subject:(Fibrillin 1)

1. Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa, Yoshihiko. Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro.

Degree: 博士（歯学）, 2016, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000043/

►

The ciliary zonule in the eye, also known as Zinn's zonule, is composed of oxytalan fibers, which are bundles of microfibrils consisting mainly of fibrillin-1.… (more)

Subjects/Keywords: fibrillin; MAGP-1; 微細線維; オキシタラン線維; 毛様体小帯; fibrillin; MAGP-1; microfibrils; oxytalan fibers; ciliary zonule

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa, Y. (2016). Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000043/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa, Yoshihiko. “Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro.” 2016. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed February 27, 2021. http://id.nii.ac.jp/1167/00000043/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa, Yoshihiko. “Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro.” 2016. Web. 27 Feb 2021.

Vancouver:

Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa Y. Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2016. [cited 2021 Feb 27]. Available from: http://id.nii.ac.jp/1167/00000043/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fujita, Takahiro; Tsuruga, Eichi; Yamanouchi, Kaori; Sawa Y. Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. : Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2016. Available from: http://id.nii.ac.jp/1167/00000043/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

2. Taucer, Anne Irene. Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome.

Degree: MS, Biomedical Engineering, 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-1048

► Marfan syndrome, affecting approximately one out of every 5,000 people, is characterized by abnormal bone growth, ectopia lentis, and often-fatal aortic dilation and dissection. The… (more)

Subjects/Keywords: biomechanics; fibrillin-1; extracellular matrix; Marfan syndrome

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Taucer, A. I. (2009). Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1048

Chicago Manual of Style (16^th Edition):

Taucer, Anne Irene. “Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome.” 2009. Masters Thesis, Texas A&M University. Accessed February 27, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-1048.

MLA Handbook (7^th Edition):

Taucer, Anne Irene. “Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome.” 2009. Web. 27 Feb 2021.

Vancouver:

Taucer AI. Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome. [Internet] [Masters thesis]. Texas A&M University; 2009. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1048.

Council of Science Editors:

Taucer AI. Biomechanics of common carotid arteries from mice heterozygous for mgR, the most common mouse model of Marfan syndrome. [Masters Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1048

Universidade Estadual de Campinas

3. Braga, Guilherme Gambogi, 1985-. Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice.

Degree: 2015, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314061

► Abstract: Fibrillin-1 is an important component of the microfibrils network present in elastic fibers. Mutations in fibrillin-1 gene imply in the development of Marfan Syndrome.… (more)

▼ Abstract: Fibrillin-1 is an important component of the microfibrils network present in elastic fibers. Mutations in fibrillin-1 gene imply in the development of Marfan Syndrome. This disease affects elastogenesis in lungs, skin, cardiovascular system and eyes. Recent studies determined that unbalanced TGF-beta activity is an important factor in the symptoms observed this syndrome. These alterations can be reversed by the use of TGF-beta blockers such as the drug losartan. The mechanisms by which the drug losartan act are not described in the literature. Thus, using a model of primary culture cells (dermal fibroblasts) the elastogenic profile by immunofluorescence, zimograph in situ, Real-Time PCR, electronic microscopy and western-blotting of matrix proteins and signal molecules of elastic fiber synthesis and degradation was evaluated. The data presented suggest a joint reduction of the deposition of proteins MAGP-1 (83%), Tropoelastina (87.5%) and Fibilina-1 (86%) in the extracellular matrix; an increase in the activity and also the levels of gene expression of matrix metalloproteinases MMP-2 and MMP-9, activation of the signaling cascade canonical (SMAD-2) and not canonical (ERK1/2 and JNK-1) of TGF-beta and increased levels of reactive oxygen species (ROS) in cultures of fibroblasts in the dermis derived from mice deficient in fibrillin-1. While using the losartan drug (100 ?M/L) to treat these cells it was possible to observe an increase in deposition of MAGP-1 (71.5%) and Tropoelastina (68.5%) in the extracellular matrix, reduction of activity and gene expression of matrix metalloproteinases MMP-2 and MMP-9 and inactivation of canonical signaling (SMAD-2) and not canonical (ERK1/2 and JNK-1) activity of TGF-beta. In general, our data suggest an increase in the degradation of molecules components of elastic fibers in culture of fibroblasts in the dermis derived from mice deficient in fibrillin-1 as a function in the increase in the expression of MMPs 2 and 9. This increase in the degradation of the extracellular matrix may be the result of lower levels of fibrillin-1 in the matrix produced by these cells, super activating the canonical signaling (SMAD-2) and non-canonical (ERK1/2 and JNK-1) of TGF-beta, which reflects the activation of ROS and consequently the activation of proteases The treatment with losartan probably takes the reverse path reducing the super activation of the signaling cascade of TGF-beta as well as the activation of metalloproteinases, indirectly increase in the deposition of MAGP-1 and Tropoelastina in the extracellular matrix of these cells Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Werneck, Claudio Chrysostomo, 1966- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Cardoso, Alexandre Bruni (committee member), Felisbino, Sérgio Luis (committee member), Brocchi, Marcelo (committee member), Kobarg, Jörg (committee member).

