Mutations in the gene for the prion protein can cause a misfolding of the dominantly alpha helical regions into beta pleated sheets.

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Mutations in the gene HR can lead to complete hair loss, though this is not typical in humans.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

Mutations in such microRNAs ( known as oncomirs ) can lead to activation of oncogenes.

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 in the androgen receptor gene can cause problems with any of the steps involved in androgenization, from the synthesis of the androgen receptor protein itself, through the transcriptional ability of the dimerized, androgen-AR complex.

* Mutations in the OFD1 gene can also cause several other disorders with features that overlap with those of oral-facial-digital syndrome.

Mutations can be detected in 90 %.

Mutations of mitochondrial DNA can lead to a number of illnesses including exercise intolerance and Kearns-Sayre syndrome ( KSS ), which causes a person to lose full function of heart, eye, and muscle movements.

Mutations in these proteins can result in altered functionality of sub-complex assembly, copper transport, or translational regulation.

Mutations of the FOXP3 gene can prevent regulatory T cell development, causing the fatal autoimmune disease IPEX.

Mutations can be caused by copying errors in the genetic material during cell division and by exposure to radiation, chemicals, or viruses, or can occur deliberately under cellular control during the processes such as meiosis or hypermutation.

Mutations and natural selection can only " remove preexisting information.

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.

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 a number of different genes as well as RAS itself can have this effect.

Mutations in these areas can lead to non-functional proteins that can polymerise and accumulate in the liver ( infantile hepatic cirrhosis ).

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 of the gene for this enzyme can cause unusual forms of diabetes or hypoglycemia.

* SGSH Mutations can cause Sanfilippo syndrome

Mutations in several genes have been linked to several types of epilepsy.

Mutations of the thyroid-stimulating hormone receptor that cause a constitutive activation of the thyroid gland cells have been discovered recently.

Mutations of this very polymorphic gene, such as Arg151Sys ( rs1805007 ), Arg160Trp ( rs1805008 ), Asp294Sys ( rs1805009 ), Val60Leu ( rs1805005 ) and Val92Met ( rs2228479 ) have been shown to cause red hair and pale skin that does not tan in a small percentage of the human population.

Mutations that make organisms more adapted to their environment increase in the population through natural selection as organisms with favorable mutations have more offspring.

Mutations in BRCA1 and BRCA2, important risk factors for ovarian cancer and breast cancer in women, have also been implicated in prostate cancer.

Mutations in this gene have been associated with early onset obesity, adrenal insufficiency, and red hair pigmentation.

Mutations within RNase MRP have been shown to cause cartilage-hair hypoplasia, a disease associated with an array of symptoms such as short stature, sparse hair, skeletal abnormalities and a suppressed immune system that is frequent among Amish and Finnish.

Mutations in factor XII have been associated with an asymptomatic prolongation in the clotting time and possibly a tendency toward thrombophlebitis.

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 TERT have been implicated in predisposing patients to aplastic anemia, a disorder in which the bone marrow fails to produce blood cells, in 2005.

Mutations in captivity have emerged in various colors, some quite different from those observed in nature.

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 that cause Noonan Syndrome have been found in PTPN11 and SOS1.

Mutations in daf-2 have been shown by Cynthia Kenyon to double the lifespan of the worms.

Mutations in only one gene, the CLRN1 gene, have been linked to Usher syndrome type III.

Mutations in this gene have been associated with the variants of bullous congenital ichthyosiform erythroderma in which the palms and soles of the feet are affected.

Mutations in the genes expressing this protein have been associated with the PC1 variant of pachyonychia congenita, an inherited disorder of the epithelial tissues in which keratin 6A is expressed, particularly leading to structural abnormalities of the nails, the epidermis of the palms and soles, and oral epithelia.

Mutations in the genes encoding this protein have been associated with White Sponge Nevus, characterized by oral, esophageal, and anal leukoplakia.

Mutations in the KRT3 encoding this protein have been associated with Meesmanns Corneal Dystrophy.

Mutations in the gene encoding this protein and keratin 4 have been associated with the autosomal dominant disorder White Sponge Nevus.

Mutations in this gene have been linked to cryptogenic cirrhosis.

Mutations have been identified in residues between transmembrane domains III and IV which make up the fast inactivation gate of Na < sub > v </ sub > 1. 4.

Mutations have also been found on the cytoplasmic loops between the S4 and S5 helices of domains II, III and IV, which are the binding sites of the inactivation gate.