Target intelligence / Profile preview

Protein sel-1 homolog 3 (SEL1L3)

Target
SEL1L3
Molecular classification
Other (predicted transmembrane protein; not a classical enzyme, receptor, ion channel, or transporter)[2][3][5]
01

Overview

Protein sel-1 homolog 3 (SEL1L3) is a human transmembrane protein encoded by the SEL1L3 gene and is part of the SEL1-like family[3][5]. Its exact physiological function is not well established, though it shares homology with SEL1L, which is a key component of the endoplasmic reticulum–associated degradation (ERAD) system that manages misfolded proteins[2]. SEL1L3 mRNA is broadly expressed in tissues, with particularly notable cytoplasmic expression in the gastrointestinal tract[9]. Recent research has identified hyper-N-glycosylated SEL1L3 as an auto-antigen in a subset of primary vitreoretinal lymphoma (PVRL): in these patients, SEL1L3 is recognized by the B-cell receptor (BCR), triggers BCR-dependent cell signaling, and may drive proliferation of malignant B-cells[4]. However, there are no established drugs targeting SEL1L3, no mechanism of drug action, and it is not currently classified as a standard druggable therapeutic target or receptor. Its involvement in disease remains an active area of research, with potential roles noted in cancer, prion diseases, and possibly other disease contexts as revealed by gene expression studies[2][3][4][8][10].

Other names
SEL1L3KIAA0746Sel-1L3Suppressor of lin-12-like protein 3sel-1 suppressor of lin-12-like 3protein sel-1 homolog 3
02

Mechanism of action

Not established; no therapeutics reported to directly target SEL1L3

03

Biological functions

Possibly involved in endoplasmic reticulum-associated degradation (ERAD) of proteins by analogy to paralog SEL1L[1][2]May function in membrane-associated quality control of misfolded proteins[2]May act as an auto-antigen in B-cell lymphomas, triggering BCR-dependent signaling[4]
04

Disease associations

Cancer (primary vitreoretinal lymphoma, potential involvement in diffuse large B-cell lymphoma subtypes)[4]Neurodegenerative disease (possible relation to prion diseases suggested by gene expression changes)[2]Renal cell carcinoma and atherosclerosis (bioinformatic evidence for association, functional role not confirmed)[8][10]
05

Safety considerations

None known; no therapeutic development reported or toxicity data available
06

Biomarkers

Down-regulation may be an early biomarker candidate for prion diseases (animal model evidence only)[2]Reactivity with lymphoma BCRs may serve as a biomarker for specific B-cell malignancies (primary vitreoretinal lymphoma)[4]

Beyond the preview

Go deeper on Protein sel-1 homolog 3 (SEL1L3).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Protein sel-1 homolog 3 (SEL1L3).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call