Subjects/Keywords: Marfan, Sindrome de; Fator de crescimento transformador beta; Losartan; Fibroblastos; Fibrilina-1; Marfan syndrome; Transforming growth factor beta; Losartan; Fibroblasts; Fibrillin-1

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Braga, Guilherme Gambogi, 1. (2015). Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Braga, Guilherme Gambogi, 1985-. “Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice.” 2015. Thesis, Universidade Estadual de Campinas. Accessed February 27, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Braga, Guilherme Gambogi, 1985-. “Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice.” 2015. Web. 27 Feb 2021.

Vancouver:

Braga, Guilherme Gambogi 1. Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice. [Internet] [Thesis]. Universidade Estadual de Campinas; 2015. [cited 2021 Feb 27]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Braga, Guilherme Gambogi 1. Avaliação dos mecanismos de ação do losartan em cultura de fibroblastos de derme deficientes em fibrilina-1: Evaluation of losartan action mechanism in dermal fibroblasts derived from fibrillin-1 deficient mice. [Thesis]. Universidade Estadual de Campinas; 2015. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universidade Estadual de Campinas

4. Nery-Diez, Ana Cláudia Coelho, 1980-. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.

Degree: 2013, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

► Abstract: Recent works show that an increased activation of the TGF-? is associated with most of the symptoms of the Marfan syndrome. Studies using mouse… (more)

▼ Abstract: Recent works show that an increased activation of the TGF-? is associated with most of the symptoms of the Marfan syndrome. Studies using mouse models of Marfan treated with losartan have been shown to prevent the degradation of the elastic matrix. Other investigators suggest that the metalloproteinases and the noncanonical ERK signaling are involved in the breakdown of the elastic fiber, which results in the aneurysm. In this study we investigated the role of fibrillin-1 in the arterial thrombosis model using mouse models of Marfan. We analyzed thrombus formation, platelet levels, APTT, PT and TT time, hemodynamic parameter, TGF-? levels, MMP activity as well as platelets, elastic fibers morphology and thrombus. This study demonstrated that Fbn1mg?/+ mice take about 120±21,07 minutes for the thrombus to be formed when compared with wild type, 58±7,16. When these Fbn1mg?/+ mice were treated with antihypertensive losartan and captopril the time taken for the thrombus formation was reduced in 57,5% and 67,5%, respectively. The activity of metalloproteinases and activity TGF-? was increased in the Fbn1mg?/+, however no significant difference between the hemodynamic parameters, levels of totals TGF-?, morphological platelets, elastic fiber and thrombus were observed. Finally, the results suggested that fibrillin-1 interferes with this process and antihypertensive affect the physiology of Fbn1mg?/+ mice. This study suggested that somehow drugs interfere with elastic matrix remodeling due to a decrease in the activity of matrix metalloproteinases which results in the recovery time of thrombus formation Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Werneck, Claudio Chrysostomo, 1966- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Pimentel, Edson Rosa (committee member), Brocchi, Marcelo (committee member), Monteiro, Robson de Queiroz (committee member), Oliva, Maria Luiza Vilela (committee member).

