HCSGD entry for KRAS
1. General information
Official gene symbol | KRAS |
---|---|
Entrez ID | 3845 |
Gene full name | v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog |
Other gene symbols | C-K-RAS K-RAS2A K-RAS2B K-RAS4A K-RAS4B KI-RAS KRAS1 KRAS2 NS NS3 RASK2 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0000165 | MAPK cascade | TAS | biological_process |
GO:0000186 | Activation of MAPKK activity | TAS | biological_process |
GO:0001934 | Positive regulation of protein phosphorylation | IMP | biological_process |
GO:0003924 | GTPase activity | IEA | molecular_function |
GO:0005515 | Protein binding | IPI | molecular_function |
GO:0005525 | GTP binding | IEA | molecular_function |
GO:0005739 | Mitochondrion | IEA | cellular_component |
GO:0005886 | Plasma membrane | TAS | cellular_component |
GO:0007173 | Epidermal growth factor receptor signaling pathway | TAS | biological_process |
GO:0007264 | Small GTPase mediated signal transduction | IEA TAS | biological_process |
GO:0007265 | Ras protein signal transduction | TAS | biological_process |
GO:0007411 | Axon guidance | TAS | biological_process |
GO:0007596 | Blood coagulation | TAS | biological_process |
GO:0008286 | Insulin receptor signaling pathway | TAS | biological_process |
GO:0008543 | Fibroblast growth factor receptor signaling pathway | TAS | biological_process |
GO:0010628 | Positive regulation of gene expression | IMP | biological_process |
GO:0016020 | Membrane | IEA | cellular_component |
GO:0019002 | GMP binding | IEA | molecular_function |
GO:0019003 | GDP binding | IEA | molecular_function |
GO:0019221 | Cytokine-mediated signaling pathway | IEA | biological_process |
GO:0030275 | LRR domain binding | IEA | molecular_function |
GO:0032403 | Protein complex binding | IDA | molecular_function |
GO:0035176 | Social behavior | IEA | biological_process |
GO:0038095 | Fc-epsilon receptor signaling pathway | TAS | biological_process |
GO:0043406 | Positive regulation of MAP kinase activity | IEA | biological_process |
GO:0045087 | Innate immune response | TAS | biological_process |
GO:0045121 | Membrane raft | IEA | cellular_component |
GO:0048011 | Neurotrophin TRK receptor signaling pathway | TAS | biological_process |
GO:0050900 | Leukocyte migration | TAS | biological_process |
GO:0051000 | Positive regulation of nitric-oxide synthase activity | IEA | biological_process |
GO:0051092 | Positive regulation of NF-kappaB transcription factor activity | IEA | biological_process |
GO:0051384 | Response to glucocorticoid | IEA | biological_process |
GO:0051385 | Response to mineralocorticoid | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.9698317199 | 0.0361271950 | 0.9999902473 | 0.3581466717 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Down | -0.1827511987 |
GSE13712_SHEAR | Down | -0.1273390973 |
GSE13712_STATIC | Down | -0.1320920214 |
GSE19018 | Down | -0.1198017115 |
GSE19899_A1 | Down | -0.2321162789 |
GSE19899_A2 | Down | -0.0514883746 |
PubMed_21979375_A1 | Down | -0.1565576161 |
PubMed_21979375_A2 | Down | -0.3951774861 |
GSE35957 | Up | 0.0451835023 |
GSE36640 | Up | 0.0310170231 |
GSE54402 | Down | -0.0504590529 |
GSE9593 | Up | 0.1575151800 |
GSE43922 | Down | -0.3776710875 |
GSE24585 | Down | -0.5466236002 |
GSE37065 | Down | -0.2010728971 |
GSE28863_A1 | Up | 0.1189217047 |
GSE28863_A2 | Down | -0.1355683562 |
GSE28863_A3 | Down | -0.7776503196 |
GSE28863_A4 | Up | 0.2829030221 |
GSE48662 | Down | -0.3122131532 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
---|---|---|
[(3,7,11-TRIMETHYL-DODECA-2,6,10-TRIENYLOXYCARBAMOYL)-METHYL]-PHOSPHONIC ACID | DB07771 | - |
FARNESYL DIPHOSPHATE | DB07780 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-126-3p | MIMAT0000445 | MIRT006450 | Immunohistochemistry//Luciferase reporter assay//Microarray//qRT-PCR//Western blot | Functional MTI | 22384141 |
hsa-miR-18a-3p | MIMAT0002891 | MIRT000230 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 19372139 |
