The IFITM5 mutation in osteogenesis imperfecta type V is associated with an ERK/SOX9-dependent osteoprogenitor differentiation defect
Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced tr...
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| Published in | The Journal of clinical investigation Vol. 134; no. 15; pp. 1 - 17 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Clinical Investigation
01.08.2024
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| Abstract | Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITM5). Here, we generated a conditional Rosa26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V. |
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| AbstractList | Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITM5). Here, we generated a conditional Rosa26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V.Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITM5). Here, we generated a conditional Rosa26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V. Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 ( IFITM5 ). Here, we generated a conditional Rosa26- knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V. Disruptions to osteo-chondroprogenitor cell differentiation due to activated ERK/SOX9 signaling contributes to the abnormal skeletal development in osteogenesis imperfecta type V. Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITM5). Here, we generated a conditional Rosa26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V. Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITM5). Here, we generated a conditional Roso26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with OI type V. Surprisingly, expression of mutant Ifitm5 in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant Ifitm5 had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of OI type V. Osteogenesis imperfecta (DI) type V is the second most common form of DI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes, in addition to the bone fragility. It is caused by a recurrent, dominant pathogenic variant (c.-14C>T) in interferon-induced transmembrane protein 5 (IFITMS). Here, we generated a conditional Roso26-knockin mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant IfitmS in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in patients with DI type V. Surprisingly, expression of mutant IfitmS in mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with an increase in the skeletal progenitor cell population within the periosteum. Lineage tracing showed that chondrogenic cells expressing the mutant IfitmS had decreased differentiation into osteoblastic cells in diaphyseal bone. Moreover, mutant IFITM5 disrupted early skeletal homeostasis in part by activating ERK signaling and downstream S0X9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. These data identify the contribution of a signaling defect altering osteo-chondroprogenitor differentiation as a driver in the pathogenesis of DI type V. |
| Audience | Academic |
| Author | Rossi, Vittoria C Berrier, Ava S Park, Dongsu Shenava, Vinitha Wallace, Maegen Washington, Megan E Stroup, Bridget M Castellon, Alexis Adeyeye, Mary Ortinau, Laura Batkovskyte, Dominyka Lee, Brendan H Tran, Alyssa A Ambrose, Catherine G Orwoll, Eric Chen, Yuqing Jiang, Ming-Ming Nagamani, Sandesh Cs Heaney, Jason D Huang, Shixia Lietman, Caressa D Busse, Emily C Lorenzo, Isabel Jeong, Youngjae Jain, Mahim Cela, Racel Song, I-Wen Meyers, D Nicole Marom, Ronit Leynes, Carolina Dawson, Brian C Turner, Alicia |
| AuthorAffiliation | 1 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA 2 Texas Children’s Hospital, Houston, Texas, USA 6 Department of Molecular and Cellular Biology, and Huffington Department of Education, Innovation, and Technology, Advanced Technology Cores, and 8 Orthopaedic Surgery, University of Nebraska Medical Center, Children’s Hospital and Medical Center, Omaha, Nebraska, USA 3 Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas, USA 4 Medical Scientist Training Program, UT Health Houston MD Anderson Cancer Center, Houston, Texas, USA 9 Department of Medicine, Bone and Mineral Unit, Oregon Health and Science University, Portland, Oregon, USA 5 Department of Orthopaedic Surgery, McGovern Medical School at UT Health, Houston, Texas, USA 7 Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas, USA |
| AuthorAffiliation_xml | – name: 3 Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas, USA – name: 6 Department of Molecular and Cellular Biology, and Huffington Department of Education, Innovation, and Technology, Advanced Technology Cores, and – name: 5 Department of Orthopaedic Surgery, McGovern Medical School at UT Health, Houston, Texas, USA – name: 9 Department of Medicine, Bone and Mineral Unit, Oregon Health and Science University, Portland, Oregon, USA – name: 7 Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas, USA – name: 8 Orthopaedic Surgery, University of Nebraska Medical Center, Children’s Hospital and Medical Center, Omaha, Nebraska, USA – name: 2 Texas Children’s Hospital, Houston, Texas, USA – name: 1 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – name: 4 Medical Scientist Training Program, UT Health Houston MD Anderson Cancer Center, Houston, Texas, USA |
