Transcriptional suppression of Sox9 expression in chondrocytes by retinoic acid

Journal of Cellular Biochemistry

Volumn 81, Issue SUPPL. 36, 2001, Pages 71-78

  He, Nonggao ^a   Brysk, Henry ^a   Tyring, Stephen K ^a   Ohkubo, Iwao ^a,b   Brysk, Miriam M ^a  

^a University of Texas Medical Branch School of Medicine   (United States)

^b SHIGA UNIVERSITY OF MEDICAL SCIENCE   (Japan)

Author keywords

Chondrocyte; Retinoic acid; SOX9; Transcription; Type II collage

Indexed keywords

COLLAGEN TYPE 2; MESSENGER RNA; RETINOIC ACID; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR SOX9; UNCLASSIFIED DRUG; HIGH MOBILITY GROUP PROTEIN; SOX-9 TRANSCRIPTION FACTOR;

ANIMAL CELL; ANIMAL TISSUE; ARTICLE; CARTILAGE CELL; CELL NUCLEUS; CONTROLLED STUDY; ENHANCER REGION; GENE EXPRESSION REGULATION; GENE REPRESSION; MOUSE; NEWBORN; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; RIB CARTILAGE; TRANSCRIPTION REGULATION; ANIMAL; CELL CULTURE; DOWN REGULATION; GENETIC TRANSCRIPTION; GENETICS; INSTITUTE FOR CANCER RESEARCH MOUSE; METABOLISM; NORTHERN BLOTTING; WESTERN BLOTTING;

ANIMALS; BLOTTING, NORTHERN; BLOTTING, WESTERN; CELLS, CULTURED; CHONDROCYTES; DOWN-REGULATION; ENHANCER ELEMENTS (GENETICS); HIGH MOBILITY GROUP PROTEINS; MICE; MICE, INBRED ICR; RNA, MESSENGER; TRANSCRIPTION FACTORS; TRANSCRIPTION, GENETIC; TRETINOIN;

EID: 0035029259     PISSN: 07302312     EISSN: None     Source Type: Journal    
DOI: 10.1002/jcb.1077     Document Type: Article

References (38)

1. SOX9 directly regulates the type-II collagen gene
2. Modulation of the rabbit chondrocyte phenotype by retinoic acid terminates type II collagen synthesis without inducing type I collagen: The modulated phenotype differs from that produced by subculture
3. Retinoic acid alters the proportion of high mannose to complex type oligosaccharides on fibronectin secreted by cultured chondrocytes
4. Sox9 is required for cartilage formation
5. Alterations in chondrocyte cytoskeletal architecture during phenotypic modulation by retinoic acid and dihydrocytochalasin B-induced reexpression
6. Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction
7. Transcriptional control in the production of liver-specific mRNAs
8. Campomelic dysplasia and autosomal sex reversal caused by mutations in an SRY-related gene
9. The HMG domain of lymphoid enhancer factor 1 bends DNA and facilitates assembly of functional nucleoprotein structures
10. A gene mapping to the sex-determining region of the mouse Y chromosome is a member of a novel family of embryonically expressed genes
11. Definition of a consensus DNA binding site for SRY
12. Identification of a phenotype-specific enhancer in the first intron of the rat collagen II gene
13. Retinoic acid rapidly reduces cartilage matrix synthesis by altering gene transcription in chondrocytes
14. Nucleolar transcription factor hUBF contains a DNA-binding motif with homology to HMG proteins
15. Characterization of primary cultures of chondrocytes from type II collagen/betagalactosidase transgenic mice
16. SOX9 is a potent activator of the chondrocyte-specific enhancer of the pro alpha1(II) collagen gene
17. Function of retinoic acid receptor gamma in the mouse
18. Function of the retinoic acid receptors (RARs) during development (I). Craniofacial and skeletal abnormalities in RAR double mutants
19. Characterization of three RXR genes that mediate the action of 9cis retinoic acid
20. The nuclear receptor superfamily: The second decade
21. The DNA-binding specificity of SOX9 and other SOX proteins
22. Transcription factor AP-2 is expressed in neural crest cell lineages during mouse embryogenesis
23. SOX9 binds DNA, activates transcription, and coexpresses with type II collagen during chondrogenesis in the mouse
24. Embryonic retinoic acid synthesis is essential for early mouse post-implantation development
25. Specific organization of the negative response elements for retinoic acid and thyroid hormone receptors in keratin gene family
26. The role of SOX9 in autosomal sex reversal and campomelic dysplasia
27. Transcription factor AP-2 essential for cranial closure and craniofacial development
28. SOX9 enhances aggrecan gene promoter/enhancer activity and is upregulated by retinoic acid in a cartilage-derived cell line, TC6
29. Autosomal sex reversal and campomelic dysplasia are caused by mutations in and around the SRY-related gene SOX9
30. From head to toes: The multiple facets of Sox proteins
31. The Sry-related gene Sox9 is expressed during chondrogenesis in mouse embryos
32. Seven new members of the Sox gene family expressed during mouse development
33. Deletion of long-range regulatory elements upstream of SOX9 causes campomelic dysplasia
34. Regulation of the mouse cartilage-derived retinoic acid-sensitive protein gene by the transcription factor AP-2
35. Trans-activation of the mouse cartilage-derived retinoic acid-sensitive protein gene by Sox9
36. Retardation of skeletal development and cervical abnormalities in transgenic mice expressing a dominant-negative retinoic acid receptor in chondrogenic cells
37. Neural tube, skeletal and body wall defects in mice lacking transcription factor AP-2
38. Parallel expression of Sox9 and Col2a1 in cells undergoing chondrogenesis