Target intelligence / Profile preview

Protein transport protein Sec23B (SEC23B)

Target
SEC23B
Molecular classification
Vesicle trafficking protein, Coat protein complex II (COPII) component, Transporter (subcellular protein transport), GTPase-activating protein (GAP)
01

Overview

Protein transport protein Sec23B is a core component of the coat protein complex II (COPII), which mediates vesicle formation from the endoplasmic reticulum (ER) to the Golgi apparatus[1][3][4]. SEC23B acts as a GTPase-activating protein for SAR1, facilitating vesicle budding and cargo selection during ER-to-Golgi transport[1][5]. It is structurally composed of five domains (zinc finger, trunk, β-barrel, α-helix, and gelsolin-like domains)[1], and has functional overlap with its paralog SEC23A, though SEC23B’s deficiency in humans primarily leads to congenital dyserythropoietic anemia type II due to defective red blood cell maturation[3]. SEC23B is also involved in regulating autophagy and maintaining secretory tissue integrity[1][5]. Abnormal SEC23B function is implicated in certain rare genetic diseases and has emerging links to cancer biology, but there are currently no clinically approved drugs that target it directly[1][3].

Other names
SEC23 homolog B, COPII componentSEC23BhSec23BCDA-IICDAIIHEMPASSEC23-related protein BCDAN2CWS7SEC23-like protein Btransport protein SEC23Bcoat complex II componentprotein transport protein Sec23B
02

Mechanism of action

Not applicable; not directly targeted by small molecules or biologics in current clinical practice[3].

03

Biological functions

Protein transport from endoplasmic reticulum (ER) to Golgi apparatusCargo recognition and selectionRegulation of COPII-coated vesicle formationAutophagy regulationEmbryonic development, especially in secretory and hematopoietic tissues
04

Disease associations

Congenital dyserythropoietic anemia type II (CDA-II)Secretory tissue degenerationCancer (involved variably, e.g., possible role in tumor cell proliferation, survival, and autophagy)
05

Safety considerations

Loss-of-function can cause severe anemia (CDA-II) in humans and degeneration of secretory tissues in model organisms[3][5].Essential for viability in some tissues; therefore, inhibition likely to have significant toxicity.
06

Biomarkers

SEC23B gene mutations serve as a genetic biomarker for congenital dyserythropoietic anemia type II[3]

Beyond the preview

Go deeper on Protein transport protein Sec23B (SEC23B).

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 transport protein Sec23B (SEC23B).

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