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@ARTICLE{Hebert:301740,
      author       = {J. D. Hebert and H. Xu and Y. J. Tang and P. A. Ruiz and C.
                      R. Detrick and J. Wang and N. W. Hughes and O. Donosa and V.
                      P. Siah and L. Andrejka and S. Karmakar and I. Aboiralor and
                      R. Tang and R. Sotillo$^*$ and J. Sage and L. Cong and D. A.
                      Petrov and M. M. Winslow},
      title        = {{E}fficient and multiplexed somatic genome editing with
                      {C}as12a mice.},
      journal      = {Nature biomedical engineering},
      volume       = {nn},
      issn         = {2157-846X},
      address      = {Tokyo},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2025-01124},
      pages        = {nn},
      year         = {2025},
      note         = {epub},
      abstract     = {Somatic genome editing in mouse models has increased our
                      understanding of the in vivo effects of genetic alterations.
                      However, existing models have a limited ability to create
                      multiple targeted edits, hindering our understanding of
                      complex genetic interactions. Here we generate transgenic
                      mice with Cre-regulated and constitutive expression of
                      enhanced Acidaminococcus sp. Cas12a (enAsCas12a), which
                      robustly generates compound genotypes, including diverse
                      cancers driven by inactivation of trios of tumour suppressor
                      genes or an oncogenic translocation. We integrate these
                      modular CRISPR RNA (crRNA) arrays with clonal barcoding to
                      quantify the size and number of tumours with each array, as
                      well as the impact of varying the guide number and position
                      within a four-guide array. Finally, we generate tumours with
                      inactivation of all combinations of nine tumour suppressor
                      genes and find that the fitness of triple-knockout genotypes
                      is largely explainable by one- and two-gene effects. These
                      Cas12a alleles will enable further rapid creation of disease
                      models and high-throughput investigation of coincident
                      genomic alterations in vivo.},
      cin          = {B220 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B220-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40447760},
      doi          = {10.1038/s41551-025-01407-7},
      url          = {https://inrepo02.dkfz.de/record/301740},
}