| Author_xml | – sequence: 1 givenname: Ronit surname: Marom fullname: Marom, Ronit organization: Texas Children's Hospital, Houston, Texas, USA – sequence: 2 givenname: I-Wen surname: Song fullname: Song, I-Wen organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 3 givenname: Emily C surname: Busse fullname: Busse, Emily C organization: Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas, USA – sequence: 4 givenname: Megan E surname: Washington fullname: Washington, Megan E organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 5 givenname: Ava S surname: Berrier fullname: Berrier, Ava S organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 6 givenname: Vittoria C surname: Rossi fullname: Rossi, Vittoria C organization: Texas Children's Hospital, Houston, Texas, USA – sequence: 7 givenname: Laura surname: Ortinau fullname: Ortinau, Laura organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 8 givenname: Youngjae surname: Jeong fullname: Jeong, Youngjae organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 9 givenname: Ming-Ming surname: Jiang fullname: Jiang, Ming-Ming organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 10 givenname: Brian C surname: Dawson fullname: Dawson, Brian C organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 11 givenname: Mary surname: Adeyeye fullname: Adeyeye, Mary organization: Medical Scientist Training Program, UT Health Houston MD Anderson Cancer Center, Houston, Texas, USA – sequence: 12 givenname: Carolina surname: Leynes fullname: Leynes, Carolina organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 13 givenname: Caressa D surname: Lietman fullname: Lietman, Caressa D organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 14 givenname: Bridget M surname: Stroup fullname: Stroup, Bridget M organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 15 givenname: Dominyka surname: Batkovskyte fullname: Batkovskyte, Dominyka organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 16 givenname: Mahim surname: Jain fullname: Jain, Mahim organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 17 givenname: Yuqing surname: Chen fullname: Chen, Yuqing organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 18 givenname: Racel surname: Cela fullname: Cela, Racel organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 19 givenname: Alexis surname: Castellon fullname: Castellon, Alexis organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 20 givenname: Alyssa A surname: Tran fullname: Tran, Alyssa A organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 21 givenname: Isabel surname: Lorenzo fullname: Lorenzo, Isabel organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 22 givenname: D Nicole surname: Meyers fullname: Meyers, D Nicole organization: Department of Orthopaedic Surgery, McGovern Medical School at UT Health, Houston, Texas, USA – sequence: 23 givenname: Shixia surname: Huang fullname: Huang, Shixia organization: Department of Molecular and Cellular Biology, and Huffington Department of Education, Innovation, and Technology, Advanced Technology Cores, and – sequence: 24 givenname: Alicia surname: Turner fullname: Turner, Alicia organization: Texas Children's Hospital, Houston, Texas, USA – sequence: 25 givenname: Vinitha surname: Shenava fullname: Shenava, Vinitha organization: Department of Orthopedic Surgery, Baylor College of Medicine, Houston, Texas, USA – sequence: 26 givenname: Maegen surname: Wallace fullname: Wallace, Maegen organization: Orthopaedic Surgery, University of Nebraska Medical Center, Children's Hospital and Medical Center, Omaha, Nebraska, USA – sequence: 27 givenname: Eric surname: Orwoll fullname: Orwoll, Eric organization: Department of Medicine, Bone and Mineral Unit, Oregon Health and Science University, Portland, Oregon, USA – sequence: 28 givenname: Dongsu surname: Park fullname: Park, Dongsu organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 29 givenname: Catherine G surname: Ambrose fullname: Ambrose, Catherine G organization: Department of Orthopaedic Surgery, McGovern Medical School at UT Health, Houston, Texas, USA – sequence: 30 givenname: Sandesh Cs surname: Nagamani fullname: Nagamani, Sandesh Cs organization: Texas Children's Hospital, Houston, Texas, USA – sequence: 31 givenname: Jason D surname: Heaney fullname: Heaney, Jason D organization: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA – sequence: 32 givenname: Brendan H surname: Lee fullname: Lee, Brendan H organization: Texas Children's Hospital, Houston, Texas, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38885336$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:159297534$$DView record from Swedish Publication Index |
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| Copyright | COPYRIGHT 2024 American Society for Clinical Investigation Copyright American Society for Clinical Investigation Aug 2024 2024 Marom et al. 2024 Marom et al. |
