Glomerular deposition of homotrimeric type I collagen in the COL1A2 deficient mouse

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Glomerular deposition of homotrimeric type I collagen in the COL1A2 deficient mouse

Please use this identifier to cite or link to this item: http://hdl.handle.net/10355/4479

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dc.contributor.advisor Phillips, Charlotte L. en
dc.contributor.author Brodeur, Amanda C., 1978- en_US
dc.date.accessioned 2010-01-12T17:08:11Z
dc.date.available 2010-01-12T17:08:11Z
dc.date.issued 2006 en_US
dc.date.submitted 2006 Spring en
dc.identifier.other BrodeurA-041706-D5065 en_US
dc.identifier.uri http://hdl.handle.net/10355/4479
dc.description Title from title screen of research.pdf file (viewed on December 22, 2006). en_US
dc.description The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. en_US
dc.description "May 2006" en_US
dc.description Vita. en_US
dc.description Includes bibliographical references. en_US
dc.description Thesis (Ph. D.) University of Missouri-Columbia 2006. en_US
dc.description Dissertations, Academic -- University of Missouri--Columbia -- Biochemistry (Medicine). en_US
dc.description.abstract Type I collagen is the most abundant structural protein in the body. Type I collagen generally exists as a heterotrimeric protein; however, a homotrimeric isotype of type I collagen has been identified. Our lab currently studies the COL1A2 deficient mouse model which is homozygous for a mutation that causes the mice to synthesize homotrimeric type I collagen exclusively. We recently identified deposition of type I collagen in the kidneys of the COL1A2 deficient mouse model and under normal physiologic conditions such accumulation is pathologic. The primary goal of this research is to investigate the molecular mechanisms involved in the regulation of type I collagen within the kidney by evaluating synthetic and degradative pathways. As presented here, the accumulation of homotrimeric type I collagen in the kidneys of the COL1A2 deficient mice occurs postnatally and appears to be due to an increase in the synthetic pathway, as well as an alteration in the degradative pathway. Gaining a further understanding of the mechanisms behind the deposition of collagen within the kidney will hopefully lead to a greater understanding of secondary renal injury seen in the progression to end-stage renal disease, a complication of a variety diseases, including diabetic and IgA nephropathy. Further, characterization of the role of homotrimeric type I collagen will also lead to a greater understanding of its role in developmental and pathological events. en_US
dc.language.iso en_US en_US
dc.publisher University of Missouri--Columbia en_US
dc.subject.lcsh Kidney glomerulus -- Diseases en_US
dc.subject.lcsh Cytoskeletal proteins en_US
dc.subject.mesh Collagen Type I -- metabolism en_US
dc.subject.mesh Kidney Glomerulus -- pathology en_US
dc.subject.mesh Mice, Mutant Strains en_US
dc.subject.mesh Osteogenesis Imperfecta -- genetics en_US
dc.subject.mesh Osteogenesis Imperfecta -- pathology en_US
dc.title Glomerular deposition of homotrimeric type I collagen in the COL1A2 deficient mouse en_US
dc.type Thesis en_US
thesis.degree.discipline Biochemistry (Medicine) en_US
thesis.degree.grantor University of Missouri--Columbia en_US
thesis.degree.name Ph. D. en_US
thesis.degree.level Doctoral en_US
dc.identifier.merlin .b57475180 en_US
dc.relation.ispartofcommunity University of Missouri-Columbia. Graduate School. Theses and Dissertations. Dissertations. 2006 Dissertations
dc.relation.ispartofcollection 2006 Freely available dissertations (MU)


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