Subjects/Keywords: Fibrilina-1; Matriz extracelular; Trombose; Agentes hipotensores; Fator de crescimento transformador beta; Fibrillin-1; Extracellular matrix; Thrombosis; Antihypertensive agents; Transforming growth factor beta1

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1. (2013). Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1980-. “Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.” 2013. Thesis, Universidade Estadual de Campinas. Accessed February 27, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1980-. “Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.” 2013. Web. 27 Feb 2021.

Vancouver:

Nery-Diez, Ana Cláudia Coelho 1. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. [Internet] [Thesis]. Universidade Estadual de Campinas; 2013. [cited 2021 Feb 27]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Nery-Diez, Ana Cláudia Coelho 1. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. [Thesis]. Universidade Estadual de Campinas; 2013. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Egana, Isabel. Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan.

Degree: Docteur es, Sciences, technologie, santé. Biologie cellulaire et physiopathologie, 2013, Université de Bordeaux Segalen

URL: http://www.theses.fr/2013BOR22052

► La formation de podosomes dans les cellules endothéliales (Ces) aortiques en réponse au TGFβ est bien décrite in vitro (dans des boîtes de culture) et… (more)

▼ La formation de podosomes dans les cellules endothéliales (Ces) aortiques en réponse au TGFβ est bien décrite in vitro (dans des boîtes de culture) et ex vivo (dans des segments de vaisseaux aortiques vivants). Le projet de cette thèse était de franchir l’étape suivante en démontrant la présence de podosomes in vivo en réponse à du TGFβ d’origine endogène. Pour ce faire, nous avons choisi d’utiliser un modèle de souris génétiquement modifiées présentant spontanément des niveaux de TGFβ élevés dans la paroi aortique, raisonnant que cet environnement devrait être propice à l’apparition des structures. La souris Marfan (FbnC1039G/+) constitue le modèle murin de la maladie humaine appelée « syndrome de Marfan ». Chez la souris comme chez l’homme, une mutation dans le gène codant pour la fibrilline-1 conduit à une augmentation des niveaux de TGFβ dans la paroi aortique et dans le sang circulant. Nous avons utilisé ce modèle pour rechercher la présence de podosomes dans l'endothélium aortique. La visualisation « en face » de l'endothélium marqué pour l’actine fibrillaire, la cortactine, la protéine adaptatrice Tks5 et la metalloprotéase MT1-MMP, a révélé des rosettes de podosomes semblables à celles détectées ex vivo en réponse à du TGFβ d’origine exogène. Ces rosettes peuvent être trouvées dans l'endothélium de l'aorte ascendante ou descendante. L’analyse du tissu sous-jacent révèle une détérioration de la lame basale qui apparait parsemée de zones dépourvues d’un de ses constituants majeurs, le collagène IV. Nous émettons l'hypothèse que les rosettes de podosomes sont impliquées dans la formation de ces zones de dégradation du collagène IV. Pour examiner les conséquences du déficit en fibrilline-1 pour les CEs et confirmer les données in vivo concernant la souris Marfan, nous avons utilisé deux approches in vitro. D’abord, nous avons mis au point un protocole pour isoler les CEs aortiques à partir des souris Marfan. Ensuite, nous avons, par la stratégie des siRNA, procédé à la déplétion en fibrilline-1 de CEs aortiques d’origine bovine (BAEc). Les cellules endothéliales aortiques isolées des souris Marfan conservent in vitro le phénotype « TGFβ » et forment podosomes capables de dégrader la matrice extracellulaire sans aucune stimulation exogène. Dans le modèle des cellules BAE, le dosage du TGFβ indique que, in vitro, la déplétion de ces cellules en fibrilline-1 provoque une augmentation de TGFβ biologiquement actif associé à la fraction cellulaire. Ce TGFβ conduit alors à la formation de podosomes dans les CEs. Nous avons observé d’autres conséquences du déficit en fibriline-1 dans l’endothélium in situ. L’analyse topologique de la surface de l’endothélium aortique de la souris Marfan révèle des phénomènes de « blebbing », des filopodes, des anomalies des jonctions cellules-cellules. L’analyse ultrastructurale en microscopie électronique à transmission révèle que l’endothélium de la souris Marfan a une apparence radicalement distincte de celui observé chez les témoins sauvages. La lame élastique, fragilisée par le… Advisors/Committee Members: Kramer, Ijsbrand M. (thesis director).

