Draft:N2G mouse
Severely immunodeficient laboratory mouse strain
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The N2G mouse (NOD–2–Genes knockout) is a severely immunodeficient laboratory mouse strain developed on a NOD background. The strain was generated by GEMCRO Inc. (South Korea) using CRISPR/Cas9 to delete large genomic regions of Prkdc, which encodes DNA-dependent protein kinase catalytic subunit (DNA-PKcs), and Il2rg, which encodes the interleukin-2 receptor common gamma chain (γc).[1]
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Submission declined on 25 September 2025 by Shocksingularity (talk). This draft appears to be generated by a large language model (such as ChatGPT). You cannot use LLMs to generate article content.
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Comment: Prose and possibly-hallucinated infobox is making me sus ai Shocksingularity (talk) 04:37, 25 September 2025 (UTC)
Genetics and immunophenotype
Loss of Prkdc function disrupts V(D)J recombination, resulting in the absence of mature T and B lymphocytes. Deletion of Il2rg additionally prevents natural killer cell development. The combined deficiency produces a T−B−NK− phenotype comparable to that of the NSG mouse and NOG mouse strains, which carry loss-of-function mutations in the same two genes.[1][2][3]
Applications
Human cancer xenografts
N2G mice support subcutaneous engraftment of human cancer cell lines and have been used to evaluate targeted therapies in vivo. The strain has been employed to investigate aurora kinase B inhibition as a strategy to overcome resistance to MET-targeted drugs in MET-amplified lung cancer models.[4] In a separate study, N2G mice were used to examine the role of dysfunctional adipocytes in tumor progression through YAP/TAZ-dependent cancer-associated adipocyte transformation.[5]
Hematopoietic stem cell engraftment
The strain supports engraftment of human hematopoietic stem cells (HSCs) and subsequent reconstitution of human immune cell populations.[1]
Cell therapy evaluation
A derivative strain, N2G-F8, carries an additional deletion of the F8 gene and has been used to evaluate iPSC-derived cell therapies for haemophilia A. A functionally enhanced factor VIII gene integrated into the AAVS1 locus of patient-derived iPSCs was assessed in N2G-F8 mice.[6]
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