KRAS
GTPase KRas
Also known as: K-Ras4B, KRAS1, KRAS2, RASK_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P01116
- Gene
- KRAS
- Ensembl
- ENSG00000133703
- Chromosome
- 12
- Canonical length
- 189 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, FDA approved drug targets, Human disease related genes, Predicted intracellular proteins, RAS pathway related proteins
- Subcellular location
- Cytosol
OverviewNCBI Gene
This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
189 residues, UniProt reviewed canonical sequence.
>P01116|KRAS
1 MTEYKLVVVG AGGVGKSALT IQLIQNHFVD EYDPTIEDSY RKQVVIDGET CLLDILDTAG
61 QEEYSAMRDQ YMRTGEGFLC VFAINNTKSF EDIHHYREQI KRVKDSEDVP MVLVGNKCDL
121 PSRTVDTKQA QDLARSYGIP FIETSAKTRQ RVEDAFYTLV REIRQYRLKK ISKEEKTPGC
181 VKIKKCIIMLocalizationUniProt · AlphaFold · HPA
Whether an antibody against KRAS can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.29
- Highest tissue expression
- 21 nTPM
Expression across tissuesHPA
Tissue
- rectum: 21 nTPM
- colon: 20 nTPM
- stomach: 19 nTPM
- cerebral cortex: 17 nTPM
- small intestine: 17 nTPM
- esophagus: 17 nTPM
Single-cell type
- neutrophils: 509 nCPM
- esophageal apical cells: 504 nCPM
- neutrophil progenitors: 198 nCPM
- colonocytes: 193 nCPM
- syncytiotrophoblasts: 190 nCPM
- suprabasal keratinocytes: 169 nCPM
Immune cell
- basophil: 32 nTPM
- non-classical monocyte: 22 nTPM
- neutrophil: 18 nTPM
- intermediate monocyte: 16 nTPM
- eosinophil: 14 nTPM
- naive CD4 T-cell: 13 nTPM
Brain region
- hypothalamus: 27 nTPM
- cerebral cortex: 26 nTPM
- basal ganglia: 26 nTPM
- cerebellum: 24 nTPM
- thalamus: 22 nTPM
- hippocampal formation: 22 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about KRAS.
Disease | AllUniProt
Conditions KRAS is implicated in, by any mechanism.
- Leukemia, acute myelogenous (AML) MIM:601626
- Leukemia, juvenile myelomonocytic (JMML) MIM:607785
- Noonan syndrome 3 (NS3) MIM:609942
- Gastric cancer (GASC) MIM:613659
- Cardiofaciocutaneous syndrome 2 (CFC2) MIM:615278
- Oculoectodermal syndrome (OES) MIM:600268
- Schimmelpenning-Feuerstein-Mims syndrome (SFM) MIM:163200
Disease | GeneticClinVar
96 pathogenic / likely-pathogenic of 547 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- RASopathy
- Noonan syndrome 3
- Noonan syndrome
- Non-small cell lung carcinoma
- Cardiofaciocutaneous syndrome 2
Disease | ImmuneIEDB
Conditions an epitope on KRAS was assayed in.
- collecting duct carcinoma T cell
- ovary serous adenocarcinoma T cell
- melanoma T cell
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.24
- gnomAD pLI
- 0
- gnomAD missense Z
- 2.32
- DepMap mean gene effect
- -0.56
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 9% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- actin cytoskeleton organization
- cardiac muscle cell proliferation
- cytokine-mediated signaling pathway
- epithelial tube branching involved in lung morphogenesis
- female pregnancy
- forebrain astrocyte development
- gene expression
- glial cell proliferation
- homeostasis of number of cells within a tissue
- liver development
- MAPK cascade
- myoblast proliferation
- negative regulation of epithelial cell differentiation
- negative regulation of neuron apoptotic process
- neuron apoptotic process
- positive regulation of cellular senescence
- positive regulation of gene expression
- positive regulation of glial cell proliferation
- positive regulation of Rac protein signal transduction
- Rac protein signal transduction
- Ras protein signal transduction
- regulation of long-term neuronal synaptic plasticity
- regulation of synaptic transmission, GABAergic
- response to glucocorticoid
- response to gravity
- response to isolation stress
- skeletal muscle cell differentiation
- striated muscle cell differentiation
- type I pneumocyte differentiation
- visual learning
- response to mineralocorticoid
Molecular functions
- G protein activity
- GDP binding
- GMP binding
- GTP binding
- GTPase activity
- identical protein binding
- LRR domain binding
- protein-containing complex binding
- protein-membrane adaptor activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of KRAS in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads KRAS as an antibody target. Whether an autoantibody or antibody against KRAS could matter depends on whether native KRAS is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
KRAS is annotated at the cell surface, where native KRAS is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label KRAS as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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