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Loss-of-Function Mutations in HPSE2 Cause the Autosomal Recessive Urofacial Syndrome

  • Junfeng Pang
    ,
  • Shu Zhang
    ,
  • Ping Yang
    ,
  • Bobbilynn Hawkins Lee
    ,
  • Jixin Zhong
    ,
  • Yushan Zhang
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

Previously, we localized the defective gene for the urofacial syndrome (UFS) to a region on chromosome 10q24 by homozygosity mapping. We now report evidence that Heparanse 2 (HPSE2) is the culprit gene for the syndrome. Mutations with a loss of function in the Heparanase 2 (HPSE2) gene were identified in all UFS patients originating from Colombia, the United States, and France. HPSE2 encodes a 592 aa protein that contains a domain showing sequence homology to the glycosyl hydrolase motif in the heparanase (HPSE) gene, but its exact biological function has not yet been characterized. Complete loss of HPSE2 function in UFS patients suggests that HPSE2 may be important for the synergic action of muscles implicated in facial expression and urine voiding.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 957-962 (6 pages)

Journal (Volume, Issue Number)

American journal of human genetics (Volume 86, Issue 6)

Publication milestones

  • Published - 07/11/2010

Publication status

Published - 07/11/2010

ISSN

0002-9297

Publication IDs

  • Scopus: 77953229417
  • PubMed: 20560209

Publication metrics

Metrics

Scopus
citations
Fractional count
5
Fractional count
0.36
Fractional count
9
Fractional count
0.64
Fractional count
5
Fractional count
1
SciVal
citations
53
SciVal
FWCI
1.35
SciVal
Author count
14
SciVal
Paper percentile
91
SciVal
Top percentile
10

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Captures
40
Citation count
72

Funding Details

We are grateful to the affected subjects and their family members for participating in this study. We are also grateful to Leszek Ignatowicz for his great suggestion for manuscript preparation and Yan Jiao for her advice in high-throughput mutation screening. This work was supported by grants from the National Institutes of Health (DK074957 to C.-Y.W. and DK53266 to J.-X.S.).
FundersFunding numbers
NIH
DK53266
NIDDK
R21DK074957