Page last updated: 2024-08-17

methionine and Achondroplasia

methionine has been researched along with Achondroplasia in 2 studies

Research

Studies (2)

Timeframe	Studies, this research(%)	All Research%
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	2 (100.00)	29.6817
2010's	0 (0.00)	24.3611
2020's	0 (0.00)	2.80

Authors

Authors	Studies
Boot-Handford, RP; Briggs, MD; Heinegård, D; Kadler, KE; Knowles, L; Meadows, RS; Piróg-Garcia, KA; Thornton, DJ	1
Buckley, MF; Elakis, G; Gardener, G; Inglis, G; Roscioli, T; Susman, RD; Zankl, A	1

Other Studies

2 other study(ies) available for methionine and Achondroplasia

Article	Year
Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP. Human molecular genetics, 2007, Sep-01, Volume: 16, Issue:17 Topics: Achondroplasia; Animals; Apoptosis; Cell Proliferation; Chondrocytes; Disease Models, Animal; Dwarfism; Endoplasmic Reticulum; Extracellular Matrix Proteins; Female; Glycoproteins; Male; Matrilin Proteins; Methionine; Mice; Mice, Knockout; Mutation; Osteochondrodysplasias; Phenotype; Protein Structure, Tertiary; Threonine	2007
Prenatal and postnatal presentation of severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) due to the FGFR3 Lys650Met mutation. American journal of medical genetics. Part A, 2008, Jan-15, Volume: 146A, Issue:2 Topics: Acanthosis Nigricans; Achondroplasia; Amino Acid Substitution; Developmental Disabilities; Female; Fetus; Humans; Infant, Newborn; Lysine; Male; Methionine; Mutation, Missense; Pregnancy; Receptor, Fibroblast Growth Factor, Type 3; Ultrasonography, Prenatal	2008

Article

Year

Reduced cell proliferation and increased apoptosis are significant pathological mechanisms in a murine model of mild pseudoachondroplasia resulting from a mutation in the C-terminal domain of COMP.

Human molecular genetics, 2007, Sep-01, Volume: 16, Issue:17

Topics: Achondroplasia; Animals; Apoptosis; Cell Proliferation; Chondrocytes; Disease Models, Animal; Dwarfism; Endoplasmic Reticulum; Extracellular Matrix Proteins; Female; Glycoproteins; Male; Matrilin Proteins; Methionine; Mice; Mice, Knockout; Mutation; Osteochondrodysplasias; Phenotype; Protein Structure, Tertiary; Threonine

2007

Prenatal and postnatal presentation of severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) due to the FGFR3 Lys650Met mutation.

American journal of medical genetics. Part A, 2008, Jan-15, Volume: 146A, Issue:2

Topics: Acanthosis Nigricans; Achondroplasia; Amino Acid Substitution; Developmental Disabilities; Female; Fetus; Humans; Infant, Newborn; Lysine; Male; Methionine; Mutation, Missense; Pregnancy; Receptor, Fibroblast Growth Factor, Type 3; Ultrasonography, Prenatal

2008