| + |
LZTR1 | down-regulates activity 
ubiquitination
|
KRAS |
0.253 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269068 |
Lys170 |
IRQYRLKkISKEEKT |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 30442762 |
By trapping LZTR1 complexes from intact mammalian cells, we identified the guanosine triphosphatase RAS as a substrate for the LZTR1-CUL3 complex. Ubiquitome analysis showed that loss of Lztr1 abrogated Ras ubiquitination at lysine-170. LZTR1-mediated ubiquitination inhibited RAS signaling by attenuating its association with the membrane. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates 
phosphorylation, binding
|
MAP3K1 |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-92793 |
Ser67 |
RQLRKVRsVELDQLP |
Homo sapiens |
|
| pmid |
sentence |
| 12228228 |
Activation of ras may lead to two distinct ras-dependent pathways involving either a raf1/mek/mapk module or a mekk/sek/sapk module; jnk/sapk binds to the d domain near the nh2 terminus of mekk1 from approximately residues 6270 (9, 10). Pak1 can phosphorylate mekk1 on serine 67 within its jnk/sapk-binding d domain. Phosphorylation of mekk1 on serine 67 alters the state of the d domain, thereby decreasing its affinity for jnk/sapk. Under these conditions jnk/sapk is not recruited into the mekk1 signaling module. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-41953 |
Ser67 |
RQLRKVRsVELDQLP |
Homo sapiens |
B-lymphocyte, Lymphoma Cell |
| pmid |
sentence |
| 8649450 |
Activation of ras may lead to two distinct ras-dependent pathways involving either a raf1/mek/mapk module or a mekk/sek/sapk module; jnk/sapk binds to the d domain near the nh2 terminus of mekk1 from approximately residues 6270 (9, 10). Pak1 can phosphorylate mekk1 on serine 67 within its jnk/sapk-binding d domain. Phosphorylation of mekk1 on serine 67 alters the state of the d domain, thereby decreasing its affinity for jnk/sapk. Under these conditions jnk/sapk is not recruited into the mekk1 signaling module. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32620 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 7744823 |
Mitogen-activated protein kinase kinase kinase (mekk1) is a serine-threonine kinase that regulates sequential protein kinase pathways involving stress-activated protein kinases and mitogen-activated protein kinases. Mekk1 is activated in response to growth factor stimulation of cells and by expression of activated ras. mekk1 directly binds ras.GTP. Thus, ras interacts with protein kinases of both the raf and mekk families. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
PTPN11 | up-regulates activity
dephosphorylation
|
KRAS |
0.647 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255982 |
Tyr32 |
QNHFVDEyDPTIEDS |
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 26617336 |
Here we identify SHP2 as the ubiquitously expressed tyrosine phosphatase that preferentially binds to and dephosphorylates Ras to increase its association with Raf and activate downstream proliferative Ras/ERK/MAPK signalling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, FLT3-ITD signaling, Noonan syndrome |
| + |
KRAS | up-regulates 
|
MAP4K5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64262 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 9949177 |
Bcr-abl_mediated ras activation is crucial for the ability of bcr-abl to activate gckr and is consistent with the previously known requirement for ras in bcr-abl_induced sapk activation how ras activates gckr remains enigmatic. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PTPN2 | down-regulates activity
dephosphorylation
|
KRAS |
0.279 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33122197 |
Mechanistically, PTPN2 negatively regulates tyrosine phosphorylation of KRAS, which, in turn, affects the activation KRAS and its downstream signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
phosphorylation
|
TCF3 |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-56144 |
|
|
Homo sapiens |
B-lymphocyte |
| pmid |
sentence |
| 9528794 |
Our results are consistent with a model in which notch and deltex act on e47 by inhibiting signaling through ras. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RASGEF1A | up-regulates
guanine nucleotide exchange factor
|
KRAS |
0.402 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183826 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19201597 |
Gefs catalyse the transition from gdp-bound, inactive ras to gtp-bound, active ras. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PIK3CA |
0.907 |
| 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 |
| + |
KRAS | down-regulates activity 
|
CARM1 |
0.275 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267640 |
|
|
Homo sapiens |
PANC-1 Cell |
| pmid |
sentence |
| 27840030 |
Interestingly, overexpression of KRASG12V (an activating mutant) in BxPC-3 cells, a PDAC cell line carrying wild-type KRAS, led to a 40% decrease of CARM1 protein and consequent hypomethylation or activation of MDH1|These observations indicate that KRAS suppresses CARM1-mediated MDH1 methylation, contributing to Gln metabolism in pancreatic cancer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RASGEF1C | up-regulates
binding
|
KRAS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-161508 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19201597 |
Gefs catalyse the transition from gdp-bound, inactive ras to gtp-bound, active ras. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOS1 | up-regulates
guanine nucleotide exchange factor
|
