HCSGD entry for KRAS


1. General information

Official gene symbolKRAS
Entrez ID3845
Gene full namev-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
Other gene symbolsC-K-RAS K-RAS2A K-RAS2B K-RAS4A K-RAS4B KI-RAS KRAS1 KRAS2 NS NS3 RASK2
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000165MAPK cascadeTASbiological_process
GO:0000186Activation of MAPKK activityTASbiological_process
GO:0001934Positive regulation of protein phosphorylationIMPbiological_process
GO:0003924GTPase activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005525GTP bindingIEAmolecular_function
GO:0005739MitochondrionIEAcellular_component
GO:0005886Plasma membraneTAScellular_component
GO:0007173Epidermal growth factor receptor signaling pathwayTASbiological_process
GO:0007264Small GTPase mediated signal transductionIEA TASbiological_process
GO:0007265Ras protein signal transductionTASbiological_process
GO:0007411Axon guidanceTASbiological_process
GO:0007596Blood coagulationTASbiological_process
GO:0008286Insulin receptor signaling pathwayTASbiological_process
GO:0008543Fibroblast growth factor receptor signaling pathwayTASbiological_process
GO:0010628Positive regulation of gene expressionIMPbiological_process
GO:0016020MembraneIEAcellular_component
GO:0019002GMP bindingIEAmolecular_function
GO:0019003GDP bindingIEAmolecular_function
GO:0019221Cytokine-mediated signaling pathwayIEAbiological_process
GO:0030275LRR domain bindingIEAmolecular_function
GO:0032403Protein complex bindingIDAmolecular_function
GO:0035176Social behaviorIEAbiological_process
GO:0038095Fc-epsilon receptor signaling pathwayTASbiological_process
GO:0043406Positive regulation of MAP kinase activityIEAbiological_process
GO:0045087Innate immune responseTASbiological_process
GO:0045121Membrane raftIEAcellular_component
GO:0048011Neurotrophin TRK receptor signaling pathwayTASbiological_process
GO:0050900Leukocyte migrationTASbiological_process
GO:0051000Positive regulation of nitric-oxide synthase activityIEAbiological_process
GO:0051092Positive regulation of NF-kappaB transcription factor activityIEAbiological_process
GO:0051384Response to glucocorticoidIEAbiological_process
GO:0051385Response to mineralocorticoidIEAbiological_process
Entries Per Page
Displaying Page of

4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.96983171990.03612719500.99999024730.3581466717