Subjects/Keywords: Podosomes; Aorte; Syndrome de Marfan; TGFβ; Endothélium aortique; Anévrisme; Remodelage vasculaire; Fibrilline-1; Podosomes; Aorta; Marfan’s syndrome; TGFβ; Aortic endothelium; Aneurysm; Vascular remodeling; Fibrillin-1

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Egana, I. (2013). Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan. (Doctoral Dissertation). Université de Bordeaux Segalen. Retrieved from http://www.theses.fr/2013BOR22052

Chicago Manual of Style (16^th Edition):

Egana, Isabel. “Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan.” 2013. Doctoral Dissertation, Université de Bordeaux Segalen. Accessed February 27, 2021. http://www.theses.fr/2013BOR22052.

MLA Handbook (7^th Edition):

Egana, Isabel. “Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan.” 2013. Web. 27 Feb 2021.

Vancouver:

Egana I. Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan. [Internet] [Doctoral dissertation]. Université de Bordeaux Segalen; 2013. [cited 2021 Feb 27]. Available from: http://www.theses.fr/2013BOR22052.

Council of Science Editors:

Egana I. Specific features of the aortic endothelium in a murine model of Marfan Syndrome : Spécificités de l’endothélium aortique dans un modèle de souris Marfan. [Doctoral Dissertation]. Université de Bordeaux Segalen; 2013. Available from: http://www.theses.fr/2013BOR22052

6. Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa, Yoshihiko. Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro.

Degree: 博士（歯学）, 2014, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000005/

►

The ciliary zonule, also known as Zinn's zonule, is composed of oxytalan fibers. However, the mechanism by which epithelial cells in the ciliary body form… (more)

Subjects/Keywords: Fibrillin-1; Fibrillin-2; microfibrils; oxytalan fibers; ciliary zonule; Cells, Cultured; Ciliary Body; Epithelial Cells; Extracellular Matrix; Extracellular Matrix Proteins; Gene Expression Regulation; Gene Knockdown Techniques; Humans; Microfilament Proteins; Pigmentation; RNA, Small Interfering

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa, Y. (2014). Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000005/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa, Yoshihiko. “Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed February 27, 2021. http://id.nii.ac.jp/1167/00000005/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa, Yoshihiko. “Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro.” 2014. Web. 27 Feb 2021.

Vancouver:

Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa Y. Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2021 Feb 27]. Available from: http://id.nii.ac.jp/1167/00000005/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yamanouchi, Kaori; Tsuruga, Eichi; Oka, Kyoko; Sawa Y. Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. : Fibrillin-1 and fibrillin-2 are essential for formation of thick oxytalan fibers in human nonpigmented ciliary epithelial cells in vitro. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000005/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Oxford

7. Robertson, Ian Butler. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.

Degree: PhD, 2012, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

► Many studies have demonstrated a connection between the fibrillin matrix and TGFβ signalling, but at present the mechanistic basis for this link is unclear. An… (more)

▼ Many studies have demonstrated a connection between the fibrillin matrix and TGFβ signalling, but at present the mechanistic basis for this link is unclear. An interaction between the C-terminus of Latent TGFβ Binding Protein 1 (LTBP1) and the N-terminus of fibrillin1 has previously been identified, and may have the potential to directly link the fibrillin matrix to TGFβ signalling. To investigate the structural basis for this interaction, several multi-domain fragments of fibrillin1 and LTBP1 were expressed prokaryotically and refolded in vitro. After initial characterisation to confirm folding, the structure, dynamics, and interdomain interactions of these fragments were investigated in more detail using NMR techniques. Domains in both LTBP1 and fibrillin1 appear to demonstrate folds consistent with homologous structures, and while the LTBP1 C-terminal cbEGF14-TB3-EGF3-cbEGF15 region contains many flexible linkers and few interdomain interactions, the fibrillin1 EGF2-EGF3-hyb1-cbEGF1 region appears rigid, with interfaces forming between all domains present. SPR studies were used to demonstrate binding between distinct LTBP1 and fibrillin fragments, suggesting interactions between multiple domains are involved in the LTBP1-fibrillin1 interaction. The binding sites involved were then mapped to specific residues using HSQC titration studies, and structural models for the LTBP1-fibrillin1 interaction were generated based on these data. Predictions from these models were used to target residues for site-directed mutagenesis, based on their potential involvement in salt bridges, and when certain residues were replaced with those of opposite charge, reductions in binding could be seen in the SPR assay. These key residues were consistent with a particular model of the LTBP1-fibrillin1 interaction, as derived from the HSQC titration data. The conservation of potential binding site residues through deuterostome evolution also supports an important biological role for the LTBP-fibrillin interaction.

