Search for dissertations about: "CAG"
Showing result 1 - 5 of 51 swedish dissertations containing the word CAG.
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1. The Kallikrein-Related Peptidases hK2 and PSA with Emphasis on Genetic Variation, Secretion, and Sperm Motility
Abstract : Prostate-specific antigen (PSA) and human glandular kallikrein 2 (hK2) are secreted by the prostate into seminal plasma and through leakage into blood. This leakage increases rapidly in prostate disease, and PSA is used worldwide as a marker of prostate cancer. READ MORE
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2. Impact of Lifestyle, Hormones, and Genes on Breast Cancer
Abstract : Approximately 7000 women are diagnosed and 1500 women die from breast cancer in Sweden every year. The aim of this thesis was to study the interplay of polymorphisms, hormone levels, lifestyle, and the use of concomitant medication in relation to risk and prognosis in two cohorts: one composed of young healthy women from high-risk breast cancer families and the other of breast cancer patients from the general population. READ MORE
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3. Functional characterisation of the CAG polymorphism in the androgen receptor- in vitro and in vivo
Abstract : The androgen receptor (AR) is the mediator of androgen actions. In the AR coding region there is a polymorphic CAG repeat encoding a stretch of the amino acid glutamine (Q). The repeat length modulates receptor activity and is normally distributed between 10-30 CAG with a median length of 22 repeats in white men. READ MORE
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4. Genetic, environmental and life-style effects on androgen receptor function
Abstract : Androgens regulate male reproductive function and their effects are mediated through the androgen receptor (AR). The AR gene contains a polymorphic CAG repeat, encoding a stretch of glutamines, affecting the transcriptional activity of the AR. READ MORE
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5. Expression and functional analysis of the SCA7 disease protein ataxin-7
Abstract : Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disease characterized by cerebellar ataxia and visual problems due to a progressive and selective loss of neurons within the cerebellum, brainstem and retina. The disease is caused by the expansion of a CAG repeat in the first coding exon of the SCA7 gene, resulting in an expanded polyglutamine domain in the N-terminal part of ataxin-7, a protein of unknown function. READ MORE