Target intelligence / Profile preview

SEC61 translocon subunit gamma (SEC61G)

Target
SEC61G
Molecular classification
Transporter, Channel subunit, Translocon complex (Endoplasmic reticulum translocon)
01

Overview

The SEC61G divergent transcript (SEC61G-DT) is not a well-established molecule in standard scientific databases. There is no evidence that "SEC61G-DT" (SEC61G divergent transcript) is recognized as a canonical molecule or therapeutic target. All functional and therapeutic relevance described is associated with the canonical SEC61G protein, which is the gamma subunit of the SEC61 translocon complex, a key component controlling translocation and membrane integration of nascent proteins in the ER. It plays essential roles in protein processing, immune evasion (by stabilization and glycosylation of immune checkpoint molecules such as PD-L1), and tumor cell survival. Overexpression and amplification of SEC61G are associated with several cancers, notably EGFR-amplified glioblastoma. Pharmacological blockade of the SEC61 complex is under investigation as a cancer therapy. If the intent was SEC61G, it is considered a therapeutic target.

Other names
SEC61GSSS1Sec61 translocon gamma subunitSEC61 translocon subunit gamma
02

Mechanism of action

Inhibition of protein translocation into ER, downregulation of immune checkpoint glycosylation, suppression of antigen processing and presentation, induction of tumor cell death by disrupting ER function

03

Biological functions

Protein translocation across ER membraneglycosylation of membrane proteinsimmune evasionregulation of antigen presentation
04

Disease associations

Cancer (e.g., glioblastoma, poor prognosis in chemotherapy/radiotherapy)congenital neutropeniaother solid tumors
05

Safety considerations

Potential for broad cytotoxicity due to central role in protein translocationrisk of systemic toxicity if not tumor-selective
06

Interacting drugs

Sec61 inhibitors (e.g., Coibamide A, KZR-261; investigational)
07

Biomarkers

SEC61G amplification/overexpressioncoamplification with EGFR in glioblastoma

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