TWIST: A new piece to the puzzle on fiat bones ossification;TWIST: Un nouvel acteur de l'ossification des os plats

Medecine/Sciences

Volumn 17, Issue 12, 2001, Pages 1281-1288

  El Ghouzzi, V ^a   Bonaventure, J ^a   Munnich, A ^a  

^a HÔPITAL NECKER ENFANTS MALADES   (France)

Author keywords

[No Author keywords available]

Indexed keywords

FIBROBLAST GROWTH FACTOR RECEPTOR; HELIX LOOP HELIX PROTEIN; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR TWIST; UNCLASSIFIED DRUG;

ACROCEPHALOSYNDACTYLY; BONE DEVELOPMENT; CELL DIFFERENTIATION; GENE MUTATION; HUMAN; NONHUMAN; OSSIFICATION; OSTEOBLAST; REVIEW; SKULL SUTURE;

EID: 0035679225     PISSN: 07670974     EISSN: None     Source Type: Journal    
DOI: 10.1051/medsci/200117121281     Document Type: Review

References (30)

1. Mutations of the TWIST gene in the Saethre-Chotzen syndrome
2. Mutations in TWIST, a basic helix-loop-helix transcription factor, in Saethre-Chotzen syndrome
3. Helix-loop-helix proteins: Regulators of transcription in eucaryotic organisms
4. The variable expressivity and incomplete penetrance of the twist-null heterozygous mouse phenotype resemble those of human Saethre-Chotzen syndrome
5. Mutations within or upstream of the basic helix-loop-helix domain of the TWIST gene are specific to Saethre-Chotzen syndrome
6. Mutations in the human TWIST gene
7. A comprehensive screen for TWIST mutations m patients with craniosynostosis identifies a new microdeletion syndrome of chromosome band 7p21.1
8. Saethre-Chotzen mutations cause TWIST protein degradation or impaired nuclear location
9. Mutations in the basic domain and the loop-helix II junction of TWIST abolish DNA binding in Saethre-Chotzen syndrome
10. Increased bone formation and decreased osteocalcin expression induced by reduced Twist dosage in Saethre-Chotzen syndrome
11. Quality control of mRNA function
12. Expression patterns of Twist and Fgfr1, -2 and -3 in the developing mouse coronal suture suggest a key role for twist in suture initiation and biogenesis
13. Fgfr1 and Fgfr2 have distinct differentiation-and proliferation-related roles in the developing mouse skull vault
14. Integration of FGF and TWIST in calvarial bone and suture development
15. Spatio-temporal expression of FGFR 1, 2 and 3 genes during human embryo-fetal ossification
16. Differential expression of fibroblast growth factor receptor-1, -2, and -3 and syndecan-1, -2, and 4 in neonatal rat mandibular condyle and calvaria during osteogenic differentiation in vitro
17. Two FGF-receptor homologues of Drosophila: One is expressed in mesodermal primordium m early embryos
18. Analysis of the murine model of the Saethre-Chotzen syndrome suggests a functional relationship between TWIST and FGFR2
19. Establishment of distinct MyoD, E2A, and twist DNA binding specificities by different basic region-DNA conformations
20. Füchtbauer EM M-twist is an inhibitor of muscle differentiation
21. The basic domain of myogenic basic helix-loop-helix (bHLH) proteins is the novel target for direct inhibition by another bHLHprotein, Twist
22. TWIST, a basic helix-loop-helix transcription factor can regulate the human osteogenic lineage
23. Twist is a potential oncogene that inhibits apoptosis
24. Functional haploinsufficiency of the human homeobox gene MSX2 causes defects in skull ossification
25. Msx2 deficiency in mice causes pleiotropic defects in bone, growth and ectodermal organ formation
26. The ALX4 homeobox gene is mutated in patients with ossification defects of the skull (foramina parietalia permagna, OMIM 168500)
27. Haploinsufficiency of the human homeobox gene ALX4 causes skull ossification defects
28. Mutations involving the transcription factor CBFA1 cause cleidocranial dysplasia
29. Deletion of the basic helix-loop-helix domain in TWIST increases apoptosis in osteoblasts in the Saethre-Chotzen craniosynostosis