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发布于:2019-4-11 09:18:51  访问:20 次 回复:0 篇
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R thyroid carcinoma [49], pancreatic carcinoma [50], and Schimmelpenning-Feuerstein-Mims syndrome [51], also as
R thyroid order Vemurafenib carcinoma [49], pancreatic carcinoma [50], and Schimmelpenning-Feuerstein-Mims syndrome [51], as well as bladder [52], lung [53], and gastric cancers [54]. A comprehensive list of all considerable co-occurrences of human illness and yeast phenotypic alterations PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27484364 is often discovered in Added file 2. Interestingly, probably the most considerable disease-phenotype co-occurrence was Wilson‘s illness, a human genetic disorder in which copper accumulates in tissues, with the yeast phenotype connected to "Gain of function; metal resistance: increased." This yeast phenotype was derived from a study that analyzed a mutated copper-transporter gene, which resulted within a gain of function mutation that enabled the manage of intracellular levels of cadmium by way of an enhanced cadmium efflux method [61]. When the partnership involving the two phenotypes for the Wilson‘s illness example appears to become clear, for many of your significant co-occurrence of phenotypes identified with our system, theTable 7 Human ailments and yeast phenotypic alterations that co-occur at domain sitesHuman Disease Wilson‘s illness (WD) (OMIM:277900) Hereditary non-polyposis colorectal cancer sort 2 (OMIM:609310) Susceptibility to Breast-Ovarian Cancer, Familial (OMIM:604370) Nemaline myopathy type three (OMIM: 161800) Familial hyperinsulinemic hypoglycemia form 1 (OMIM: 256450) Costello syndrome (OMIM:190020) Methemoglobinemia, kind 1 (OMIM:250800) Crouzon syndrome (OMIM: 123500) Yeast Phenotypic Modify Acquire of function; metal resistance: enhanced (PMID: 10743563) Mutation frequency: improved (PMID: 16492773) Reduction of function; protein/peptide accumulation: improved (PMID: 10218484) Reduction of function; replicative lifespan: decreased (PMID: 21931558) Inviable (PMID.R thyroid carcinoma [49], pancreatic carcinoma [50], and Schimmelpenning-Feuerstein-Mims syndrome [51], at the same time as bladder [52], lung [53], and gastric cancers [54]. While each HRAS and KRAS belong for the very same protein household and are as a result usually implicated in the exact same studies, domain position five also aligns to position 38 of a gene from a diverse household, GNAT1, which can be not comparable in sequence to HRAS (i.e., HRAS-GNAST1 E-value of 0.53 utilizing BLAST [55]) or KRAS (i.e., KRAS-GNAST1 BLAST E-value of 0.42). The GNAT1 mutation has been related with congenital stationary evening blindness [56]. Moreover, other mutations were discovered in the GTP/Mg++ binding pocket that were not members of position-based domain hotspots in either organism that we had been capable to determine using our feature-based domain hotspots. These mutations, sharing common functional annotation with position-based domain hotspots in bothspecies, have been associated with autoimmune lymphoproliferative syndrome [57], somatic pilocytic astrocytoma [58], Noonan syndrome [59], and chylomiccron retention disease [60]. As a result, by extrapolating hotspots in human and yeast to prevalent PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27107493 functional function positions, we had been capable to determine a popular functional disruption of the GTP/Mg++ binding pocket that causes different phenotypes when mutated in distinctive genes sharing the identical domain inside the identical organism as well as across organisms. Furthermore, the domain-centric strategy across species introduced here could also be extended to compare the unique phenotypes across organisms that may be associated through mutations clustered with this approach, analogous for the phenotype similarities described by McGary et al. [12] employing gene orthology.
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