Subjects/Keywords: 572; Medical sciences; Biology (medical sciences); Cardiovascular disease; Physiology; Extracellular matrix; Biochemistry; structural biology; fibrillin; Latent TGF beta binding protein; marfan syndrome; transforming growth factor beta; TGFbeta; TGFb; nuclear magnetic resonance; surface plasmon resonance; microfibril; fibrillin 1

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robertson, I. B. (2012). An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

Chicago Manual of Style (16^th Edition):

Robertson, Ian Butler. “An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.” 2012. Doctoral Dissertation, University of Oxford. Accessed February 27, 2021. http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932.

MLA Handbook (7^th Edition):

Robertson, Ian Butler. “An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction.” 2012. Web. 27 Feb 2021.

Vancouver:

Robertson IB. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2021 Feb 27]. Available from: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932.

Council of Science Editors:

Robertson IB. An investigation into the molecular mechanism of the fibrillin1-LTBP1 interaction. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:e154e0a2-c0cb-42bd-8b90-7a13460700c0 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669932

8. Santos, Thayna Meirelles. Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica.

Degree: PhD, Cardiologia, 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25112014-111305/ ;

► A Síndrome de Marfan (SMF) é a enfermidade hereditária mais comum dentre as que afetam o sistema conjuntivo, causada por mutações da glicoproteína fibrilina-1, o… (more)

▼ A Síndrome de Marfan (SMF) é a enfermidade hereditária mais comum dentre as que afetam o sistema conjuntivo, causada por mutações da glicoproteína fibrilina-1, o principal componente estrutural das microfibrilas elásticas da matriz extracelular. As manifestações fenotípicas da SMF são sistêmicas e acometem tipicamente os sistemas ocular, esquelético e cardiovascular, este uma importante causa de morbi-mortalidade. Entretanto, não está claro como a mutação induz a doença. Estudos anteriores sugerem anomalias morfológicas do retículo endoplasmático (RE) ou retenção intracelular da fibrilina-1 nos estágios avançados da SMF. Entretanto, a contribuição do enovelamento da fibrilina-1 mutada e do estresse do RE na fisiopatologia celular da SMF não é conhecida. Proteínas mal-enoveladas podem levar à retenção intracelular e/ou aumento da degradação através da via de degradação associada ao RE (ERAD), além da indução da resposta a proteínas mal-enoveladas (UPR), ambas com potencial contribuição à fisiopatologia de doenças, incluindo a SMF. Assim, estudamos em fibroblastos embrionários isolados de camundongos (MEFs) com SMF se a fibrilina-1 mutada é reconhecida pelo controle de qualidade do RE pelo seu mal- enovelamento e induz estresse do RE por sua retenção intracelular. Demonstramos que a mutação na fibrilina-1 per se não promoveu chaperonas marcadoras de UPR ou geração de oxidantes. Além disso, não levou a uma maior sensibilização das células à indução exógena de estresse do RE, nem promoveu maior morte celular após inibição do proteassoma. Além disso, não foi observada retenção intracelular da fibrilina-1 nas células SMF, e mesmo após inibição da via secretora ou indução de estresse do RE, a inibição da secreção da fibrilina-1 foi similar nos MEFs SMF e wild-type (WT). A dissulfeto isomerase proteica (PDI), uma importante chaperona redox do RE, interage com fibrilina-1, e seu silenciamento levou a um aumento na secreção da fibrilina-1 pelos MEFs WT, mas não SMF. Além disso, o silenciamento da PDI promoveu a desorganização da matriz extracelular depositada de fibrilina-1 nos MEFs WT, enquanto nos MEFs SMF, a desorganização basal da matriz não foi adicionalmente alterada. Em paralelo, investigações in vivo mostraram que o estresse do RE não é induzido em camundongos SMF com 1 ou 3 meses de idade, apesar de manifestações fenotípicas evidentes. Entretanto, concomitante à progressão da doença, detectamos a ocorrência de estresse do RE nas aortas ascendentes dos camundongos aos 6 meses. Esta detecção foi exclusiva desta região da aorta e não ocorreu em outros órgãos afetados ou não afetados pela SMF. Assim, a manifestação do fenótipo clássico da SMF não requer uma perda da homeostase do RE diretamente induzida pela fibrilina-1 mutada. Ao contrário, esta é capaz de evadir mecanismos de controle de qualidade mediados pela PDI, sendo secretada normalmente. Assim, esta evasão do controle de qualidade pela PDI é uma condição permissiva essencial para o fenótipo da SMF. Por outro lado, o estresse do RE é uma característica evolutiva… Advisors/Committee Members: Laurindo, Francisco Rafael Martins.

