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Biography and Research Information
OverviewAI-generated summary
Milena Dimori's research focuses on developing and utilizing animal models, primarily mice and swine, to investigate human genetic disorders, with a particular emphasis on osteogenesis imperfecta and Ehlers-Danlos syndrome. Her work examines the intricate relationship between skeletal defects and respiratory function, exploring how alterations in collagen type I impact lung development and physiological processes. Dimori's publications detail the creation of new mouse models to dissect specific genetic contributions to these conditions, such as the role of COL5A1 haploinsufficiency in classical Ehlers-Danlos syndrome and the effects of Rab33b missense mutations on bone resorption and protein glycosylation in Smith-McCort dysplasia. She also investigates the cellular mechanisms underlying bone mass regulation, including the role of autophagy in bone density. Dimori collaborates with researchers at the University of Arkansas for Medical Sciences, including Roy Morello, Melda Onal, Charles A. O’Brien, and Jeff D. Thostenson, with whom she has co-authored multiple publications.
Metrics
- h-index: 10
- Publications: 29
- Citations: 348
Selected Publications
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Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function (2026)
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A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta (2024)
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A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation (2023)
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Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta (2022)
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Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome (2022)
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Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022)
Collaboration Network
Top Collaborators
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
Showing 5 of 6 shared publications
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- A Rab33b missense mouse model for Smith-McCort dysplasia shows bone resorption defects and altered protein glycosylation
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
- Haploinsufficiency of <i>Col5a1</i> causes intrinsic lung and respiratory changes in a mouse model of classical Ehlers‐Danlos syndrome
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- A new <i>Col1a1</i> conditional knock-in mouse model to study osteogenesis imperfecta
- A New Mouse Model to Dissect the Contribution of Intrinsic Lung Defects Versus Extrinsic Skeletal Defects to Impaired Lung Function in Osteogenesis Imperfecta
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Distinct type I collagen alterations cause intrinsic lung and respiratory defects of variable severity in mouse models of osteogenesis imperfecta
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