Gene content  |
| KRAS ( by HUGO) |
| Kirsten Rat Sarcoma Viral Oncogene Homolog |
| Oncogene |
| Kirsten Rat Sarcoma Viral Oncogene Homolog KRAS2 RASK2 V-Ki-Ras2 Kirsten Rat Sarcoma 2 Viral Oncogene Homolog V-Ki-Ras2 Kirsten Rat Sarcoma Viral Oncogene Homolog c-Ki-ras K-Ras 2 CFC2 NS C-K-RAS K-RAS2A K-RAS2B K-RAS4A K-RAS4B KI-RAS KRAS1 NS3 C-Kirsten-Ras Protein Cellular C-Ki-Ras2 Proto-Oncogene GTPase KRas K-Ras P21 Protein Oncogene KRAS2 PR310 C-K-Ras Oncogene Transforming Protein P21 Ki-Ras c-K-ras |
| NCBI: 12p12.1 Ensembl: 12p12.1 |
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Subunit: Interacts with PHLPP. Interacts (active GTP-bound form preferentially) with RGS14 (By similarity) Selected PDB 3D structures from [IMAGE] and Proteopedia [IMAGE] for KRAS (see all 28): 1D8D (3D) [IMAGE] 1D8E (3D) [IMAGE] 1KZO (3D) [IMAGE] 1KZP (3D) [IMAGE] 3GFT (3D) [IMAGE] 4DSN (3D) [IMAGE]
Function: UniProtKB/Swiss-Prot Summary: RASK_HUMAN, P01116 Function: Ras proteins bind GDP/GTP and possess intrinsic GTPase activity Enzyme regulation: Alternates between an inactive form bound to GDP and an active form bound to GTP. Activated by a guanine nucleotide-exchange factor (GEF) and inactivated by a GTPase-activating protein (GAP) Gene Ontology (GO): Selected molecular function terms (see all 7): About this table GO ID Qualified GO term Evidence PubMed IDs GO:0003924 GTPase activity -- -- GO:0005515 protein binding IPI 12732644 GO:0005525 GTP binding IEA -- GO:0019002 GMP binding IEA -- GO:0019003 GDP binding IEA -- [IMAGE] Find genes that share ontologies with KRAS About GenesLikeMe Phenotypes: 3 GenomeRNAi human phenotypes for KRAS: Decreased TP53 protein express Decreased viability Synthetic lethal with Ras Selected MGI mutant phenotypes (inferred from 14 alleles[IMAGE]) (MGI details for Kras) (see all 23): behavior/neurological cardiovascular system cellular digestive/alimentary embryogenesis endocrine/exocrine gland growth/size/body hematopoietic system homeostasis/metabolism immune system integument limbs/digits/tail liver/biliary system mortality/aging muscle [IMAGE] Find genes that share phenotypes with KRAS About GenesLikeMe Animal Models: MGI mouse knock-outs for KRAS: Krastm1Epa Krastm1Mok Krastm1Tyj [IMAGE] inGenious Targeting Laboratory: Let us create your new Knockout/Knockin mouse model for KRAS [IMAGE] inGenious Targeting Laboratory: Contact us about creating complex and humanized mouse models for KRAS [IMAGE] genOway customized KO model: permanent, tissue-specific or time-controlled inactivation for KRAS [IMAGE] genOway customized Knockin model: humanization, point mutation, expression monitoring, etc. for KRAS miRNA Products: miRTarBase miRNAs that target KRAS: hsa-mir-181c-5p (MIRT003210), hsa-mir-143-3p (MIRT000312), hsa-mir-217 (MIRT006501), hsa-mir-18a-3p (MIRT000230), hsa-let-7a-5p (MIRT001855), hsa-mir-622 (MIRT006220), hsa-mir-193b-3p (MIRT016516), hsa-let-7g-5p (MIRT000399), hsa-mir-181a-5p (MIRT025201), hsa-mir-126-3p (MIRT006450), hsa-mir-96-5p (MIRT005553), hsa-mir-155-5p (MIRT005100) [IMAGE] Block miRNA regulation of human, mouse, rat KRAS using miScript Target Protectors [IMAGE] Selected qRT-PCR Assays for microRNAs that regulate KRAS (see all 122): hsa-miR-323-3p hsa-miR-193a-3p hsa-miR-300 hsa-miR-15a hsa-miR-134 hsa-miR-605 hsa-miR-30d hsa-miR-3653 [IMAGE] Browse SwitchGear 3'UTR luciferase reporter plasmids Inhib. RNA Products: [IMAGE] OriGene RNAi products in human, mouse, rat for KRAS [IMAGE] Predesigned siRNA for gene silencing in human, mouse, rat KRAS Gene Editing