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This paradigm indicates that specific, critical mutations produce abnormal cell proliferation leading to cancer, rather than ER-mediated abnormal cell proliferation that generates random mutations [1, 6 10].
On the contrary, some missense mutations produce abnormal proteins that are present at normal levels inside cells.
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Markers include mutations that produce abnormal movement [ dpy-10 (cn64 ), rol-6 (su1006 ), unc-22 (loss-of-function)] or repair of a conditional lethal mutation [ pha-1 (e2123 ) (Arribere et al. 2014; Kim et al. 2014; Ward 2015].
Due to a procollagen α2 gene recessive mutation, homozygous oim mice produce abnormal homotrimeric collagen type I (Col1- α1)3) which results in a phenotype mimicking the human type III osteogenesis imperfecta (small body weight, skeletal deformities and brittle bones) [47].
Single nucleotide mutations in α1 or α2 genes produce abnormal α-chain hemoglobins.
Mutations of lamin A/C (Lmna) gene or the Zmpste24 gene produce abnormal lamins, such as progerin or prelamin A, respectively [ 16], which can cause disassembly of the nuclear envelope proteins, subsequently accompanied by accelerated aging due to laminopathies [ 16].
Sleeping pills also produce abnormal sleep patterns and reduce alertness the next day.
Mild head injury may or may not produce abnormal EEG readings.
Aberrations in neuronal excitability can produce abnormal electrical discharges in the brain leading to seizure activity.
Dysfunction in such a feedback structure can produce abnormal synchronization under pathological conditions.
Hemiarthroplasties produce abnormal stress levels on the acetabulum which in turn causes degeneration [ 21, 40].
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