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.1827511987
GSE13712_SHEARDown-0.1273390973
GSE13712_STATICDown-0.1320920214
GSE19018Down-0.1198017115
GSE19899_A1Down-0.2321162789
GSE19899_A2Down-0.0514883746
PubMed_21979375_A1Down-0.1565576161
PubMed_21979375_A2Down-0.3951774861
GSE35957Up0.0451835023
GSE36640Up0.0310170231
GSE54402Down-0.0504590529
GSE9593Up0.1575151800
GSE43922Down-0.3776710875
GSE24585Down-0.5466236002
GSE37065Down-0.2010728971
GSE28863_A1Up0.1189217047
GSE28863_A2Down-0.1355683562
GSE28863_A3Down-0.7776503196
GSE28863_A4Up0.2829030221
GSE48662Down-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 ACIDDB07771 -
FARNESYL DIPHOSPHATEDB07780 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-126-3pMIMAT0000445MIRT006450Immunohistochemistry//Luciferase reporter assay//Microarray//qRT-PCR//Western blotFunctional MTI22384141
hsa-miR-18a-3pMIMAT0002891MIRT000230Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI19372139
hsa-miR-143-3pMIMAT0000435MIRT000312qRT-PCR//Western blotFunctional MTI19157460
hsa-miR-143-3pMIMAT0000435MIRT000312Luciferase reporter assay//qRT-PCR//MicroarrayFunctional MTI19137007
hsa-miR-143-3pMIMAT0000435MIRT000312Western blotFunctional MTI23276710
hsa-let-7g-5pMIMAT0000414MIRT000399Luciferase reporter assayFunctional MTI18308936
hsa-miR-217MIMAT0000274MIRT006501Luciferase reporter assay//Reporter assayFunctional MTI20675343
hsa-miR-622MIMAT0003291MIRT006220Luciferase reporter assay//Western blotFunctional MTI22016468
hsa-let-7a-5pMIMAT0000062MIRT001855Luciferase reporter assay//MicroarrayFunctional MTI15766527
hsa-let-7a-5pMIMAT0000062MIRT001855Western blotFunctional MTI20033209
hsa-let-7a-5pMIMAT0000062MIRT001855qRT-PCR//Western blotFunctional MTI16651716
hsa-miR-181c-5pMIMAT0000258MIRT003210Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20080834
hsa-miR-155-5pMIMAT0000646MIRT005100MicroarrayFunctional MTI (Weak)19193853
hsa-miR-155-5pMIMAT0000646MIRT005100pSILAC//ProteomicsFunctional MTI (Weak)18668040
hsa-miR-155-5pMIMAT0000646MIRT005100Reporter assay;OtherNon-Functional MTI20584899
hsa-miR-96-5pMIMAT0000095MIRT005553Immunoblot//Immunohistochemistry//Northern blot//Quantitative proteomic approach//Western blot//Reporter assay;Western blot;qRT-PCR;OtherFunctional MTI20610624
hsa-miR-96-5pMIMAT0000095MIRT005553SequencingFunctional MTI (Weak)20371350
hsa-miR-193b-3pMIMAT0002819MIRT016516MicroarrayFunctional MTI (Weak)20304954
hsa-miR-181a-5pMIMAT0000256MIRT025201SequencingFunctional MTI (Weak)20371350
Entries Per Page
Displaying Page of
  • 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-5pMIMAT00000627hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000622hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000621hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000624hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000626hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000628hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000623hsa-let-7a15766527
hsa-let-7a-5pMIMAT00000625hsa-let-7a15766527
hsa-miR-143-3pMIMAT00004351hsa-miR-143{Western blot}{overexpression by miRNA precursor transfection}19137007
hsa-miR-143-3pMIMAT00004352hsa-miR-143{Western blot}{overexpression by miRNA precursor transfection}19137007
hsa-miR-181c-5pMIMAT00002581hsa-miR-181c20080834
hsa-miR-18a-3pMIMAT00028911hsa-miR-18a*{Western blot}{downregulation by anti-miRNA oligonucleotide}19372139
hsa-miR-217MIMAT00002741hsa-miR-217{Western blot}{overexpression by miRNA precursor transfection}20675343
hsa-miR-622MIMAT00032911hsa-miR-622{Western blot}{overexpression by miRNA mimics tranfection}22016468
hsa-miR-622MIMAT00032912hsa-miR-622{Western blot}{overexpression by miRNA mimics tranfection}22016468
hsa-miR-622MIMAT00032913hsa-miR-622{Western blot}{overexpression by miRNA mimics tranfection}22016468
Entries Per Page
Displaying Page of

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

27141064In contrast, serous cystadenomas without OSBTs do not show Kras or Braf mutations
27141064In OSBTs, Kras mutations range from 17% to 39
27141064The former is comparable with the range of Kras mutations in ovarian low-grade serous carcinomas (OLGSCa), 19%-54
27141064In contrast, OSBTs without a Braf mutation may progress to OLGSCa due to Kras mutation or some other genetic alterations
27141064Nevertheless, LGSCa as a recurrence of an OSBT can originate from OSBTs with or without detectable Kras mutations
27141064Also, it appears to be an association between Kras G12v mutation and a more aggressive phenotype of OSBT that recurred as LGSCa
27141064It has been reported that cancer cell lines with Kras G12v mutation are more sensitive to selumetinib than cell lines with wild-type Kras
25461770A heterogeneous combination of genetic mutations, including KRAS, INK4a/CDKN2A and p53, underpin the propensity of pancreatic cancer to rapidly invade and disseminate
25188864In 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
24618719Elevated CUX1 expression in a transgenic mouse model enables the emergence of mammary tumors with spontaneous activating Kras mutations
23904845No pathogenetic mutations in CDKN2A, BRAF, NRAS, KRAS, cKIT, TP53 and PTEN genes were observed
23535008Therefore, 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
23535008Increased 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
23174937Most studies investigating aberrations in borderline tumors have focused on KRAS/BRAF mutations
23174937KRAS c
22964484MCT2 knockdown suppressed KRAS mutant colorectal tumor growth in vivo
22654667KRAS mutant lung cancers are generally refractory to chemotherapy as well targeted agents
22654667We 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
22654667Moreover, the suppression of Twist1 to physiological levels is sufficient to cause Kras mutant lung tumors to undergo senescence and lose their neoplastic features
20972333KRAS is one of the most frequently mutated human oncogenes
20972333In some settings, oncogenic KRAS can trigger cellular senescence, whereas in others it produces hyperproliferation
20972333Using 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
20972333Deletion 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
20972333In human lung cancer cell lines dependent on oncogenic KRAS, WT1 loss decreased proliferation and induced senescence
20972333Furthermore, WT1 inactivation defined a gene expression signature that was prognostic of survival only in lung cancer patients exhibiting evidence of oncogenic KRAS activation
20972333These 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
19723919Cox 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)
17450133In 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
Entries Per Page
Displaying Page of