![]() (1984) reexamined the Hutterite family, making use of other markers thought to be on 1p (6PGD, Colton, UMPK1) and concluded that crossover or mutation indeed had occurred. Hopefully, Rh antigen will be isolated for characterisation but there has been nothing published since the report of Plapp et al. Except for Steinberg's one crossover, there have been no exceptions to the inheritance of Rh antigens in tight haplotype packages. (Illegitimacy was excluded by the mores of the sect and by marker studies.) Rosenfield (1981) wrote: 'We still know nothing about Rh. Race and Sanger (1975) considered a recessive suppressor likely. Mutation and, much less likely, a recessive suppressor of the D antigen were mentioned as other possibilities. Steinberg (1965) thought this was an instance of crossing-over. Steinberg (1965) described a Hutterite family in which the father was CDe-cde, mother cde-cde, 4 children cde-cde, 3 children CDe-cde, and 1 child (the 6th born) Cde-cde. No completely certain example of recombination within a postulated gene complex has been described. Rh antigen still eludes chemical definition (Tippett, 1978), but it is thought to be a lipoprotein. (1977) observed only 1 recombination in 58 opportunities between the alpha-fucosidase locus (FUCA1 612280) and the Rh locus. (1974) did not have deletion of the PGM1 locus in the mutant clone, the Rh locus is probably distal to the PGM1 locus. (1973) that the PGM1 locus, which is linked to Rh, is on the short arm of chromosome 1. The conclusion is consistent with the finding of Douglas et al. ![]() They concluded that the Rh locus probably lies on the distal segment of the short arm at some point between 1p32 and the end of the short arm. ![]() Nucleated hemopoietic precursors were circulating in his blood, and these cells had an abnormal chromosome complement from which part of the short arm of chromosome 1 had been deleted. (1974) found Rh-negative erythrocytes in an Rh-positive man suffering from myelofibrosis. Although the Rh and Duffy loci are both on chromosome 1, they are too far apart to demonstrate linkage in family studies (Sanger et al., 1973). Renwick (1971) suggested that PGM1 is on the side of Rh, remote from 6PGD and about 30 centimorgans from Rh. (1970) published family data consistent with loose linkage of Duffy and PGM1. (1970) reported data suggesting a loose linkage between a translocation breakpoint near the end of the long arm of chromosome 1 and Rh. Information from cell hybridization studies placed the Rh-elliptocytosis-PGM(1)-6PGD linkage group on chromosome 1. The first 2 loci appear to lie between the latter 2 (Renwick, 1971). Rh, elliptocytosis, PGM1, and 6PGD are all on the same chromosome. Industry Insights with Yuning Chen on Recombinant Proteins.ExpertAnswers: Yuning Chen on Antibody Production.Universal Vaccine Advancement through AI and Recombinant Technology.Nanobodies: An Important Tool for the Next Generation of Tumor Diagnostics and Therapeutics.ExpertAnswers: Amy Sheng on Antibody Screening and Discovery.Recombinant DNA Technology and Its Impact on Drug Discovery.CAR-T Cell Therapy Development: From Personalized to off the Shelf Approaches.BioBuzz with Sino | Episode 1: ChatGPT in Biotech. ![]()
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