By Michael M. Gottesman
Thoughts had to isolate mutant mobile traces and to exploit the mutants to clone and map the genes are offered intimately. this can be the 1st e-book within which such method and molecular biology are combined.The hottest cellphone traces for genetic research are awarded within the first part, by way of specified options for separating a variety of mutants. the rest of the publication is dedicated to genetic mapping and cloning of mutant genes. the ultimate part provides unique innovations in gene rules.
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Additional info for Molecular Genetics of Mammalian Cells
Ribonucleotide reductase alterations with abnormal responsiveness to dGTP Ribonucleotide reductase alterations with abnormal responsiveness to dATP Ribonucleotide reductase alterations with abnormal responsiveness to dTTP Adenylosuccinate synthase deficiency CTP synthase refractory to inhibition by CTP Deoxycytidylate deaminase deficiency AMP deaminase deficiency IMP dehydrogenase alterations Nucleoside transport deficiency Nucleoside transport functions insensitive to complete inhibition by NBMPR, a potent inhibitor of nucleoside transport Reference 22 23, 24 25 26 25, 27 25, 27 28 29 29- 31 30, 32, 33 34 35, 36 37 38, 39 40 41 42 43, 44 Glucocorticoid Response Altered ploidy of receptor gene Altered glucocorticoid binding by receptor Altered nuclear transport of receptor Independence of glucoeorticoid sensitivity from other responses 45, 46 47-49 47-51 5, 52 Cyclic AMP response Altered or deficient cAMP-dependent kinaseb Revertants of kinase mutants Mutants resistant to cAMP-induced cytolysis Mutants with altered or deficient adenylate cyclaseb Mutants with altered cAMP phosphodiesteraseb Mutants deficient in fl-adrenergic receptors Mutants with altered cAMP transport 6, 53-70 14, 16, 17 67, 71 72-82 80, 83-85 86 87 Miscellaneous Ornithine decarboxylase overproduction Lectin resistance~ Surface antigen (thy) deficiency~ 8, 88, 89 5,90,91 92, 93 a Available from ATCC.
3). Dedifferentiated variants have been isolated from both biochemically marked sublines as well as from the original H4II EC3 cells. In addition, Killary et al. 34 have isolated a thymidine kinase-deficient strain of H4II EC3, a useful mutant for cell hybridization and gene transfer. FU5 and its derivatives have been maintained primarily in F I 2 medium with 5% fetal calf serum. Faza has been maintained in our laboratory in MEM/MAB 87/3 + 10°/o FBS for several years without apparent loss of hepatospecific properties.
Niwa, and D. W. Nebert,Biochem. Pharmacol. 22, 2766 (1973). 5 H. Baumann and G. P. Jahreis, J. Cell Biol. 97, 728 (1983). 6 F. D. Ledley,unpublished observations. 7G. J. Darlington, J. Papaconstantinou, D. W. Sammons, P. C. Brown, E. Y. Wong, A. L. Esterman, and J. Kang, Somatic Cell Genet. 8, 451 (1982). s O. Hankinson, Somatic Cell Genet. 7, 373 (1981). 22 CELL LINES FOR GENETIC ANALYSIS [31 TABLE I Hepa PHENOTYPES Hepa phenotypes Designation Reference Albumin Alcohol dehydrogenase (liver isoform) Aldolase A Aldolase B ot-Fetoprotein Amylase AMY- 1 Induction of AMY- 1 by dexamethasone Amylase AMY-2 Induction of AMY-2 by dexamethasone Aryl hydrocarbon hydroxylase (AHH) Inducibility of AHH by phenobarbitol Ceruloplasmin C3 Esterase 1 Esterase 2 Fibrinogen Glycogen storage Haptoglobin Phenylalanine hydroxylase Pseudocholinesterase Transferrin Tyrosine aminotransferase (TAT) Inducibility of TAT by dexamethasone Xanthine oxidase + + + + 1 1 1 1 1 3 + - 3 3 + + 3 4 + + + -+ + + + - 4 1 1 1 1 1 1 5 6 1 1 1 1 1 overlay has been performed by Sammons et al.