Back to discover

Protein / target

Lysosome-associated membrane glycoprotein 2

Encoded byLAMP2P13473Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Protein-macromolecule adaptor

Strongest disease association

Cardiomyopathy, Hypertrophic

Via encoding gene LAMP2 · Genetic evidence · score 0.84

Research activity

Emerging research

1 papers · latest 2020

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

Lysosomal membrane glycoprotein which plays an important role in lysosome biogenesis, lysosomal pH regulation and autophagy.

View complete UniProt function annotation

Lysosomal membrane glycoprotein which plays an important role in lysosome biogenesis, lysosomal pH regulation and autophagy (PubMed:11082038, PubMed:18644871, PubMed:24880125, PubMed:27628032, PubMed:36586411, PubMed:37390818, PubMed:8662539). Acts as an important regulator of lysosomal lumen pH regulation by acting as a direct inhibitor of the proton channel TMEM175, facilitating lysosomal acidification for optimal hydrolase activity (PubMed:37390818). Plays an important role in chaperone-mediated autophagy, a process that mediates lysosomal degradation of proteins in response to various stresses and as part of the normal turnover of proteins with a long biological half-live (PubMed:11082038, PubMed:18644871, PubMed:24880125, PubMed:27628032, PubMed:36586411, PubMed:8662539). Functions by binding target proteins, such as GAPDH, GPX4, NLRP3 and MLLT11, and targeting them for lysosomal degradation (PubMed:11082038, PubMed:18644871, PubMed:24880125, PubMed:36586411, PubMed:8662539). In the chaperone-mediated autophagy, acts downstream of chaperones, such as HSPA8/HSC70, which recognize and bind substrate proteins and mediate their recruitment to lysosomes, where target proteins bind LAMP2 (PubMed:36586411). Plays a role in lysosomal protein degradation in response to starvation (By similarity). Required for the fusion of autophagosomes with lysosomes during autophagy (PubMed:27628032). Cells that lack LAMP2 express normal levels of VAMP8, but fail to accumulate STX17 on autophagosomes, which is the most likely explanation for the lack of fusion between autophagosomes and lysosomes (PubMed:27628032). Required for normal degradation of the contents of autophagosomes (PubMed:27628032). Required for efficient MHC class II-mediated presentation of exogenous antigens via its function in lysosomal protein degradation; antigenic peptides generated by proteases in the endosomal/lysosomal compartment are captured by nascent MHC II subunits (PubMed:15894275, PubMed:20518820). Is not required for efficient MHC class II-mediated presentation of endogenous antigens (PubMed:20518820)

Subcellular location

Lysosome membraneEndosome membraneCell membraneCytoplasmic vesicle, autophagosome membrane
Domains and Gene Ontology detail (37)

Gene Ontology

  • Cautolysosome
  • Cautophagosome membrane
  • Cazurophil granule membrane
  • Cchaperone-mediated autophagy translocation complex
  • Cextracellular exosome
  • Cextracellular space
  • Cficolin-1-rich granule membrane
  • Clate endosome
  • Clate endosome membrane
  • Clysosomal lumen
  • Clysosomal membrane
  • Clysosome

410 aa · 45 kDa · 3 isoforms

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 LAMP2

Gene-level evidence surfaced through the gene LAMP2that 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.

Cardiomyopathy, Hypertrophic
0.89Well supported

Genetic evidence dominant · Open Targets 0.53

Cardiomyopathy, Dilated
0.85Well supported

Genetic evidence dominant · Open Targets 0.51

Cardiomyopathies
0.80Well supported

Genetic evidence dominant · Open Targets 0.49

Familial hypertrophic cardiomyopathy
0.51Moderately supported

Genetic evidence dominant · Open Targets 0.31

Neoplasms
0.12Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

View evidence synthesis (5)
Cardiomyopathy, HypertrophicWell supported
0.89
agreement 0.771.00
Genetic75%Animal model24%Literature2%

Open Targets aggregate 0.53 · 3 independent evidence families

Cardiomyopathy, DilatedWell supported
0.85
agreement 0.730.97
Genetic79%Animal model20%Literature1%

Open Targets aggregate 0.51 · 3 independent evidence families

CardiomyopathiesWell supported
0.80
agreement 0.660.94
Genetic93%Literature7%

Open Targets aggregate 0.49 · 2 independent evidence families

Familial hypertrophic cardiomyopathyModerately supported
0.51
agreement 0.370.65
Genetic98%Literature2%

Open Targets aggregate 0.31 · 2 independent evidence families

NeoplasmsPreliminary
0.12
agreement 0.000.40
Literature100%

Open Targets aggregate 0.10 · 1 independent evidence family · no direct causal or clinical evidence

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
Cardiomyopathy, Hypertrophic0.53
Cardiomyopathy, Dilated0.51
Cardiomyopathies0.49
Familial hypertrophic cardiomyopathy0.31
Neoplasms0.10

Tractability

AntibodiesEmerging

Feasibility evidence (uniprot loc high conf and go cc high conf) — no clinical-stage drug of this modality recorded.

Protein degradersEmerging

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

View underlying tractability evidence (4)
AB · UniProt loc high confAB · GO CC high confAB · UniProt SigP or TMHMMPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2020

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.