@article{(Open Science Index):https://publications.waset.org/pdf/10682,
	  title     = {Proteins Length and their Phenotypic Potential},
	  author    = {Tom Snir and  Eitan Rubin},
	  country	= {},
	  institution	= {},
	  abstract     = {Mendelian Disease Genes represent a collection of single points of failure for the various systems they constitute. Such genes have been shown, on average, to encode longer proteins than 'non-disease' proteins. Existing models suggest that this results from the increased likeli-hood of longer genes undergoing mutations. Here, we show that in saturated mutagenesis experiments performed on model organisms, where the likelihood of each gene mutating is one, a similar relationship between length and the probability of a gene being lethal was observed. We thus suggest an extended model demonstrating that the likelihood of a mutated gene to produce a severe phenotype is length-dependent. Using the occurrence of conserved domains, we bring evidence that this dependency results from a correlation between protein length and the number of functions it performs. We propose that protein length thus serves as a proxy for protein cardinality in different networks required for the organism's survival and well-being. We use this example to argue that the collection of Mendelian Disease Genes can, and should, be used to study the rules governing systems vulnerability in living organisms.
},
	    journal   = {International Journal of Biomedical and Biological Engineering},
	  volume    = {3},
	  number    = {6},
	  year      = {2009},
	  pages     = {320 - 324},
	  ee        = {https://publications.waset.org/pdf/10682},
	  url   	= {https://publications.waset.org/vol/30},
	  bibsource = {https://publications.waset.org/},
	  issn  	= {eISSN: 1307-6892},
	  publisher = {World Academy of Science, Engineering and Technology},
	  index 	= {Open Science Index 30, 2009},
	}