Abstract:
:Nuclear FGFR1 acts as a developmental gene regulator in cooperation with FGF-2, RSK1, and CREB-binding protein (CBP). FRAP analysis revealed three nuclear FGFR1 populations: i) a fast mobile, ii) a slower mobile population reflecting chromatin-bound FGFR1, and iii) an immobile FGFR1 population associated with the nuclear matrix. Factors (cAMP, CBP) that induce FGFR1-mediated gene activation shifted FGFR1 from the nuclear matrix (immobile) to chromatin (slow) and reduced the movement rate of the chromatin-bound population. Transcription inhibitors accelerated FGFR1 movement; the content of the chromatin-bound slow FGFR1 decreased, whereas the fast population increased. The transcriptional activation appears to involve conversion of the immobile matrix-bound and the fast nuclear FGFR1 into a slow chromatin-binding population through FGFR1's interaction with CBP, RSK1, and the high-molecular-weight form of FGF-2. Our findings support a general mechanism in which gene activation is governed by protein movement and collisions with other proteins and nuclear structures.
journal_name
Mol Biol Celljournal_title
Molecular biology of the cellauthors
Dunham-Ems SM,Lee YW,Stachowiak EK,Pudavar H,Claus P,Prasad PN,Stachowiak MKdoi
10.1091/mbc.e08-06-0600subject
Has Abstractpub_date
2009-05-01 00:00:00pages
2401-12issue
9eissn
1059-1524issn
1939-4586pii
E08-06-0600journal_volume
20pub_type
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