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Protein / target

NAD-dependent protein deacetylase sirtuin-3, mitochondrial

Encoded bySIRT3Q9NTG7Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
2
Research papers

Protein at a glance

Biological role

NAD-dependent protein lysine deacetylase

Strongest disease association

Intracranial Aneurysm

Via encoding gene SIRT3 · Genetic evidence · score 0.23

Research activity

Emerging research

2 papers · latest 2024

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

NAD-dependent protein deacetylase.

View complete UniProt function annotation

NAD-dependent protein deacetylase (PubMed:12186850, PubMed:12374852, PubMed:16788062, PubMed:18680753, PubMed:18794531, PubMed:19535340, PubMed:23283301, PubMed:24121500, PubMed:24252090). Activates or deactivates mitochondrial target proteins by deacetylating key lysine residues (PubMed:12186850, PubMed:12374852, PubMed:16788062, PubMed:18680753, PubMed:18794531, PubMed:23283301, PubMed:24121500, PubMed:24252090, PubMed:38146092). Known targets include ACSS1, IDH, GDH, SOD2, PDHA1, LCAD, SDHA, MRPL12 and the ATP synthase subunit ATP5PO (PubMed:16788062, PubMed:18680753, PubMed:19535340, PubMed:24121500, PubMed:24252090, PubMed:38146092). Contributes to the regulation of the cellular energy metabolism (PubMed:24252090). Important for regulating tissue-specific ATP levels (PubMed:18794531). In response to metabolic stress, deacetylates transcription factor FOXO3 and recruits FOXO3 and mitochondrial RNA polymerase POLRMT to mtDNA to promote mtDNA transcription (PubMed:23283301). Acts as a regulator of ceramide metabolism by mediating deacetylation of ceramide synthases CERS1, CERS2 and CERS6, thereby increasing their activity and promoting mitochondrial ceramide accumulation (By similarity). Regulates hepatic lipogenesis (By similarity). Uses NAD(+) substrate imported by SLC25A47, triggering downstream activation of PRKAA1/AMPK-alpha signaling cascade that ultimately downregulates sterol regulatory element-binding protein (SREBP) transcriptional activities and ATP-consuming lipogenesis to restore cellular energy balance (By similarity). In addition to protein deacetylase activity, also acts as a protein-lysine deacylase by recognizing other acyl groups, such as benzoyl and lactoyl, leading to protein debenzoylation and delactylation, respectively (PubMed:39524354, PubMed:36896611, PubMed:37720100). Catalyzes debenzoylation of PPIF and ACLY (PubMed:37720100). Mediates delactylation of CCNE2 and 'Lys-16' of histone H4 (H4K16la) (PubMed:36896611, PubMed:37720100)

Subcellular location

Mitochondrion matrix
Domains and Gene Ontology detail (25)

Domains & features

Deacetylase sirtuin-type

Gene Ontology

  • Cmitochondrial matrix
  • Cmitochondrion
  • Cnucleoplasm
  • Cnucleus
  • Cprotein-containing complex
  • Fenzyme binding
  • Fhistone deacetylase activity, NAD-dependent
  • FNAD+ binding
  • FNAD-dependent protein lysine deacetylase activity
  • FNAD-dependent protein lysine delactylase activity
  • Fprotein lysine deacetylase activity
  • Fsequence-specific DNA binding

399 aa · 44 kDa · 2 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Lipid & lipoprotein metabolismUniProt
View supporting evidence

Lipid & lipoprotein metabolism

  • ·NAD-dependent protein deacetylase (PubMed:12186850, PubMed:12374852, PubMed:16788062, Pu…

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

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 SIRT3

Gene-level evidence surfaced through the gene SIRT3that 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.

Coronary Artery Disease
0.29Limited support

Genetic evidence dominant · Open Targets 0.12

Intracranial Aneurysm
0.23Preliminary

Genetic evidence dominant · Open Targets 0.14

Female reproductive system disorder
0.21Preliminary

Genetic evidence dominant · Open Targets 0.13

Neurodegenerative Diseases
0.15Preliminary

Pathway evidence dominant · Open Targets 0.19 · no direct causal or clinical evidence

Neoplasms
0.14Preliminary

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

View evidence synthesis (5)
Coronary Artery DiseaseLimited support
0.29
agreement 0.170.41
Genetic55%Animal model33%Literature12%

Open Targets aggregate 0.12 · 3 independent evidence families

Intracranial AneurysmPreliminary
0.23
agreement 0.110.35
Genetic100%

Open Targets aggregate 0.14 · 1 independent evidence family

Female reproductive system disorderPreliminary
0.21
agreement 0.090.33
Genetic100%

Open Targets aggregate 0.13 · 1 independent evidence family

Neurodegenerative DiseasesPreliminary
0.15
agreement 0.000.33
Pathway80%Literature20%

Open Targets aggregate 0.19 · 2 independent evidence families · no direct causal or clinical evidence

NeoplasmsPreliminary
0.14
agreement 0.000.42
Literature100%

Open Targets aggregate 0.12 · 1 independent evidence family · 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 Diseases0.19
Intracranial Aneurysm0.14
Female reproductive system disorder0.13
Coronary Artery Disease0.12
Neoplasms0.12
Acute Kidney Injury0.11
Carcinoma, Hepatocellular0.11

Tractability

Small moleculesEmerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

View underlying tractability evidence (6)
SM · Structure with LigandSM · High-Quality LigandSM · High-Quality PocketSM · Druggable FamilyPR · Half-life DataPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

regulation of catalytic activityToxCast

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

2 papers · to 2024

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Recent

Europe PMC papers linked directly to this protein.

Related family literature

7

Papers about “Sirtuins” — a broader family this protein belongs to. Shown as context; not counted as papers specifically about this protein.

Regulation of SIRT1 and Its Roles in Inflammation.

Yang Y · Frontiers in immunology · 2022

via Sirtuins

The sirtuin family in health and disease.

Wu QJ · Signal transduction and targeted therapy · 2022

via Sirtuins

NAD<sup>+</sup> homeostasis in renal health and disease.

Ralto KM · Nature reviews. Nephrology · 2020

via Sirtuins

Europe PMC literature, reached through curated HGNC family membership. Membership is a taxonomic relationship — it does not imply this protein participates in every mechanism these papers discuss.