Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Enlargement of the skull vault occurs by appositional growth at the fibrous joints between the bones, termed cranial sutures. Relatively little is known about the developmental biology of this process, but genetically determined disorders of premature cranial suture fusion (craniosynostosis) provide one route to the identification of some of the key molecules involved. Mutations of the MSX2, FGFR1, FGFR2, FGFR3 and TWIST genes yield new insights, both into normal and abnormal cranial suture biogenesis and into problems of broad interest, such as the conservation of molecular pathways in development, and mechanisms of mutation and dominance.

Original publication

DOI

10.1093/hmg/6.10.1647

Type

Journal article

Journal

Hum Mol Genet

Publication Date

1997

Volume

6

Pages

1647 - 1656

Keywords

Amino Acid Sequence, Animals, Craniosynostoses, DNA-Binding Proteins, Homeodomain Proteins, Humans, Molecular Sequence Data, Mutation, Nuclear Proteins, Point Mutation, Protein-Tyrosine Kinases, Receptor Protein-Tyrosine Kinases, Receptor, Fibroblast Growth Factor, Type 1, Receptor, Fibroblast Growth Factor, Type 2, Receptor, Fibroblast Growth Factor, Type 3, Receptors, Fibroblast Growth Factor, Sequence Alignment, Transcription Factors, Twist-Related Protein 1