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Target intelligence / Profile preview
Zinc finger SWIM domain-containing protein 8 (ZSWIM8)
- Target
- ZSWIM8
- Molecular classification
- E3 ubiquitin-protein ligase (Cullin-RING ligase type), SCF-like ubiquitin ligase complex substrate receptor, Protein with zinc finger SWIM domain
01
Overview
Zinc finger SWIM domain-containing protein 8 (ZSWIM8) is a substrate recognition component of a **Cullin-RING E3 ubiquitin ligase complex** that promotes **target-directed microRNA degradation (TDMD)**, a post-transcriptional gene-silencing regulatory process. ZSWIM8 binds Argonaute (AGO) proteins loaded with specific microRNAs extensively paired to targets, enabling ubiquitination and proteasomal degradation of AGO, which then exposes the microRNA for degradation[1][5][4][2]. ZSWIM8 also recognizes misfolded proteins such as ROBO3 and DAB1 for quality control during neural development, and is implicated in axon guidance, embryonic tissue development, and myogenic differentiation[1][3][4]. It contains a characteristic zinc finger SWIM domain, Cul2/VHL boxes, and is evolutionarily conserved from invertebrates to vertebrates[1][2]. No drugs currently target this protein, and it is not classified as a direct therapeutic target, but its biological roles are critical in normal development and disease pathogenesis.
- Other names
- KIAA09134832404P21RikPeladoDoradoZSWIM8Zswim8 (mouse ortholog; sometimes written in lowercase)
02
Mechanism of action
Not applicable/no known drugs
03
Biological functions
Target-directed microRNA degradation (TDMD), mediating degradation of microRNAs by facilitating the ubiquitination and degradation of Argonaute (AGO) proteinsProtein ubiquitination and subsequent proteasomal degradation of substrate proteinsRegulation of axon guidance via degradation of misfolded Robo receptorsRegulation of protein quality control, e.g., DAB1 degradationModulation of embryonic development (heart, lung, brain)Modulation of myogenic differentiation (muscle cell differentiation)
04
Disease associations
Developmental abnormalities (e.g., Acromelic Frontonasal Dysostosis)Potential roles in neural development defects (linked to axon guidance pathways)Modulation of antiviral response (Zika virus manipulation of STAT2 degradation)Possibly cancer, though evidence is indirect (cell viability/fitness screens)
05
Safety considerations
Not specifically reported as a safety concern; loss-of-function mutations are associated with severe developmental abnormalitiesZSWIM8 knockout is lethal in some model organisms, indicating essential developmental roles
06
Interacting drugs
None known or reported
07
Biomarkers
None established or reported
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