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Parp1-/- is a genetically modified mouse strain that lacks the expression of the Parp1 gene. Parp1 encodes the enzyme Poly(ADP-ribose) Polymerase 1, which is involved in DNA repair processes. This mouse strain can be used in research to study the role of Parp1 in various biological systems.

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Balb c, by Charles River Laboratories (1 mentions) Fvb mice, by Charles River Laboratories (1 mentions) C57bl 6j mice, by Jackson ImmunoResearch (1 mentions)

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Parp1 null (2 citations)

2 protocols using parp1

1

Genetically Modified Mice for Vision Research

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Animals rd1 mice were the albino FVB strain, which carries the Pde6brd1 allele (MGI: 1856373). BALB/c, CD1, and FVB mice were purchased from Charles River Laboratories. Due to availability, some of the FVB mice were purchased from Taconic, and we did not notice any difference between the two sources in terms of cone degeneration rate. C57BL/6J, rd10, and Parp1-/- mice were purchased from The Jackson Laboratories and bred in house. C57BL/6J and rd10, which is on C57BL/6J background, carry a null mutation in the Nnt gene (Freeman et al., 2006 (link)), but not in the other strains (i.e., rd1, Rho-/-, Parp1-/-, CD1, and BALB/c). We crossed the Parp1-/- mice with FVB mice to generate homozygous Parp1-/-rd1 and Parp1+/+rd1 mice. Genotyping of these mice was done by Transnetyx (Cordova, TN). The Rho-/- mice were kindly provided by Janice Lem (Tufts University, MA) (Lem et al., 1999 (link)).
Xue Y., Wang S.K., Rana P., West E.R., Hong C.M., Feng H., Wu D.M, & Cepko C.L. (2021). AAV-Txnip prolongs cone survival and vision in mouse models of retinitis pigmentosa. eLife, 10, e66240.
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2

Mouse Models of Neurological Disorders

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All procedures were approved by the Institutional Animal Care and Use Committee of Weill Cornell Medical College. Experiments were conducted in C57BL/6J mice (The Jackson Laboratories), in mice lacking PARP-1 (The Jackson Laboratories) or Nox2, bred on a C56BL/6J background55 (link),5 (link), and in transgenic mice overexpressing the Swedish mutation of APP (tg2576)17 (link). TRPM2-null mice57 (link) and WT controls were generously provided by Drs Herson and Traystman. All mice were male and 3- to 4-month-old. Age-matched nontransgenic littermates served as controls. Mice were randomly assigned to the experimental groups and experiments were performed in a blinded manner.
Park L., Wang G., Moore J., Girouard H., Zhou P., Anrather J, & Iadecola C. (2014). The key role of transient receptor potential melastatin-2 channels in amyloid-β-induced neurovascular dysfunction. Nature communications, 5, 5318.
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