Seroatlas · Human Serome Atlas

AKT1

RAC-alpha serine/threonine-protein kinase

Also known as: AKT, AKT1_HUMAN, PKB, PRKBA, RAC, RAC-alpha

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
P31749
Gene
AKT1
Ensembl
ENSG00000142208
Chromosome
14
Canonical length
480 aa
Protein class
Cancer-related genes, Disease related genes, Enzymes, Human disease related genes, Potential drug targets, Predicted intracellular proteins, RAS pathway related proteins, Transporters
Subcellular location
Nucleoplasm,Microtubules,Primary cilium,Basal body,Perinuclear theca,Calyx,Principal piece,End piece

OverviewNCBI Gene

This gene encodes one of the three members of the human AKT serine-threonine protein kinase family which are often referred to as protein kinase B alpha, beta, and gamma. These highly similar AKT proteins all have an N-terminal pleckstrin homology domain, a serine/threonine-specific kinase domain and a C-terminal regulatory domain. These proteins are phosphorylated by phosphoinositide 3-kinase (PI3K). AKT/PI3K forms a key component of many signalling pathways that involve the binding of membrane-bound ligands such as receptor tyrosine kinases, G-protein coupled receptors, and integrin-linked kinase. These AKT proteins therefore regulate a wide variety of cellular functions including cell proliferation, survival, metabolism, and angiogenesis in both normal and malignant cells. AKT proteins are recruited to the cell membrane by phosphatidylinositol 3,4,5-trisphosphate (PIP3) after phosphorylation of phosphatidylinositol 4,5-bisphosphate (PIP2) by PI3K. Subsequent phosphorylation of both threonine residue 308 and serine residue 473 is required for full activation of the AKT1 protein encoded by this gene. Phosphorylation of additional residues also occurs, for example, in response to insulin growth factor-1 and epidermal growth factor. Protein phosphatases act as negative regulators of AKT proteins by dephosphorylating AKT or PIP3. The PI3K/AKT signalling pathway is crucial for tumor cell survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating AKT1 which then phosphorylates and inactivates components of the apoptotic machinery. AKT proteins also participate in the mammalian target of rapamycin (mTOR) signalling pathway which controls the assembly of the eukaryotic translation initiation factor 4F (eIF4E) complex and this pathway, in addition to responding to extracellular signals from growth factors and cytokines, is disregulated in many cancers. Mutations in this gene are associated with multiple types of cancer and excessive tissue growth including Proteus syndrome and Cowden syndrome 6, and breast, colorectal, and ovarian cancers. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2020]

Canonical amino-acid sequenceUniProt

480 residues, UniProt reviewed canonical sequence.

>P31749|AKT1
     1  MSDVAIVKEG WLHKRGEYIK TWRPRYFLLK NDGTFIGYKE RPQDVDQREA PLNNFSVAQC
    61  QLMKTERPRP NTFIIRCLQW TTVIERTFHV ETPEEREEWT TAIQTVADGL KKQEEEEMDF
   121  RSGSPSDNSG AEEMEVSLAK PKHRVTMNEF EYLKLLGKGT FGKVILVKEK ATGRYYAMKI
   181  LKKEVIVAKD EVAHTLTENR VLQNSRHPFL TALKYSFQTH DRLCFVMEYA NGGELFFHLS
   241  RERVFSEDRA RFYGAEIVSA LDYLHSEKNV VYRDLKLENL MLDKDGHIKI TDFGLCKEGI
   301  KDGATMKTFC GTPEYLAPEV LEDNDYGRAV DWWGLGVVMY EMMCGRLPFY NQDHEKLFEL
   361  ILMEEIRFPR TLGPEAKSLL SGLLKKDPKQ RLGGGSEDAK EIMQHRFFAG IVWQHVYEKK
   421  LSPPFKPQVT SETDTRYFDE EFTAQMITIT PPDQDDSMEC VDSERRPHFP QFSYSASGTA

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against AKT1 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)
0.3
Highest tissue expression
94 nTPM

Expression across tissuesHPA

Tissue

  • heart muscle: 94 nTPM
  • pancreas: 85 nTPM
  • seminal vesicle: 68 nTPM
  • adipose tissue: 61 nTPM
  • lung: 61 nTPM
  • esophagus: 61 nTPM

Single-cell type

  • breast lactating cells: 153 nCPM
  • alveolar cells type 2: 90 nCPM
  • megakaryocytes: 87 nCPM
  • alveolar cells type 1: 67 nCPM
  • breast hormone-responsive cells: 58 nCPM
  • transitional alveolar cells: 57 nCPM

Immune cell

  • eosinophil: 24 nTPM
  • neutrophil: 8.4 nTPM
  • NK-cell: 6.6 nTPM
  • non-classical monocyte: 6 nTPM
  • intermediate monocyte: 4.8 nTPM
  • memory CD8 T-cell: 3.8 nTPM

Brain region

  • medulla oblongata: 71 nTPM
  • choroid plexus: 69 nTPM
  • spinal cord: 66 nTPM
  • thalamus: 65 nTPM
  • midbrain: 61 nTPM
  • pons: 60 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about AKT1.

Disease | AllUniProt

Conditions AKT1 is implicated in, by any mechanism.

Disease | GeneticClinVar

4 pathogenic / likely-pathogenic of 962 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
0.32
gnomAD pLI
0.98
gnomAD missense Z
3.48
DepMap mean gene effect
-0.12
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of AKT1 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 AKT1 as an antibody target. Whether an autoantibody or antibody against AKT1 could matter depends on whether native AKT1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

AKT1 is annotated at the cell surface, where native AKT1 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 AKT1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/AKT1. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

© 2026 · Seroatlas, Discover Oregon LLC · Terms of use

Loading the interactive Seroatlas protein explorer...