
|
| Publications: |
3 |
Organism: |
Mus Musculus, Homo Sapiens, Chlorocebus Aethiops |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
| + |
motesanib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-194569 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KIT | up-regulates activity
phosphorylation
|
STAP1 |
0.484 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261820 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10679268 |
STAP-1 was tyrosine-phosphorylated by activated c-kit. An in vitro binding assay suggested that the STAP-1 SH2 domain interacted with several tyrosine-phosphorylated proteins including c-kit and STAT5. These suggest that STAP-1 functions as an adaptor molecule downstream of c-kit in hematopoietic stem cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
tandutinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207212 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
pazopanib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257736 |
|
|
Homo sapiens |
HUVEC Cell |
| pmid |
sentence |
| 18620382 |
Pyrimidine 13 showed good potency against all the human VEGFR receptors with an IC50 of 10, 30, and 47 nM for VEGFR-1, -2, and -3, respectively. Significant activity was also seen against the closely related tyrosine receptor kinases PDGFRβ, c-Kit, FGF-R1, and c-fms with IC50’s of 84, 74, 140, and 146 nM, respectively. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
pazopanib hydrochloride | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-201250 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
imatinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-193375 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
sunitinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257851 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20570526 |
Sunitinib [inhibits KDR, PDGFR2, PDGFRβ, c-KIT and FLT3; approved for the treatment of renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors], |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258291 |
|
|
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: |
2 |
Organism: |
Homo Sapiens, In Vitro |
| + |
sunitinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-176760 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21993628 |
The action of kit kinase inhibitors, especially imatinib, sunitinib, dasatinib and pkc412, on different primary and secondary mutants is discussed. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KIT | up-regulates activity
binding
|
PIK3R1 |
0.716 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255948 |
|
|
Chlorocebus aethiops |
|
| 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 |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
KIT | up-regulates activity
phosphorylation
|
PTPN11 |
0.671 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256140 |
|
|
Mus musculus |
32D Cell |
| pmid |
sentence |
| 22806893 |
SHP2 can be phosphorylated at 2 C-terminal tyrosyl residues by receptor tyrosine kinases, including KIT as well as cytosolic tyrosine kinases, including Src and Abl. The level of tyrosyl phosphorylation of SHP2 has been associated with its recruitment to the receptor.Thus, pharmacologic inhibition of SHP2 phosphatase function might permit SHP2 to return to its inactive conformation resulting in reduced tyrosine phosphorylation. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
quizartinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258271 |
|
|
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 |
| + |
KIT | up-regulates activity 
|
ERK1/2 |
0.31 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254947 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 15526160 |
A number of studies have demonstrated the ability of SCF to activate the Ras-Erk pathway. The adapter protein Grb2 can directly associate with phosphorylated Y703 and Y936 in c-Kit |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma |
| + |
CBL | down-regulates activity
ubiquitination
|
KIT |
0.601 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260104 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15315962 |
KIT binds to and induces the phosphorylation of Cbl proteins, which in turn act as E3 ligases, mediating the ubiquitination and degradation of KIT and themselves. Tyrosine kinase binding and RING finger domains of Cbl are essential for Cbl-mediated ubiquitination and degradation of KIT. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML |
| + |
AML1-ETO | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255699 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29236325 |
We report here that AML1/ETO transactivates c-KIT expression through directly binding to and mediating the long-range interaction between the promoter and intronic enhancer regions of c-KIT. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML |
| + |
lapatinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-257901 |
|
|
Homo sapiens |
HUVEC Cell |
| pmid |
sentence |
| 21443688 |
YN968D1 potently suppressed the kinase activities of VEGFR-2, c-kit and c-src, and inhibited cellular phosphorylation of VEGFR-2, c-kit and PDGFRβ. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
4-amino-5-fluoro-3-[5-(4-methyl-1-piperazinyl)-1,3-dihydrobenzimidazol-2-ylidene]-2-quinolinone | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-191409 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FUBP1 | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259132 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30500954 |
Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RUNX1 | up-regulates quantity by expression
transcriptional regulation
|
KIT |
0.341 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259133 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30500954 |
Notably, upregulation of c-KIT expression by FUBP1 and RUNX1 promotes cell proliferation and renders cells more resistant to the c-KIT inhibitor imatinib mesylate, a common therapeutic drug. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
| + |
masitinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258244 |
|
|
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 |
| + |
Telatinib | down-regulates
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-207227 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
sorafenib tosylate | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259226 |
|
|
in vitro |
|
| pmid |
sentence |
| 16757355 |
Further characterization of sorafenib revealed that this molecule was a multikinase inhibitor that targeted the vascular endothelial growth factor receptor family (VEGFR-2 and VEGFR-3) and platelet-derived growth factor receptor family (PDGFR-beta and Kit), which play key roles in tumor progression and angiogenesis. The in vitro and cellular profile of sorafenib is summarized in Table I. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
KITLG | up-regulates activity
binding
|
KIT |
0.933 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254946 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17259966 |
The most relevant and still unique mast-cell growth factor is SCF, which is the ligand of KIT, a receptor with tyrosine-kinase activity that is expressed on the surface of all human and murine mast cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma |
| + |
imatinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258225 |
|
|
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 |
| + |
CHEK2 | up-regulates
phosphorylation
|
KIT |
0.291 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-197281 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22558186 |
In this report, we characterize the binding of sh2(chk) to specific phosphotyrosine sites on the c-kit protein sequence. the sh2(chk) binding to the two sites is direct and not through phosphorylated intermediates such as fyn or shc. this indicates that chk binds to the same site on c-kit to which fyn binds, possibly bringing the two into proximity on associated c-kit subunits and leading to the down-regulation of fyn by chk. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
GRB2 | down-regulates
|
KIT |
0.635 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-157956 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 17904548 |
Grb2 mediates c-kit degradation through recruitment of cbl to c-kit, leading to ubiquitination of c-kit followed by internalization and degradation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma |
| + |
KIT | up-regulates activity
binding
|
JAK2 |
0.597 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254954 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15526160 |
C-Kit stimulates rapid and transient tyrosine phosphorylation of JAK2. JAK2 was found to be constitutively associated with c-Kit, with increased association after ligand stimulation of c-Kit |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Onco-fusion proteins in AML, KIT in AML |
| + |
ponatinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259272 |
|
|
Homo sapiens |
HMC-1 Cell |
| pmid |
sentence |
| 23539538 |
Ponatinib was found to inhibit the kinase activity of KIT G560V and KIT D816V in the human mast cell leukemia cell line HMC-1. In addition, ponatinib was found to block Lyn- and STAT5 activity in neoplastic mast cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOCS6 | down-regulates
ubiquitination
|
KIT |
0.665 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-169145 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21030588 |
Suppressor of cytokine signaling 6 (socs6) is a member of the socs family of e3 ubiquitin ligases that can interact with c-kit and suppress c-kit-dependent pathways. / we demonstrate that socs6 has ubiquitin ligase activity toward c-kit and regulates c-kit protein turnover in cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
axitinib | down-regulates activity
chemical inhibition
|
KIT |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258073 |
|
|
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 |
| + |
KIT | up-regulates activity
binding
|
GRB2 |
0.635 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-248283 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10377264 |
We furthermore demonstrate that the adapter protein Grb2 is a specific binding partner for both phosphorylated Tyr-703 and phosphorylated Tyr-936, whereas the adapter protein Grb7 binds selectively to phosphorylated Tyr-936. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, KIT in AML, Malignant Melanoma |
3.0
KIT
- 
- 