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9 Mar 2019
I was reading a section in my Cell Bio book regarding lamins and premature aging. While the disease is rare, it seems to be one that makes a large impact on developmental science and medicine. The book mentions that the symptoms for this disease are caused by a mutation in the LMNA gene, resulting in the protein staying in the nuclear membrane instead of the lamina.
My question is, how do the cells of those affected with this disease compare to normally aging individuals? Do older adults experience similar mutations of the LMNA genes as those affected by the disease? Also, what exactly would a treatment target and how does the localization of progerin cause the disease symptoms?
I was reading a section in my Cell Bio book regarding lamins and premature aging. While the disease is rare, it seems to be one that makes a large impact on developmental science and medicine. The book mentions that the symptoms for this disease are caused by a mutation in the LMNA gene, resulting in the protein staying in the nuclear membrane instead of the lamina.
My question is, how do the cells of those affected with this disease compare to normally aging individuals? Do older adults experience similar mutations of the LMNA genes as those affected by the disease? Also, what exactly would a treatment target and how does the localization of progerin cause the disease symptoms?
Trinidad TremblayLv2
10 Mar 2019
