Add like
Add dislike
Add to saved papers

Compound pathogenic mutation in the USH2A gene in Chinese RP families detected by whole‑exome sequencing.

Retinitis pigmentosa (RP) is a common form of inherited retinal degeneration that causes progressive loss of vision or adult blindness, characterized by the impairment of rod and cone photoreceptors. At present, mutations in >60 pathogenic genes have been confirmed to cause RP. The predominant modes of inheritance are autosomal dominant, autosomal recessive and X‑linked. In addition, other modes of inheritance, including digenic or mitochondrial inheritance, have been reported. In previous decades, with the development of sequencing techniques, significant advances in identifying novel RP pathogenic genes and screening mutations have been made. In the present study, whole‑exome sequencing was performed on samples from two Chinese pedigrees diagnosed with RP. A compound heterozygous mutation in the gene usherin 2A (USH2A; c.6,485+5G>A/c.11,156G>A) and a heterozygous X‑linked mutation in the gene retinitis pigmentosa 2 (RP2) ARL3 GTPase‑activating protein (RP2; c.358C>T) were identified by Sanger sequencing and co‑segregation analysis, of which the pathogenic mutation (c.6,485+5G>A) in USH2A has not been previously reported among Chinese patients. The findings of the present study may expand on current knowledge of RP among the Chinese population, providing essential assistance in the molecular diagnosis and screening of RP, and promoting further investigation of the pathogenesis of RP.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app