Protein / target

Alanine aminotransferase 1

Encoded byGPTP24298Homo sapiensSwiss-Prot

UniProt: P24298 Ensembl: ENSG00000167701 HGNC: HGNC:4552 NCBI Gene: 2875

Degrader-tractable

Druggability

Half-life Data

Research papers

Protein at a glance

Biological role

L-alanine:2-oxoglutarate aminotransferase

Strongest disease association

Liver Diseases

Via encoding gene GPT · Genetic evidence · score 0.32

Research activity

Emerging research

3 papers · latest 2021

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Catalyzes the reversible transamination between alanine and 2-oxoglutarate to form pyruvate and glutamate.

View complete UniProt function annotation

Catalyzes the reversible transamination between alanine and 2-oxoglutarate to form pyruvate and glutamate. Participates in cellular nitrogen metabolism and also in liver gluconeogenesis starting with precursors transported from skeletal muscles (By similarity)

Subcellular location

Cytoplasm

Domains and Gene Ontology detail (5)

Gene Ontology

Ccytosol
Cextracellular exosome
FL-alanine:2-oxoglutarate aminotransferase activity
Fpyridoxal phosphate binding
PL-alanine catabolic process

496 aa · 55 kDa

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene GPT

Gene-level evidence surfaced through the gene GPTthat encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Liver Diseases

0.41Limited support

Genetic evidence dominant · Open Targets 0.22

Intelligence

0.21Preliminary

Genetic evidence dominant · Open Targets 0.13

Non-alcoholic Fatty Liver Disease

0.21Preliminary

Literature evidence dominant · Open Targets 0.13

Neurodegenerative Diseases

0.17Preliminary

Pathway evidence dominant · Open Targets 0.26 · no direct causal or clinical evidence

Carcinoma, Hepatocellular

0.17Preliminary

Literature evidence dominant · Open Targets 0.12 · no direct causal or clinical evidence

View evidence synthesis (5)

Liver DiseasesLimited support

0.41

agreement 0.27–0.55

Genetic71%Literature29%

Open Targets aggregate 0.22 · 2 independent evidence families

IntelligencePreliminary

0.21

agreement 0.09–0.33

Genetic100%

Open Targets aggregate 0.13 · 1 independent evidence family

Non-alcoholic Fatty Liver DiseasePreliminary

0.21

agreement 0.07–0.35

Literature68%Genetic32%

Open Targets aggregate 0.13 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary

0.17

agreement 0.00–0.35

Pathway97%Literature3%

Open Targets aggregate 0.26 · 2 independent evidence families · no direct causal or clinical evidence

Carcinoma, HepatocellularPreliminary

0.17

agreement 0.00–0.36

Literature83%RNA expression17%

Open Targets aggregate 0.12 · 2 independent evidence families · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Neurodegenerative Diseases0.26

Liver Diseases0.22

Non-alcoholic Fatty Liver Disease0.13

Intelligence0.13

Carcinoma, Hepatocellular0.12

Metabolic Syndrome0.12

Diabetes Mellitus0.12

Neoplasms0.12

Tractability

Protein degraders — Emerging

Feasibility evidence (half-life data) — no clinical-stage drug of this modality recorded.