Pathology of Genetically Engineered and Other Mutant Mice
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Pathology of Genetically Engineered and Other Mutant Mice: краткое содержание, описание и аннотация
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An updated and comprehensive reference to pathology in every organ system in genetically modified mice Pathology of Genetically Engineered and Other Mutant Mice
Pathology of Genetically Engineered and Other Mutant Mice
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20 20 Penner, J.D. and Prieur, D.J. (1987). A comparative study of the lesions in cultured fibroblasts of humans and four species of animals with Chediak‐Higashi syndrome. Am. J. Med. Genet. 28 (2): 445–454.
21 21 Penner, J.D. and Prieur, D.J. (1987). Interspecific genetic complementation analysis with fibroblasts from humans and four species of animals with Chediak‐Higashi syndrome. Am. J. Med. Genet. 28 (2): 455–470.
22 22 Schofield, P.N., Vogel, P., Gkoutos, G.V., and Sundberg, J.P. (2012). Exploring the elephant: histopathology in high‐throughput phenotyping of mutant mice. Dis. Models Mech. 5 (1): 19–25.
23 23 Mezick, J.A., Bhatia, M.C., and Capetola, R.J. (1984). Topical and systemic effects of retinoids on horn‐filled utriculus size in the rhino mouse. A model to quantify “antikeratinizing” effects of retinoids. J. Invest. Dermatol. 83 (2): 110–113.
24 24 Ashton, R.E., Connor, M.J., and Lowe, N.J. (1984). Histologic changes in the skin of the rhino mouse (Hrrh/Hrrh) induced by retinoids. J. Invest. Dermatol. 82 (6): 632–635.
25 25 Bryce, G.F., Bogdan, N.J., and Brown, C.C. (1988). Retinoic acids promote the repair of the dermal damage and the effacement of wrinkles in the UVB‐irradiated hairless mouse. J. Invest. Dermatol. 91 (2): 175–180.
26 26 Kligman, L.H. (1989). Prevention and repair of photoaging: sunscreens and retinoids. Cutis 43 (5): 458–465.
27 27 Sundberg, J.P., Dunstan, R.W., and Compton, J.G. (1989). Hairless mouse, HRS/J hr/hr. In: Integument and Mammary Glands Monographs on Pathology of Laboratory Animals (eds. T.C. Jones, U. Mohr and R.D. Hunt), 192–197. Heidelberg: Springer‐Verlag.
28 28 Sundberg, J.P., Price, V.H., and King, L.E. Jr. (1999). The “hairless” gene in mouse and man. Arch. Dermatol. 135 (6): 718–720.
29 29 Ahmad, W., Faiyaz ul Haque, M., Brancolini, V. et al. (1998). Alopecia universalis associated with a mutation in the human hairless gene. Science 279 (5351): 720–724.
30 30 Ahmad, W., Irvine, A.D., Lam, H. et al. (1998). A missense mutation in the zinc‐finger domain of the human hairless gene underlies congenital atrichia in a family of Irish travellers. Am. J. Hum. Genet. 63 (4): 984–991.
31 31 Ahmad, W., Panteleyev, A.A., Henson‐Apollonio, V. et al. (1998). Molecular basis of a novel rhino (hrrhChr) phenotype: a nonsense mutation in the mouse hairless gene. Exp. Dermatol. 7 (5): 298–301.
32 32 Ahmad, W., Panteleyev, A.A., Sundberg, J.P., and Christiano, A.M. (1998). Molecular basis for the rhino (Hrrh‐8J) phenotype: a nonsense mutation in the mouse hairless gene. Genomics 53 (3): 383–386.
33 33 Panteleyev, A.A., Ahmad, W., Malashenko, A.M. et al. (1998). Molecular basis for the rhino Yurlovo (hr(rhY)) phenotype: severe skin abnormalities and female reproductive defects associated with an insertion in the hairless gene. Exp. Dermatol. 7 (5): 281–288.
34 34 Panteleyev, A.A., Paus, R., Ahmad, W. et al. (1998). Molecular and functional aspects of the hairless (Hr) gene in laboratory rodents and humans. Exp. Dermatol. 7 (5): 249–267.
35 35 Tuttle, A.H., Philip, V.M., Chesler, E.J., and Mogil, J.S. (2018). Comparing phenotypic variation between inbred and outbred mice. Nat. Methods 15 (12): 994–996.
36 36 McElwee, K.J., Niiyama, S., Freyschmidt‐Paul, P. et al. (2003). Dietary soy oil content and soy‐derived phytoestrogen genistein increase resistance to alopecia areata onset in C3H/HeJ mice. Exp. Dermatol. 12 (1): 30–36.
37 37 Ward, J.M. and Devor‐Henneman, D.E. (2004). Mouse models of human familial cancer syndromes. Toxicol. Pathol. 32 (Suppl 1): 90–98.
38 38 Kuperwasser, C., Hurlbut, G.D., Kittrell, F.S. et al. (2000). Development of spontaneous mammary tumors in BALB/c p53 heterozygous mice. A model for Li‐Fraumeni syndrome. Am. J. Pathol. 157 (6): 2151–2159.