KRAS |
0.821 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-201703 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25624485 |
Because the KRAS-GDP to KRAS-GTP transition catalyzed by the GEF, son of sevenless 1 (SOS1), represents the rate-limiting step for nucleotide exchange, disrupting the activating SOS1/KRAS protein interaction has also been the focus of drug development efforts |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141647 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25624485 |
Because the KRAS-GDP to KRAS-GTP transition catalyzed by the GEF, son of sevenless 1 (SOS1), represents the rate-limiting step for nucleotide exchange, disrupting the activating SOS1/KRAS protein interaction has also been the focus of drug development efforts |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175256 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25624485 |
Because the KRAS-GDP to KRAS-GTP transition catalyzed by the GEF, son of sevenless 1 (SOS1), represents the rate-limiting step for nucleotide exchange, disrupting the activating SOS1/KRAS protein interaction has also been the focus of drug development efforts |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-122075 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25624485 |
Because the KRAS-GDP to KRAS-GTP transition catalyzed by the GEF, son of sevenless 1 (SOS1), represents the rate-limiting step for nucleotide exchange, disrupting the activating SOS1/KRAS protein interaction has also been the focus of drug development efforts |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, COVID-19 Causal Network, Colorectal Carcinoma, Glioblastoma Multiforme, Luminal Breast Cancer, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Rhabdomyosarcoma, SARS-CoV MAPK PERTURBATION, Thyroid cancer |
| + |
Av/b3 integrin | up-regulates activity
binding
|
KRAS |
0.346 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277742 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 32745890 |
Oncogenic RAS requires a protein scaffold to induce downstream signaling and macropinocytosis, three separate studies have identified upstream and downstream regulators that help drive this process in cancer cells. Anchorage-independent growth of cancer cells is supported by avb3 integrins which can be clustered by the extracellular lectin, galectin-3 to drive mutant RAS-mediated macropinocytosis for nutrient supplementation and growth of anchorage-independent cells. Secreted galectin-3 was found to bind to the N-glycans on surface avb3 integrins, clustering the integrins on the surface of the nonadherent cells for the recruitment of mutant KRAS as a signaling platform for inducing macropinocytosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TRiC | up-regulates quantity by stabilization
binding
|
KRAS |
0.269 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272871 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 36185250 |
Mammalian cells contain an evolutionarily conserved type II chaperonin called chaperonin containing tailless complex polypeptide 1 (CCT) or tailless complex polypeptide 1 ring complex (TRiC). The CCT complex is composed of eight subunits [CCT1-8 (yeast) or CCTα-θ (mammals)] and folds substrates needed for cell invasion and proliferation, such as actin, tubulin, and cell division cycle protein 20 homolog (cdc20), as well as oncoproteins like signal transducer and activator of transcription 3 (STAT3), Kirsten rat sarcoma viral oncogene homolog (KRAS), and Myelocytomatosis (MYC). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates activity
relocalization
|
V-ATPase |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277759 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 31827278 |
V-ATPase is required for macropinocytosis. oncogenic RAS-dependent recruitment of V-ATPase to the plasma membrane constitutes an essential step in induction of macropinocytosis. Here we identify vacuolar ATPase (V-ATPase) as an essential regulator of RAS-induced macropinocytosis. Oncogenic RAS promotes the translocation of V-ATPase from intracellular membranes to the plasma membrane via a pathway that requires the activation of protein kinase A by a bicarbonate- dependent soluble adenylate cyclase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
|
MINK1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-142985 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16337592 |
Mink is activated after ras induction via a mechanism involving reactive oxygen species and mediates stimulation of the stress-activated protein kinase p38 mapk downstream of the raf/erk pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RAPGEF5 | up-regulates
guanine nucleotide exchange factor
|
KRAS |
0.414 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183735 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19201597 |
Gefs catalyse the transition from gdp-bound, inactive ras to gtp-bound, active ras. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates quantity by expression
transcriptional regulation
|
NFE2L2 |
0.437 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267361 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29731393 |
Oncogenic proteins that regulate proliferation, such as KRAS, BRAF, and MYC increase the transcription of NRF2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RIN1 | up-regulates
binding
|
KRAS |
0.58 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-113970 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11784866 |