hsa-miR-143-3p | MIMAT0000435 | MIRT000312 | qRT-PCR//Western blot | Functional MTI | 19157460 |
hsa-miR-143-3p | MIMAT0000435 | MIRT000312 | Luciferase reporter assay//qRT-PCR//Microarray | Functional MTI | 19137007 |
hsa-miR-143-3p | MIMAT0000435 | MIRT000312 | Western blot | Functional MTI | 23276710 |
hsa-let-7g-5p | MIMAT0000414 | MIRT000399 | Luciferase reporter assay | Functional MTI | 18308936 |
hsa-miR-217 | MIMAT0000274 | MIRT006501 | Luciferase reporter assay//Reporter assay | Functional MTI | 20675343 |
hsa-miR-622 | MIMAT0003291 | MIRT006220 | Luciferase reporter assay//Western blot | Functional MTI | 22016468 |
hsa-let-7a-5p | MIMAT0000062 | MIRT001855 | Luciferase reporter assay//Microarray | Functional MTI | 15766527 |
hsa-let-7a-5p | MIMAT0000062 | MIRT001855 | Western blot | Functional MTI | 20033209 |
hsa-let-7a-5p | MIMAT0000062 | MIRT001855 | qRT-PCR//Western blot | Functional MTI | 16651716 |
hsa-miR-181c-5p | MIMAT0000258 | MIRT003210 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20080834 |
hsa-miR-155-5p | MIMAT0000646 | MIRT005100 | Microarray | Functional MTI (Weak) | 19193853 |
hsa-miR-155-5p | MIMAT0000646 | MIRT005100 | pSILAC//Proteomics | Functional MTI (Weak) | 18668040 |
hsa-miR-155-5p | MIMAT0000646 | MIRT005100 | Reporter assay;Other | Non-Functional MTI | 20584899 |
hsa-miR-96-5p | MIMAT0000095 | MIRT005553 | Immunoblot//Immunohistochemistry//Northern blot//Quantitative proteomic approach//Western blot//Reporter assay;Western blot;qRT-PCR;Other | Functional MTI | 20610624 |
hsa-miR-96-5p | MIMAT0000095 | MIRT005553 | Sequencing | Functional MTI (Weak) | 20371350 |
hsa-miR-193b-3p | MIMAT0002819 | MIRT016516 | Microarray | Functional MTI (Weak) | 20304954 |
hsa-miR-181a-5p | MIMAT0000256 | MIRT025201 | Sequencing | Functional MTI (Weak) | 20371350 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
---|---|---|---|---|---|---|---|
hsa-let-7a-5p | MIMAT0000062 | 7 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 2 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 1 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 4 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 6 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 8 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 3 | hsa-let-7a | 15766527 | |||
hsa-let-7a-5p | MIMAT0000062 | 5 | hsa-let-7a | 15766527 | |||
hsa-miR-143-3p | MIMAT0000435 | 1 | hsa-miR-143 | {Western blot} | {overexpression by miRNA precursor transfection} | 19137007 | |
hsa-miR-143-3p | MIMAT0000435 | 2 | hsa-miR-143 | {Western blot} | {overexpression by miRNA precursor transfection} | 19137007 | |
hsa-miR-181c-5p | MIMAT0000258 | 1 | hsa-miR-181c | 20080834 | |||
hsa-miR-18a-3p | MIMAT0002891 | 1 | hsa-miR-18a* | {Western blot} | {downregulation by anti-miRNA oligonucleotide} | 19372139 | |
hsa-miR-217 | MIMAT0000274 | 1 | hsa-miR-217 | {Western blot} | {overexpression by miRNA precursor transfection} | 20675343 | |
hsa-miR-622 | MIMAT0003291 | 1 | hsa-miR-622 | {Western blot} | {overexpression by miRNA mimics tranfection} | 22016468 | |
hsa-miR-622 | MIMAT0003291 | 2 | hsa-miR-622 | {Western blot} | {overexpression by miRNA mimics tranfection} | 22016468 | |
hsa-miR-622 | MIMAT0003291 | 3 | hsa-miR-622 | {Western blot} | {overexpression by miRNA mimics tranfection} | 22016468 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 12 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
27141064 | In contrast, serous cystadenomas without OSBTs do not show Kras or Braf mutations |
27141064 | In OSBTs, Kras mutations range from 17% to 39 |
27141064 | The former is comparable with the range of Kras mutations in ovarian low-grade serous carcinomas (OLGSCa), 19%-54 |
27141064 | In contrast, OSBTs without a Braf mutation may progress to OLGSCa due to Kras mutation or some other genetic alterations |
27141064 | Nevertheless, LGSCa as a recurrence of an OSBT can originate from OSBTs with or without detectable Kras mutations |