39 39 Sundberg, J.P. and Schofield, P.N. (2018). Living inside the box: environmental effects on mouse models of human disease. Dis. Models Mech. 11 (10): dmm035360. https://doi.org/10.1242/dmm.035360.
40 40 Sofaer, J.A. (1969). Aspects of the tabby‐crinkled‐downless syndrome. II. Observations on the reaction to changes of genetic background. J. Embryol. Exp. Morphol. 22 (2): 207–227.
41 41 Sofaer, J.A. (1969). Aspects of the tabby‐crinkled‐downless syndrome. I. The development of tabby teeth. J. Embryol. Exp. Morphol. 22 (2): 181–205.
42 42 Li, Q., Philip, V.M., Stearns, T.M. et al. (2019). Quantitative trait locus and integrative genomics revealed candidate modifier genes for ectopic mineralization in mouse models of pseudoxanthoma elasticum. J. Invest. Dermatol. 139 (12): 2447–2457.e7.
43 43 Montagutelli, X., Hogan, M.E., Aubin, G. et al. (1996). Lanceolate hair (lah): a recessive mouse mutation with alopecia and abnormal hair. J. Invest. Dermatol. 107 (1): 20–25.
44 44 Sundberg, J.P., Boggess, D., Bascom, C. et al. (2000). Lanceolate hair‐J (lahJ): a mouse model for human hair disorders. Exp. Dermatol. 9 (3): 206–218.
45 45 Chavanas, S., Bodemer, C., Rochat, A. et al. (2000). Mutations in SPINK5, encoding a serine protease inhibitor, cause Netherton syndrome. Nat. Genet. 25 (2): 141–142.
46 46 Kljuic, A., Bazzi, H., Sundberg, J.P. et al. (2003). Desmoglein 4 in hair follicle differentiation and epidermal adhesion: evidence from inherited hypotrichosis and acquired pemphigus vulgaris. Cell 113 (2): 249–260.
47 47 Price, V.H., Odom, R.B., Ward, W.H., and Jones, F.T. (1980). Trichothiodystrophy: sulfur‐deficient brittle hair as a marker for a neuroectodermal symptom complex. Arch. Dermatol. 116 (12): 1375–1384.
48 48 Gummer, C.L., Dawber, R.P., and Price, V.H. (1984). Trichothiodystrophy: an electron‐histochemical study of the hair shaft. Br. J. Dermatol. 110 (4): 439–449.
49 49 Metze, D. and Oji, V. (2020). Disorders of keratinization. In: McKee's Pathology of the Skin. 1., 5e (eds. E. Calonje, T. Brenn, A. Lazar and S.D. Billings), 53–117. China: Elsevier.
50 50 Mecklenburg, L., Paus, R., Halata, Z. et al. (2004). FOXN1 is critical for onycholemmal terminal differentiation in nude (Foxn1) mice. J. Invest. Dermatol. 123 (6): 1001–1011.
51 51 Davisson, M.T., Bergstrom, D.E., Reinholdt, L.G., and Donahue, L.R. (2012). Discovery genetics – the history and future of spontaneous mutation research. Curr. Protoc. Mouse Biol. 2: 103–118.
52 52 Probst, F.J. and Justice, M.J. (2010). Mouse mutagenesis with the chemical supermutagen ENU. Methods Enzymol. 477: 297–312.
53 53 Arnold, C.N., Barnes, M.J., Berger, M. et al. (2012). ENU‐induced phenovariance in mice: inferences from 587 mutations. BMC Res. Notes 5: 577.
54 54 Sabrautzki, S., Rubio‐Aliaga, I., Hans, W. et al. (2012). New mouse models for metabolic bone diseases generated by genome‐wide ENU mutagenesis. Mamm. Genome 23 (7‐8): 416–430.
55 55 Potter, P.K., Bowl, M.R., Jeyarajan, P. et al. (2016). Novel gene function revealed by mouse mutagenesis screens for models of age‐related disease. Nat. Commun. 7: 12444.
56 56 Wang, T., Bu, C.H., Hildebrand, S. et al. (2018). Probability of phenotypically detectable protein damage by ENU‐induced mutations in the Mutagenetix database. Nat. Commun. 9 (1): 441.
57 57 Fairfield, H., Srivastava, A., Ananda, G. et al. (2015). Exome sequencing reveals pathogenic mutations in 91 strains of mice with Mendelian disorders. Genome Res. 25 (7): 948–957.
58 58 Palmer, K., Fairfield, H., Borgeia, S. et al. (2016). Discovery and characterization of spontaneous mouse models of craniofacial dysmorphology. Dev. Biol. 415 (2): 216–227.
59 59 Andrews, T.D., Whittle, B., Field, M.A. et al. (2012). Massively parallel sequencing of the mouse exome to accurately identify rare, induced mutations: an immediate source for thousands of new mouse models. Open Biol. 2 (5): 120061. https://doi.org/10.1098/rsob.120061.
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