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| Keywords | Cartilage Bone biology Genetics Bone disease Bone development |
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| References_xml | – ident: B61 doi: 10.1016/j.ajhg.2018.07.008 – ident: B29 doi: 10.1016/j.bbrc.2011.04.136 – ident: B28 doi: 10.1038/s41586-018-0662-5 – ident: B31 doi: 10.1074/jbc.M114.576793 – ident: B21 doi: 10.1038/s41598-020-78403-1 – ident: B17 doi: 10.1089/ten.tea.2016.0559 – ident: B50 doi: 10.1101/gad.1179104 – ident: B1 doi: 10.1038/nrdp.2017.52 – ident: B24 doi: 10.1016/j.bbrc.2009.06.059 – ident: B16 doi: 10.1371/journal.pone.0184568 – ident: B18 doi: 10.1007/s00774-015-0667-1 – ident: B36 doi: 10.1002/jbmr.4011 – ident: B6 doi: 10.1007/s00198-017-4143-8 – ident: B35 doi: 10.1038/s41467-018-03720-z – ident: B9 doi: 10.1016/j.ajhg.2012.06.005 – ident: B38 doi: 10.7554/eLife.78069 – ident: B53 doi: 10.1016/j.devcel.2011.12.024 – ident: B43 doi: 10.1016/bs.ctdb.2019.01.007 – ident: B4 doi: 10.1210/endrev/bnab017 – ident: B40 doi: 10.3389/fcell.2020.585640 – ident: B41 doi: 10.1073/pnas.97.3.1113 – ident: B34 doi: 10.1083/jcb.200610046 – ident: B23 doi: 10.1002/jbm4.10707 – ident: B48 doi: 10.1002/ajmg.a.62651 – ident: B15 doi: 10.1359/jbmr.080412 – ident: B54 doi: 10.1073/pnas.0605170103 – ident: B20 doi: 10.1016/j.bone.2017.11.013 – ident: B39 doi: 10.1007/s00774-007-0804-6 – ident: B8 doi: 10.1359/jbmr.2000.15.9.1650 – volume: 13 issue: 1 year: 2018 ident: B25 article-title: Comparative analysis of gene expression identifies distinct molecular signatures of bone marrow- and periosteal-skeletal stem/progenitor cells publication-title: PLoS One doi: 10.1371/journal.pone.0190909 contributor: fullname: Deveza – ident: B42 doi: 10.1186/s13018-019-1505-2 – ident: B52 doi: 10.1093/hmg/ddu594 – ident: B37 doi: 10.1359/jbmr.060603 – ident: B19 doi: 10.1002/jbmr.2363 – ident: B49 doi: 10.1038/srep43220 – ident: B32 doi: 10.1016/j.bbadis.2018.07.034 – ident: B44 doi: 10.1073/pnas.2019152118 – ident: B46 doi: 10.1242/dev.045203 – volume: 1 issue: 1 year: 2008 ident: B59 article-title: High-efficiency Rosa26 knockin vector construction for Cre-regulated overexpression and RNAi publication-title: Pathogenetics doi: 10.1186/1755-8417-1-3 contributor: fullname: Hohenstein – ident: B2 doi: 10.1530/EJE-20-0299 – ident: B10 doi: 10.1136/jmedgenet-2012-101307 – ident: B33 doi: 10.1128/MCB.01549-08 – ident: B3 doi: 10.1097/MOP.0000000000000813 – ident: B5 doi: 10.1007/s00198-016-3709-1 – ident: B14 doi: 10.1002/ajmg.a.36025 – ident: B47 doi: 10.1016/j.bone.2019.05.027 – ident: B12 doi: 10.1002/jbmr.1891 – ident: B27 doi: 10.3389/fcell.2022.876825 – ident: B56 doi: 10.1002/jbmr.2997 – ident: B64 doi: 10.1158/0008-5472.CAN-18-1087 – ident: B63 doi: 10.1093/nar/gkv688 – ident: B7 doi: 10.1590/1678-4685-gmb-2018-0043 – ident: B26 doi: 10.1038/ncb3067 – ident: B65 doi: 10.1002/jbmr.141 – ident: B30 doi: 10.1002/jbmr.2243 – ident: B62 doi: 10.1016/j.cell.2014.11.042 – ident: B58 doi: 10.1016/j.bone.2020.115835 – ident: B22 doi: 10.1002/9780470942390.mo140150 – ident: B51 doi: 10.1093/hmg/dds305 – volume: 131 issue: 5 year: 2021 ident: B60 article-title: Nitric oxide modulates bone anabolism through regulation of osteoblast glycolysis and differentiation publication-title: J Clin Invest doi: 10.1172/JCI138935 contributor: fullname: Jin – ident: B11 doi: 10.1016/j.ajhg.2012.06.011 – ident: B55 doi: 10.3389/fendo.2023.1145125 – ident: B57 doi: 10.1002/jbmr.258 – ident: B13 doi: 10.1186/1471-2474-15-107 – ident: B45 doi: 10.1007/s00774-010-0206-z |
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| Snippet | Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous... Osteogenesis imperfecta (DI) type V is the second most common form of DI, distinguished by hyperplastic callus formation and calcification of the interosseous... |
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| SubjectTerms | Analysis Animals Biological response modifiers Bone growth Bone mass Bones Calcification Callus Cartilage Cell Differentiation Collagen Density Development and progression Endochondral bone Fractures Genetic aspects Genotype & phenotype Growth plate Growth rate Health aspects Homeostasis Humans Interferon Kinases MAP Kinase Signaling System Medicin och hälsovetenskap Membrane proteins Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Transgenic Mitogen-Activated Protein Kinase 3 Mutants Mutation Ossification Osteoblastogenesis Osteoblasts Osteoblasts - metabolism Osteoblasts - pathology Osteogenesis - genetics Osteogenesis imperfecta Osteogenesis Imperfecta - genetics Osteogenesis Imperfecta - metabolism Osteogenesis Imperfecta - pathology Osteoprogenitor cells Pathogenesis Periosteum Phenotypes Progenitor cells Proteins Risk factors Scientific equipment and supplies industry Sox9 protein SOX9 Transcription Factor - genetics SOX9 Transcription Factor - metabolism Stem Cells - metabolism Stem Cells - pathology Transgenic animals |
| Title | The IFITM5 mutation in osteogenesis imperfecta type V is associated with an ERK/SOX9-dependent osteoprogenitor differentiation defect |
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