We demonstrate that the ras effector protein rin1 binds to activated ras with an affinity (k(d), 22 nm) similar to that observed for raf1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PI3K |
0.729 |
| 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) |
| + |
KRAS | up-regulates
binding
|
RAF1 |
0.841 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-141641 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16293107 |
Among other effectors, active ras binds and activates the raf kinase, iniziating a kinase cascade involving serine phosporylation of mek1/2 (mapkk) and tyrosine and threonine phosphorylation of erk1/2. the raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases.. Association of ras with the mapk kinase kinase, raf, initiates the raf mek erk map kinase cascade. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-78911 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10882715 |
Among other effectors, active ras binds and activates the raf kinase, iniziating a kinase cascade involving serine phosporylation of mek1/2 (mapkk) and tyrosine and threonine phosphorylation of erk1/2. the raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases.. Association of ras with the mapk kinase kinase, raf, initiates the raf mek erk map kinase cascade. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, COVID-19 Causal Network, Noonan syndrome, SARS-CoV MAPK PERTURBATION |
| + |
KRAS | up-regulates
|
NFIL3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242757 |
|
|
Mus musculus |
Pro-B-lymphocyte |
| pmid |
sentence |
| 10082541 |
A constitutively active Ras protein [Ras(G12V)] regulates the stable expression of the NFIL3 transcription factor through both the Raf-MAPK and PI3-K pathways. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
FNTB | up-regulates activity
|
KRAS |
0.428 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242556 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24294527 |
Major investments have been made to target Ras through indirect routes. Inhibition of farnesyl transferase to block Ras maturation has failed in large clinical trials. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PIK3CG |
0.768 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59819 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9727023 |
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. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175213 |
|
|
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. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
EML4-ALK | up-regulates
|
KRAS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253216 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19483050 |
A recurrent gene fusion between echinoderm microtubule-associated protein-like 4 (EML4;and, occasionally, of other fusion partners) and the anaplastic lymphoma kinase (ALK) geneoccurs in of NSCLCs , resulting in activation of a potent ALK fusion protein.ALK fusion protein is usually found in never-smoker subjects. Although relatively rare, therelative paucity of fusion proteins known to contribute to lung cancer pathogenesis makes this a finding of biological interest. Although present understanding of the ALK fusion protein is limited, it may play a role in activating RAS. Thus it is negatively associated with thepresence of KRAS or EGFR mutations, and may favour ADC histology and never-smokerstatus. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates activity
binding
|
RASSF1 |
0.638 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249585 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22195963 |
Mutant K-Ras promotes MST2 activation in two ways (i.e., by direct disruption of the inhibitory Raf-1-MST2 complex (Matallanas et al., 2008) and by forming an activating (i.e., by direct disruption of the inhibitory Raf-1-MST2 complex K-Ras-RASSF1AMST2 complex, as reported here |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Non-small-cell lung cancer (NSCLC) |
| + |
RASGEF1B | up-regulates
binding
|
KRAS |
0.301 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-183835 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19201597 |
Gefs catalyse the transition from gdp-bound, inactive ras to gtp-bound, active ras. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates activity
binding
|
BRAF |
0.872 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156906 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
The raf family of proteins (raf-1, a-raf, and b-raf) is serine/threonine kinases that bind to the effector region of ras-gtp, thus inducing translocation of the protein to the plasma membrane. Once there, raf proteins are activated and phosphorylated by different protein kinases. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, BCR-ABL in AML, FLT3 in AML, Colorectal Carcinoma, FLT3-ITD signaling, Glioblastoma Multiforme, Luminal Breast Cancer, Noonan syndrome, Non-small-cell lung cancer (NSCLC), Pancreatic ductal adenocarcinoma (PDA), Rhabdomyosarcoma, Thyroid cancer |
| + |
MVD | up-regulates quantity by stabilization
|
KRAS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265887 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 12646231 |
