CARCINOFETAL ALTERATIONS IN GLYCOGEN PHOSPHORYLASE ISOZYMES IN RAT HEPATOMAS
Annals of the New York Academy of Sciences, ISSN: 1749-6632, Vol: 259, Issue: 1, Page: 273-286
1975
- 19Citations
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations19
- Citation Indexes19
- 19
- CrossRef13
Book Chapter Description
As part of a continuing study on the loss or retention of enzymes involved in specific hepatic functions in a series of rat liver neoplasms ranging widely in growth rate and degree of differentiation, isozyme patterns of glycogen phosphorylase in rat hepatomas were compared with those in rat tissues during development. A third phosphorylase isozyme, distinguishable kinetically, immunologically, electrophoretically, and by isoelectric focusing from liver and muscle types is commonly present in various rat hepatomas including Novikoff, Morris, and Yoshida hepatomas with various degrees of retention of liver type according to their degree of differentiation. This isozyme is also the sole type in the placenta and early embryo, and in liver and muscle is replaced with the organ specific liver and muscle types during development. In other organs, the replacement is only partial, and, especially in adult rat brain, this type is retained. Thus, this isozyme seems to be a prototype whose appearance in hepatomas is one of many examples of carcinofetal alterations in isozymes.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0016586626&origin=inward; http://dx.doi.org/10.1111/j.1749-6632.1975.tb25424.x; http://www.ncbi.nlm.nih.gov/pubmed/173229; https://nyaspubs.onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1975.tb25424.x; https://dx.doi.org/10.1111/j.1749-6632.1975.tb25424.x; https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1975.tb25424.x
Wiley
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