Products: [IMAGE] DNA2.0 Custom Protein Engineering Service for KRAS Clone Products: [IMAGE] OriGene clones in human, mouse for KRAS (see all 11) OriGene ORF clones in mouse, rat for KRAS OriGene custom cloning services - gene synthesis, subcloning, mutagenesis, variant library, vector shuttling [IMAGE] GenScript Custom all cDNA clones Services for KRAS [IMAGE] Sino Biological Human cDNA Clone for KRAS [IMAGE] DNA2.0 Custom Codon Optimized Gene Synthesis Service for KRAS [IMAGE] Vector BioLabs ready-to-use adenovirus/AAV for human, mouse, rat KRAS [IMAGE] Addgene plasmids for KRAS [IMAGE] Cell Line Products: [IMAGE] GenScript Custom overexpressing Cell Line Services for KRAS [IMAGE] Browse ESI BIO Cell Lines and PureStem Progenitors for KRAS [IMAGE] In Situ Assay Products: [IMAGE] Advanced Cell Diagnostics RNAscope RNA in situ hybridization assays for KRAS
Similarity: Belongs to the small GTPase superfamily. Ras family [IMAGE]
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| Disorder & Mutation |
| Source |
Disease |
| SWISS-PROT | Leukemia, acute myelogenous (AML) [MIM:601626]: A subtype of acute leukemia, a cancer of the white blood cells. AML is a malignant disease of bone marrow characterized by maturational arrest of hematopoietic precursors at an early stage of development. Clonal expansion of myeloid blasts occurs in bone marrow, blood, and other tissue. Myelogenous leukemias develop from changes in cells that normally produce neutrophils, basophils, eosinophils and monocytes. Note=The disease is caused by mutations affecting the gene represented in this entry |
| SWISS-PROT | Leukemia, juvenile myelomonocytic (JMML) [MIM:607785]: An aggressive pediatric myelodysplastic syndrome/myeloproliferative disorder characterized by malignant transformation in the hematopoietic stem cell compartment with proliferation of differentiated progeny. Patients have splenomegaly, enlarged lymph nodes, rashes, and hemorrhages. Note=The disease is caused by mutations affecting the gene represented in this entry |
| SWISS-PROT | Noonan syndrome 3 (NS3) [MIM:609942]: A form of Noonan syndrome, a disease characterized by short stature, facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears, and a high incidence of congenital heart defects and hypertrophic cardiomyopathy. Other features can include a short neck with webbing or redundancy of skin, deafness, motor delay, variable intellectual deficits, multiple skeletal defects, cryptorchidism, and bleeding diathesis. Individuals with Noonan syndrome are at risk of juvenile myelomonocytic leukemia, a myeloproliferative disorder characterized by excessive production of myelomonocytic cells. Note=The disease is caused by mutations affecting the gene represented in this entry |
| SWISS-PROT | Gastric cancer (GASC) [MIM:613659]: A malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease. Note=The disease is caused by mutations affecting the gene represented in this entry |
| SWISS-PROT | Note=Defects in KRAS are a cause of pylocytic astrocytoma (PA). Pylocytic astrocytomas are neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors |
| SWISS-PROT | Cardiofaciocutaneous syndrome 2 (CFC2) [MIM:615278]: A form of cardiofaciocutaneous syndrome, a multiple congenital anomaly disorder characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. CFC2 patients often do not have the skin abnormalities, such as ichthyosis, hyperkeratosis, and hemangioma observed in CFC1. Note=The disease is caused by mutations affecting the gene represented in this entry |