An overexpression of mot-2 resulted in reduced level of Ras and phosphorylated ERK2. These were rescued by co-expression of MPD from an exogenous promoter demonstrating a functional link between mot-2, MPD, and Ras. Ras and its oncogenic forms act as key players in controlling proliferation of normal and cancerous cells. Assigning mot-2 upstream of p21Ras offers an important mechanism for influence over cell proliferation. Therefore, we ra tionaled to investigate if overexpression of MPD could affect the steady state levels of Ras by affecting its prenylationTransient transfections of MPD-myc in COS 7 cells resulted in higher stable levels of Ras as compared to the untransfected cells (Fig. 3A, compare lanes 4 and 8 and Fig. 3B) |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
DAB2IP | down-regulates activity
gtpase-activating protein
|
KRAS |
0.497 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254746 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27858941 |
The GAP domain of DAB2IP is homologous to other Ras-GAPs, such as GAP120 and neurofibromin (NF1), and can stimulate the GTPase activity of RAS proteins both in vitro and in cancer cell lines. DAB2IP is able to stimulate in vitro and in vivo the GTPase activity of RAS proteins (H-Ras, K-Ras, and N-Ras) facilitating GTP hydrolysis to GDP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PIK3CD |
0.62 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175210 |
|
|
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 |
| + |
KRAS | up-regulates
|
Glycolysis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259372 |
|
|
Homo sapiens |
Colonic Cancer Cell Line |
| pmid |
sentence |
| 27340238 |
These alterations corresponded to mutant KRAS and BRAF-dependent increases in glucose uptake and lactate production. Metabolic reprogramming and glucose conversion to lactate in RKO cells were proportional to levels of BRAF V600E protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOS2 | up-regulates
guanine nucleotide exchange factor
|
KRAS |
0.704 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175265 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21779497 |
Grb2 binds and activates sos, which then activates ras, and this activates p110 independently of p85. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
EFR3A | up-regulates quantity
binding
|
KRAS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269094 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 34504076 |
EFR3A directly binds to active KRAS through its C-terminus. EFR3A promotes the localization and nanoclustering of KRAS at the plasma membrane. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FNTA | up-regulates activity
|
KRAS |
0.39 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242559 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24294527 |
Major investments have been made to target Ras through indirect routes. Inhibition of farnesyl transferase to block Ras maturation has failed in large clinical trials. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RAP1GDS1 | up-regulates
binding
|
KRAS |
0.426 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-171415 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21242305 |
Smggds has been previously shown to activate a wide variety of small gtpases, including the ras family members rap1a, rap1b, and k-ras, as well as the rho family members cdc42, rac1, rac2, rhoa, and rhob |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RASSF5 | up-regulates activity
binding
|
KRAS |
0.681 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249586 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22195963 |
NORE1A can bind K-Ras.GTP through its RA domain and regulate the proapoptotic activity of MST1/2 kinases |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KRAS | up-regulates
binding
|
PIK3CB |
0.701 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-175207 |
|
|
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: | Adipogenesis |
| + |
SRC | up-regulates
phosphorylation
|
KRAS |
0.645 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-47152 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9096340 |
Expression of v-src, a transforming nonreceptor tyrosine kinase, results in ras activation, and ras function in nih 3t3 cells suppresses transformation by v-src, indicating that in these cells ras-dependent signaling pathways are required for v-src to exert its biological effects. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Rhabdomyosarcoma |
| + |
LZTR1 | down-regulates quantity
ubiquitination
|
KRAS |
0.253 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269069 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 31337872 |
We demonstrate that LZTR1 facilitates the polyubiquitination and degradation of RAS via the ubiquitin-proteasome pathway, leading to the inhibition of the RAS/MAPK signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NF1 | down-regulates activity
binding
|
KRAS |
0.711 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273661 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 32697994 |
Sprouty-related, EVH1 domain-containing (SPRED) proteins negatively regulate RAS/mitogen-activated protein kinase (MAPK) signaling following growth factor stimulation. This inhibition of RAS is thought to occur primarily through SPRED1 binding and recruitment of neurofibromin, a RasGAP, to the plasma membrane. Here, we report the structure of neurofibromin (GTPase-activating protein [GAP]-related domain) complexed with SPRED1 (EVH1 domain) and KRAS. The structure provides insight into how the membrane targeting of neurofibromin by SPRED1 allows simultaneous interaction with activated KRAS. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glioblastoma Multiforme |
3.0
KRAS
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