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Both mutations can result in pheochromocytoma formation.

These mutations can result in oligospermia or azoospermia, cryptorchidism [4], and aneuploidy [5].

Alternatively, mutations can result in the carcinogenic transformation of cells and the formation of a tumour.

Another variable which influences our understanding is that proteins with translated mutations can result in interactions with other proteins.

More subtle molecular clock issues arise from the fact that mutations can result in variable amino acid replacement rates in proteins, especially among primates.

However, oncogenic mutations can result in Met overexpression and/or aberrant signaling that can lead to epithelial-to-mesenchymal transition (EMT) [8],[8]],[8]].

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There are other significant biological challenges as well as it has been shown that an identical mutation can result in different phenotypes [36].

Furthermore, we show that an acceptor-splice site mutation can result in different mutant transcripts, including a two-exon-skip involving an upstream exon.

A Gly717Arg mutation can result from a single bp change of G to A at the first base of codon717 in the eEF-2 gene.

Interestingly, the degradation of apoptotic cells utilizes many genes that also function in receptor-mediated endocytosis, and their mutation can result in various human diseases (e.g., mammalian orthologues of RAB-5 in tuberous sclerosis, Dynamin-2 and Rab7 in Charcot-Marie-Tooth disease [35] [37]).

This mutation can result in a continuous stimulation of cell growth and, consequently, in cancer.

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