Skip to content

The mechanism of splicing factor PUF60 causing congenital skeletal abnormalities by inhibiting osteogenic development

The mechanism of splicing factor PUF60 causing congenital skeletal abnormalities by inhibiting osteogenic development

Status
Active, not recruiting
Phases
Unknown
Study type
Observational
Source
ChiCTR
Registry ID
ChiCTR2500112279
Enrollment
Unknown
Registered
2025-11-12
Start date
2025-12-01
Completion date
Unknown
Last updated
2025-11-17

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Genetic Skeletal Disorders, GSD

Interventions

Gold Standard:Whole exome sequencing suggests that the child has a PUF60 mutation. After further Sanger sequencing, if the same PUF60 mutation is also detected, then the child has a PUF60 mutation sit
Index test:The sanger sequencing

Sponsors

Beijing Childrens Hospital,Capital Medical University
Lead Sponsor

Eligibility

Sex/Gender
All
Age
No minimum to 18 Years

Inclusion criteria

Inclusion criteria: 1. Age: children or adolescents aged 0-18 years. 2. Clinical and molecular diagnosis: PUF60 mutation was found in all the children with hereditary bone disease diagnosed by whole exome sequencing in our hospital.

Exclusion criteria

Exclusion criteria: 1. Children with non-hereditary bone disease and non-PUF60 gene mutation.

Design outcomes

Primary

MeasureTime frame
Sanger sequencing revealed gene mutations in the patient;Clinical skeletal (e.g., craniofacial, scapular, spine, and body condition) and nonskeletal (heart, kidney) phenotypes;

Secondary

MeasureTime frame
The height of child, the CT scan of bone;

Countries

China

Contacts

Public ContactChanjuan Hao

Beijing Childrens Hospital,Capital Medical University

hchjhchj@163.com+86 10 59616894

Outcome results

None listed

Source: ChiCTR (via WHO ICTRP) · Data processed: Feb 4, 2026