Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1

Science

Volumn 298, Issue 5600, 2002, Pages 1996-1999

  Iratni, Rabah ^a,c   Yan, Yu Ting ^b   Chen, Canhe ^b   Ding, Jixiang ^b   Zhang, Yi ^a,d   Price, Sandy M ^b   Reinberg, Danny ^a   Shen, Michael M ^b  

^a HOWARD HUGHES MEDICAL INSTITUTE   (United States)

^b RUTGERS ROBERT WOOD JOHNSON MEDICAL SCHOOL   (United States)

^c INSTITUT ALBERT BONNIOT   (France)

^d UNIVERSITY OF NORTH CAROLINA SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DNA; LIVING SYSTEMS STUDIES; PROTEINS;

POSITIVE FEEDBACK LOOP;

BIOCHEMISTRY;

DNA; PROTEIN; PROTEIN DRAP1; PROTEIN FOXH1; TRANSCRIPTION FACTOR; UNCLASSIFIED DRUG;

DNA; SIGNALING;

ANIMAL TISSUE; ARTICLE; AUTOREGULATION; BIOCHEMISTRY; CONTROLLED STUDY; DNA BINDING; EMBRYO; EMBRYO DEVELOPMENT; GASTRULATION; HETEROZYGOSITY; MAMMAL; MESODERM; MORPHOGENESIS; MOUSE; NONHUMAN; PRIORITY JOURNAL;

ALLELES; ANIMALS; CELL LINE; CROSSES, GENETIC; DNA; DNA-BINDING PROTEINS; EMBRYONIC AND FETAL DEVELOPMENT; FEMALE; FORKHEAD TRANSCRIPTION FACTORS; GASTRULA; GENE EXPRESSION REGULATION, DEVELOPMENTAL; GENE TARGETING; HETEROZYGOTE; IN SITU HYBRIDIZATION; MALE; MESODERM; MICE; MORPHOGENESIS; MUTATION; PHENOTYPE; PROTEIN BINDING; RECOMBINANT FUSION PROTEINS; REPRESSOR PROTEINS; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RNA INTERFERENCE; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTORS; TRANSFORMING GROWTH FACTOR BETA;

ANIMALIA; MAMMALIA;

EID: 2242437180     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.1073405     Document Type: Article

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29. We thank R. Behringer, H. Hamada, G. Hannon, A. Joyner, R. Krumlauf, F. Lai, F. Liu, R. Lovell-Badge, G. Martin, A. McMahon, P. Paddison, J. Rossant, M. Whitman, and C. Wright for gifts of reagents and probes, N. Desai and L. Wang for technical assistance, and C. Abate-Shen for helpful discussions and comments on the manuscript. We are particularly grateful to C. Abate-Shen and L. Vales for invaluable advice on protein interaction assays and to E. Robertson for generously providing Nodal-lacZ mice. Supported by awards from the American Heart Association (J.D.) and the Leukemia and Lymphoma Society (J.D.), and by a postdoctoral fellowship (Y.Z.) and grants from the NIH (D.R., M.M.S.). D.R. is an Investigator of the Howard Hughes Medical Institute.