Subjects/Keywords: Camundongos mutantes; Dobramento de proteína; Endoplasmic reticulum stress; Estresse do retículo endoplasmático; Fibrilina; Fibrillin 1; Isomerase de dissulfetos de proteínas; Marfan syndrome; Mice mutant strains; Protein disulfide-Isomerases; Protein folding; Síndrome de Marfan

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Santos, T. M. (2014). Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25112014-111305/ ;

Chicago Manual of Style (16^th Edition):

Santos, Thayna Meirelles. “Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica.” 2014. Doctoral Dissertation, University of São Paulo. Accessed February 27, 2021. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25112014-111305/ ;.

MLA Handbook (7^th Edition):

Santos, Thayna Meirelles. “Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica.” 2014. Web. 27 Feb 2021.

Vancouver:

Santos TM. Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Feb 27]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25112014-111305/ ;.

Council of Science Editors:

Santos TM. Processamento intracelular da fibrilina-1 mutada na síndrome de Marfan: escape do controle de qualidade pela dissulfeto isomerase proteica. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-25112014-111305/ ;

Freie Universität Berlin

9. Robinson, Peter. Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders.

Degree: 2009, Freie Universität Berlin

URL: https://refubium.fu-berlin.de/handle/fub188/13383

► Marfan syndrome (MFS) is a relatively common inherited disorder of connective tissue with prominent manifestations in the skeleton, eye, and cardiovascular system. MFS is inherited… (more)

▼ Marfan syndrome (MFS) is a relatively common inherited disorder of connective tissue with prominent manifestations in the skeleton, eye, and cardiovascular system. MFS is inherited in an autosomal dominant fashion and is caused by mutations in the gene for fibrillin-1, FBN1. Early mortality in untreated persons with MFS is mainly due to cardiovascular complications such as aortic dissection and rupture. MFS can be viewed as one of the success stories of molecular medicine in the last decades, after the characterization of the biochemical functions of fibrillin-1 and the basis of the molecular pathophysiology of MFS led to the introduction of two efficacious forms of medical therapy in mouse models for the MFS, doxycyclin and losartan. This habilitation deals with FBN1 mutations and genotype-phenotype correlations in MFS, investigations of the role of fibrillin-1 fragments in the pathogenesis of MFS, the clinical characterization of a related disorder termed Shprintzen Goldberg Syndrome (SGS), as well as molecular genetic investigations about the mechanisms of FBN1 gene expression. Mutations in FBN1 can cause not only classical MFS, but also a series of related disorders of connective tissue that have been termed type 1 fibrillinopathies. Neonatal MFS is characterized by a number of unusually severe clinical manifestations and displays a highly significant association with mutations in the middle of the FBN1 gene. Many persons presenting in specialized clinics for MFS do not actually have MFS or any identifiable syndrome. Individual relatively nonspecific features of MFS are also common in the general population, so that it is often difficult to distinguish between persons with a few anomalies of connective tissue from persons with oligosymptomatic forms of MFS. This fact has tended to lead to clinical overdiagnosis of MFS, which in turn seems to be a reason for the relatively low mutation detection rates reported in many studies on FBN1 mutation analysis. Missense mutations in cbEGF modules are the most commonly observed mutations in MFS and generally affect one of the six absolutely conserved cysteine residues or residues of the consensus sequence for calcium binding. Mutations of these residues led to destabilization of recombinant fibrillin-1 constructs in in vitro experiments. This could imply that mutant fibrillin-1 monomers represent a kind of Achilles' heel in the highly polymeric fibrillin-containing microfibrils that lead to the production of fibrillin-1 fragments. It was shown that two different recombinant fibrillin-1 fragments induce upregulation of matrix metalloproteinase expression related to either an integrin-binding RGD sequence or an elastin-binding protein (EBP) recognition motif. Taken together, our results suggest that mutations in FBN1 could lead to the production of matricryptins. It was additionally shown that aortic extracts of the mgR MFS mouse model stimulate macrophage chemotaxis via interactions with EBP and that a fibrillin-1 polypeptide with an EBP recognition motif has a similar… Advisors/Committee Members: [email protected] (contact), m (gender), Prof. Dr. J. Schmidtke/ Hannover (firstReferee), Prof. Dr. O. Rieß/ Tübingen (furtherReferee).

