RIT2
GTP-binding protein Rit2
Also known as: RIBA, RIN, RIT2_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q99578
- Gene
- RIT2
- Ensembl
- ENSG00000152214
- Chromosome
- 18
- Canonical length
- 217 aa
- Protein class
- Enzymes, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm,Golgi apparatus,Cytosol
OverviewNCBI Gene
RIN belongs to the RAS (HRAS; MIM 190020) superfamily of small GTPases (Shao et al., 1999 [PubMed 10545207]).[supplied by OMIM, Mar 2008]
Canonical amino-acid sequenceUniProt
217 residues, UniProt reviewed canonical sequence.
>Q99578|RIT2
1 MEVENEASCS PGSASGGSRE YKVVMLGAGG VGKSAMTMQF ISHQFPDYHD PTIEDAYKTQ
61 VRIDNEPAYL DILDTAGQAE FTAMREQYMR GGEGFIICYS VTDRQSFQEA AKFKELIFQV
121 RHTYEIPLVL VGNKIDLEQF RQVSTEEGLS LAQEYNCGFF ETSAALRFCI DDAFHGLVRE
181 IRKKESMPSL MEKKLKRKDS LWKKLKGSLK KKRENMTLocalizationUniProt · AlphaFold · HPA
Whether an antibody against RIT2 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)
- 0.33
- Highest tissue expression
- 62 nTPM
Expression across tissuesHPA
Tissue
- cerebellum: 62 nTPM
- basal ganglia: 23 nTPM
- hypothalamus: 22 nTPM
- cerebral cortex: 20 nTPM
- hippocampal formation: 8.9 nTPM
- amygdala: 7.2 nTPM
Single-cell type
- brain excitatory neurons: 523 nCPM
- oligodendrocyte progenitor cells: 303 nCPM
- retinal ganglion cells: 232 nCPM
- other brain neurons: 191 nCPM
- brain inhibitory neurons: 191 nCPM
- oocytes: 65 nCPM
Immune cell
- basophil: 0 nTPM
- classical monocyte: 0 nTPM
- eosinophil: 0 nTPM
- gdT-cell: 0 nTPM
- intermediate monocyte: 0 nTPM
- MAIT T-cell: 0 nTPM
Brain region
- cerebellum: 46 nTPM
- pons: 26 nTPM
- cerebral cortex: 20 nTPM
- hypothalamus: 18 nTPM
- medulla oblongata: 17 nTPM
- basal ganglia: 12 nTPM
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)
- 1.3
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.89
- DepMap mean gene effect
- 0.11
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- adenylate cyclase-activating G protein-coupled receptor signaling pathway
- chemical synaptic transmission
- intracellular signal transduction
- maintenance of protein location in cell
- negative regulation of neuron projection development
- positive regulation of MAPK cascade
- positive regulation of neuron projection development
- positive regulation of transcription by RNA polymerase II
- Ras protein signal transduction
- regulation of calcium-mediated signaling
- regulation of Cdc42 protein signal transduction
- regulation of endocytosis
- small GTPase-mediated signal transduction
Molecular functions
- calmodulin binding
- chromatin binding
- G protein activity
- GDP binding
- GTP binding
- GTPase activity
- semaphorin receptor binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of RIT2 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 RIT2 as an antibody target. Whether an autoantibody or antibody against RIT2 could matter depends on whether native RIT2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
RIT2 is annotated at the cell surface, where native RIT2 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 RIT2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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