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The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease.

Open access
Wang, Z Q, Auer, B, Stingl, L, Berghammer, H, Haidacher, D, Schweiger, M, Wagner, E F·1995·Genes & Development
DOI 10.1101/gad.9.5.509
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Abstract

Poly(ADP-ribosyl)ation is catalyzed by NAD+: protein(ADP-ribosyl) transferase (ADPRT), a chromatin-associated enzyme which, in the presence of DNA breaks, transfers ADP-ribose from NAD+ to nuclear proteins. This post-translational modification has been implicated in many fundamental processes, like DNA repair, chromatin stability, cell proliferation, and cell death. To elucidate the biological function of ADPRT and poly(ADP-ribosyl)ation in vivo the gene was inactivated in the mouse germ line. Mice homozygous for the ADPRT mutation are healthy and fertile. Analysis of mutant tissues and fibroblasts isolated from mutant fetuses revealed the absence of ADPRT enzymatic activity and poly(ADP-ribose), implying that no poly(ADP-ribosyl)ated proteins are present. Mutant embryonic fibroblasts were able to efficiently repair DNA damaged by UV and alkylating agents. However, proliferation of mutant primary fibroblasts as well as thymocytes following gamma-radiation in vivo was impaired. Moreover, mutant mice are susceptible to the spontaneous development of skin disease as approximately 30% of older mice develop epidermal hyperplasia. The generation of viable ADPRT-/-mice negates an essential role for this enzyme in normal chromatin function, but the impaired proliferation and the onset of skin lesions in older mice suggest a function for ADPRT in response to environmental stress.

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Show all 31 references

Research works printed but not linked: 23

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Metadata

Authors
Wang, Z. Q., Auer, B., Stingl, L., Berghammer, H., Haidacher, D., Schweiger, M., & Wagner, E. F.
Venue
Genes & Development
Publisher
Cold Spring Harbor Laboratory
Published
1995-03-01
Volume
9
Issue
5
Pages
509-520
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
DOI
10.1101/gad.9.5.509
OpenAlex
W2151797852
Cited by
774
References
31
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease. https://app.cochat.ai/papers/10.1101/gad.9.5.509
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Wang, Z. Q., Auer, B., Stingl, L., Berghammer, H., Haidacher, D., Schweiger, M., & Wagner, E. F. (1995). Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease. Genes & Development. https://doi.org/10.1101/gad.9.5.509

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