Subjects/Keywords: Marfan syndrome; fibrillin-1; FBN1; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Robinson, P. (2009). Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/13383

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Robinson, Peter. “Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders.” 2009. Thesis, Freie Universität Berlin. Accessed February 27, 2021. https://refubium.fu-berlin.de/handle/fub188/13383.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Robinson, Peter. “Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders.” 2009. Web. 27 Feb 2021.

Vancouver:

Robinson P. Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders. [Internet] [Thesis]. Freie Universität Berlin; 2009. [cited 2021 Feb 27]. Available from: https://refubium.fu-berlin.de/handle/fub188/13383.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Robinson P. Molecular and Clinical Investigations on Marfan Syndrome and Related Disorders. [Thesis]. Freie Universität Berlin; 2009. Available from: https://refubium.fu-berlin.de/handle/fub188/13383

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Jones, Wendell Brooks. The Role of Fibrillin-1 in Eye Development and Disease.

Degree: PhD, Biology & Biomedical Sciences (Molecular Genetics & Genomics), 2018, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/art_sci_etds/1700

► The ciliary zonule of the human eye consists of a circumferential array of fibers that connect the ocular lens to the nonpigmented ciliary epithelium… (more)

▼ The ciliary zonule of the human eye consists of a circumferential array of fibers that connect the ocular lens to the nonpigmented ciliary epithelium (NPCE) located at the inner wall of the eye. Zonular fibers consist of bundles of beaded filaments called microfibrils. Microfibrils are major structural elements of the extracellular matrix and are present in pure form in the ciliary zonule. Microfibrils are composed principally of fibrillin-1 (FBN-1); a large extracellular matrix glycoprotein. In humans, mutations in FBN1 underlie Marfan syndrome; a pleiotropic connective tissue disorder that profoundly affects the eye. Ocular manifestations include ectopia lentis (dislocated lenses), cataracts, glaucoma and axial myopia. The ocular phenotypes in Marfan syndrome suggest an important role for FBN-1 in eye development. In this report, I used mice as a model system to test the role of FBN1 in eye development and disease with an emphasis on understanding the role of FBN-1 in the synthesis of the ciliary zonule. Our lab has shown that the organization and composition of the mouse ciliary zonule is similar to humans. A recent proteomic study identified FBN-1 as the main component of the ciliary zonule, accounting for 60% to 70% of total zonule protein. In order to understand the role of FBN-1 in eye development, I had to first identify the cells in the eye responsible for expressing FBN-1 and other core components of the zonule (FBN-2, MFAP2, LTBP2 and ADAMTSL4). I used in situ hybridization on wild type mouse eye tissue to show that some zonule components (Fbn1, Fbn2, Ltbp2, Mfap2) are expressed by cells of the NPCE while others (Adamtsl4, Mfap2) are expressed by the lens. This suggests that the ciliary zonule is synthesized by both tissues. Immunofluorescence experiments on adult wild type mouse eyes using antibodies against core zonule proteins showed that the ciliary zonule is heterogeneous in composition and nonuniform along the length of fibers suggesting that the spatial distribution of proteins in the ciliary zonule could reflect the temporal expression of zonule components during eye development. The identification of NPCE cells as the likely source of FBN-1 in the zonule allowed me to test the contribution of Fbn1 directly. I used a conditional knockout approach to delete Fbn1 in the nasal and temporal regions of the mouse NPCE. Three-dimensional reconstructions of conditional Fbn1 knockout mouse eyes (Fbn1-NPCE) demonstrated that the zonule was produced in the nominal absence of its most abundant component. However, the Fbn1-NPCE mice developed ectopia lentis; the major ocular manifestation and diagnostic criterion for MFS in humans. Given the clinical importance of the disease, I decided to investigate the structural and biomechanical changes leading to ectopia lentis in the Fbn1-NPCE mouse model. Ultrastructural studies on FBN-1 deficient mouse eyes using scanning electron microscopy revealed that Fbn1-NPCE mice had significant changes in zonular fiber density and thickness. Biomechanical testing… Advisors/Committee Members: Steven Bassnett, Christina Gurnett, Todd Margolis, Robert Mecham, Alan Shiels.

