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Mutations that affect insulin-like signaling in worms, flies, and the growth hormone / IGF1 axis in mice are associated with extended lifespan.
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Mutations and affect
Mutations in genes can cause also affect skin colour through oculocutaneous albinism ( OCA ) – a lack of pigment in the eyes, skin and sometimes hair that occurs occasionally in a very small fraction of the population.
Mutations to hemagglutinin affect the binding affinity to the cell surface receptor glycan of a target species, which determines the infectivity of the virus strain to that species.
Mutations in this region can affect rate of efficiency of gene transcription, which in turn can alter levels of mRNA and, thus, protein levels in general.
Mutations in this region can affect the efficiency of gene transcription, which controls both the levels of mRNA and overall protein levels .< ref > name
Mutations that affect the normal function of these genes can result in retinitis pigmentosa and vision loss.
Mutations in elements of the Notch signaling pathway affect the earliest intestinal cell fate decisions during zebrafish development.
Mutations of the CFTR gene affect functioning of the chloride ion channels in these cell membranes, leading to cystic fibrosis and congenital absence of the vas deferens.
Mutations that cause the altered codon to produce an amino acid with similar functionality ( i. e. a mutation producing leucine instead of isoleucine ) are often also classified as silent ; if the properties of the amino acid are conserved, this mutation does not usually significantly affect protein function.
Mutations that occur early on in development will affect a greater number of cells and can result in an individual that can be identified as a mosaic strictly based on phenotype.
Mutations in BMPs and their inhibitors ( such as sclerostin ) are associated with a number of human disorders which affect the skeleton.
Mutations in the human homologues of the Mut proteins affect genomic stability, which can result in microsatellite instability ( MI ).
Mutations and signaling
Mutations in the Ras / mitogen activated protein kinase signaling pathways are known to be responsible for ~ 70 % of NS cases.
Mutations in JAG1 disrupt the signaling pathway, causing errors in development, especially of the heart, bile ducts in the liver, spinal column, eyes, blood vessels and certain facial features.
Mutations and worms
Mutations in daf-2 have been shown by Cynthia Kenyon to double the lifespan of the worms.
Mutations and flies
Mutations of the wingless gene in the fruit fly were found in wingless flies, while tumors caused by MMTV were found to have copies of the virus integrated into the genome forcing overproduction of one of several Wnt genes.
Mutations and growth
Mutations in the epidermal growth factor receptor activate signalling pathways that promote cell survival.
Mutations in the FLCN gene may interfere with the ability of folliculin to restrain cell growth and division, leading to the formation of noncancerous and cancerous tumors.
Mutations at many steps in the pathway towards the restriction point can result in cancerous growth of cells.
* Mutations associated with aberrant epithelial cell layer growth due to lack of adhesions and contact inhibition
Mutations and hormone
Mutations of the thyroid-stimulating hormone receptor that cause a constitutive activation of the thyroid gland cells have been discovered recently.
Mutations in receptors that result in increased constitutive activity underlie some inherited diseases, such as precocious puberty ( due to mutations in luteinizing hormone receptors ) and hyperthyroidism ( due to mutations in thyroid-stimulating hormone receptors ).
Mutations and /
The National Gerbil Society .< http :// www. gerbils. pwp. blueyonder. co. uk / gerbils / genetics. htm # Mutations ></ ref >
Mutations / knockout of other genes affecting the GH / IGF1 axis, such as Lit, Ghr and Irs1 have also shown extension in lifespan, but much more modest both in relative and absolute terms.
Mutations in this gene and / or its regulatory regions cause or hypohaptoglobinemia.
Mutations of the genes VHL, RET, NF1 ( Gene 17 Neurofibromatosis type 1 ), SDHB and SDHD are all known to cause familial pheochromocytoma / extra-adrenal paraganglioma.
Mutations in this gene have been associated with various behavioral phenotypes, including autonomic nervous system dysfunction, attention deficit / hyperactivity disorder, schizophrenia, and the personality trait of novelty seeking.
Mutations in nsP2 that produce noncytopathic viruses or a temperature sensitive phenotypes cluster at the P2 / P3 interface region.
Mutations and mice
Mutations of the corresponding gene in mice ( FOXP2 is fairly well conserved ; modern humans share the same allele as Neanderthals ) cause reductions in size and vocalization rate.
Mutations associated with the gene may result in changes in serotonin transporter function, and experiments with mice have identified more the 50 different phenotypic changes as a result of genetic variation.
Mutations and are
Mutations in two regulatory genes of white grapes turn off production of anthocyanins which are responsible for the color of purple grapes.
Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.
Mutations are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.
Mutations in transpeptidases that lead to reduced interactions with an antibiotic are a significant source of emerging antibiotic resistance.
Mutations are an important force driving evolution.
Mutations are permanent, transmissible changes to the genetic material ( usually DNA or RNA ) of a cell.
Mutations are considered the driving force of evolution, where less favorable ( or deleterious ) mutations are removed from the gene pool by natural selection, while more favorable ( or beneficial ) ones tend to accumulate.
Mutations leading to the loss of function of a gene are much more common than mutations that produce a new, fully functional gene.
Mutations in the tafazzin gene ( TAZ, also called G4. 5 ) are closely associated with
Mutations periodically occur within the Y chromosome and these mutations are passed on to males in subsequent generations.
Mutations are characterized as either β < sup > o </ sup > or β thalassemia major if they prevent any formation of β chains, the most severe form of β thalassemia.
Mutations are the ultimate source of genetic variation because they alter the order of bases in the nucleotides of DNA.
Mutations are likely to be rare and most mutations are neutral or deleterious, but in some instances the new alleles can be favored by natural selection.
Mutations in the Ras family of proto-oncogenes ( comprising H-Ras, N-Ras and K-Ras ) are very common, being found in 20 % to 30 % of all human tumours.
Mutations in this gene are rare.
Mutations affecting repressor are said to be recessive to wild type ( and that wild type is dominant ), and this is explained by the fact that repressor is a small protein which can diffuse in the cell.
Mutations usually sound at pitches in the harmonic series of the fundamental and, except where they are derived from unit ranks, are always tuned pure.
Mutations within the desmosome are the main cause of Arrhythmogenic right ventricular cardiomyopathy ( ARVC ).
Mutations of the WT1 gene on chromosome 11 p 13 are observed in approximately 20 % of Wilms ' tumors .< ref > At least half of the Wilms ' tumors with mutations in WT1 also carry mutations in CTNNB1, the gene encoding the proto-oncogene beta-catenin.
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