27141064 | Also, it appears to be an association between Kras G12v mutation and a more aggressive phenotype of OSBT that recurred as LGSCa |
27141064 | It has been reported that cancer cell lines with Kras G12v mutation are more sensitive to selumetinib than cell lines with wild-type Kras |
25461770 | A heterogeneous combination of genetic mutations, including KRAS, INK4a/CDKN2A and p53, underpin the propensity of pancreatic cancer to rapidly invade and disseminate |
25188864 | In this study, we correlated the morphologic and immunohistochemical phenotypes of 71 APSTs and 18 LGSCs with the mutational status of KRAS and BRAF, the most common molecular genetic changes in these neoplasms |
24618719 | Elevated CUX1 expression in a transgenic mouse model enables the emergence of mammary tumors with spontaneous activating Kras mutations |
23904845 | No pathogenetic mutations in CDKN2A, BRAF, NRAS, KRAS, cKIT, TP53 and PTEN genes were observed |
23535008 | Therefore, we investigated the role of gene silencing (DNA promoter methylation of LINE-1, PTEN), genetic aberrations (karyotype, KRAS and BRAF mutations) as well as their contribution to the proliferation rate and migratory potential that underlies "initial" and "final" passage sarcoma cells |
23535008 | Increased proliferative potential of final passage STS cells was not associated with significant differences in methylation (LINE-1, PTEN) and mutation status (KRAS, BRAF), but it was dependent on the amount of chromosomal aberrations |
23174937 | Most studies investigating aberrations in borderline tumors have focused on KRAS/BRAF mutations |
23174937 | KRAS c |
22964484 | MCT2 knockdown suppressed KRAS mutant colorectal tumor growth in vivo |
22654667 | KRAS mutant lung cancers are generally refractory to chemotherapy as well targeted agents |
22654667 | We demonstrate in both a novel transgenic mutant Kras lung cancer mouse model and in human lung tumors that the inhibition of Twist1 restores a senescence program inducing the loss of a neoplastic phenotype |
22654667 | Moreover, the suppression of Twist1 to physiological levels is sufficient to cause Kras mutant lung tumors to undergo senescence and lose their neoplastic features |
20972333 | KRAS is one of the most frequently mutated human oncogenes |
20972333 | In some settings, oncogenic KRAS can trigger cellular senescence, whereas in others it produces hyperproliferation |
20972333 | Using a combination of functional genomics and mouse genetics, we identified a role for the transcription factor Wilms tumor 1 (WT1) as a critical regulator of senescence and proliferation downstream of oncogenic KRAS signaling |
20972333 | Deletion or suppression of Wt1 led to senescence of mouse primary cells expressing physiological levels of oncogenic Kras but had no effect on wild-type cells, and Wt1 loss decreased tumor burden in a mouse model of Kras-driven lung cancer |
20972333 | In human lung cancer cell lines dependent on oncogenic KRAS, WT1 loss decreased proliferation and induced senescence |
20972333 | Furthermore, WT1 inactivation defined a gene expression signature that was prognostic of survival only in lung cancer patients exhibiting evidence of oncogenic KRAS activation |
20972333 | These findings reveal an unexpected role for WT1 as a key regulator of the genetic network of oncogenic KRAS and provide important insight into the mechanisms that regulate proliferation or senescence in response to oncogenic signals |
19723919 | Cox proportional hazard models computed hazard ratio (HR) for death, adjusted for potential confounders, including p53, cyclin D1, KRAS, BRAF, PIK3CA, LINE-1 hypomethylation, CpG island methylator phenotype (CIMP), and microsatellite instability (MSI) |
17450133 | In contrast, high levels of Ras activation - similar to those found in tumours bearing endogenous Kras2 mutations - induce cellular senescence that is Ink4a-Arf- dependent and irreversible following Ras downregulation |
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