Subjects/Keywords: Ciliary zonule, Eye, Fibrillin-1, Lens, Marfan syndrome, Non-pigmented ciliary epithelium; Genetics; Ophthalmology

…Extracellular matrix FBN-1; Fibrillin-1 FBN-2; Fibrillin-2 FUN; Fibrillin unique region FN… …THE DISSERTATION The role of fibrillin-1 in eye development and eye disease Wendell Brooks… …the ciliary zonule. Microfibrils are composed principally of fibrillin-1 (FBN-1)… …of the ciliary zonule. The first identified a protein named fibrillin-1 as the major… …study confirmed fibrillin-1 as the main component of the ciliary zonule, accounting for 60% to…

11 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jones, W. B. (2018). The Role of Fibrillin-1 in Eye Development and Disease. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/art_sci_etds/1700

Chicago Manual of Style (16^th Edition):

Jones, Wendell Brooks. “The Role of Fibrillin-1 in Eye Development and Disease.” 2018. Doctoral Dissertation, Washington University in St. Louis. Accessed February 27, 2021. https://openscholarship.wustl.edu/art_sci_etds/1700.

MLA Handbook (7^th Edition):

Jones, Wendell Brooks. “The Role of Fibrillin-1 in Eye Development and Disease.” 2018. Web. 27 Feb 2021.

Vancouver:

Jones WB. The Role of Fibrillin-1 in Eye Development and Disease. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2018. [cited 2021 Feb 27]. Available from: https://openscholarship.wustl.edu/art_sci_etds/1700.

Council of Science Editors:

Jones WB. The Role of Fibrillin-1 in Eye Development and Disease. [Doctoral Dissertation]. Washington University in St. Louis; 2018. Available from: https://openscholarship.wustl.edu/art_sci_etds/1700

Freie Universität Berlin

11. Ney, Andreas. Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct.

Degree: 2007, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-11765

► The Marfan syndrome (MFS), a relatively common autosomal dominant disorder of connective tissue, is caused by mutations in the gene for fibrillin-1 (FBN1). Fibrillin-1 is… (more)

Subjects/Keywords: Fibrillin-1; Marfan Syndrome; Matrix metalloproteinase; integrin-binding motif (RGD); elastin-binding motif (GXXPG); Versican; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ney, A. (2007). Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-11765

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ney, Andreas. “Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct.” 2007. Thesis, Freie Universität Berlin. Accessed February 27, 2021. http://dx.doi.org/10.17169/refubium-11765.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ney, Andreas. “Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct.” 2007. Web. 27 Feb 2021.

Vancouver:

Ney A. Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct. [Internet] [Thesis]. Freie Universität Berlin; 2007. [cited 2021 Feb 27]. Available from: http://dx.doi.org/10.17169/refubium-11765.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ney A. Pathogenesis of Marfan Syndrome: Analysis of (1) metalloproteinase regulation upon stimulation with recombinant fibrillin-1 constructs and (2) self- association of a recombinant versican construct. [Thesis]. Freie Universität Berlin; 2007. Available from: http://dx.doi.org/10.17169/refubium-11765

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations