Angiotensin II–Induced Stimulation of Smooth Muscle α-Actin Expression by Serum Response Factor and the Homeodomain Transcription Factor MHox

1997 ◽  
Vol 81 (4) ◽  
pp. 600-610 ◽  
Author(s):  
Martina B. Hautmann ◽  
Maria M. Thompson ◽  
Ellen A. Swartz ◽  
Eric N. Olson ◽  
Gary K. Owens
2000 ◽  
Vol 275 (13) ◽  
pp. 9814-9822 ◽  
Author(s):  
Joseph M. Miano ◽  
Michael J. Carlson ◽  
Jeffrey A. Spencer ◽  
Ravi P. Misra

2011 ◽  
Vol 50 (2) ◽  
pp. 354-362 ◽  
Author(s):  
Abel Martin-Garrido ◽  
David I. Brown ◽  
Alicia N. Lyle ◽  
Anna Dikalova ◽  
Bonnie Seidel-Rogol ◽  
...  

2000 ◽  
Vol 345 (3) ◽  
pp. 445-451 ◽  
Author(s):  
Paul R. KEMP ◽  
James C. METCALFE

Serum response factor (SRF) is a key transcriptional activator of the c-fos gene and of muscle-specific gene expression. We have identified four forms of the SRF coding sequence, SRF-L (the previously identified form), SRF-M, SRF-S and SRF-I, that are produced by alternative splicing. The new forms of SRF lack regions of the C-terminal transactivation domain by splicing out of exon 5 (SRF-M), exons 4 and 5 (SRF-S) and exons 3, 4 and 5 (SRF-I). SRF-M is expressed at similar levels to SRF-L in differentiated vascular smooth-muscle cells and skeletal-muscle cells, whereas SRF-L is the predominant form in many other tissues. SRF-S expression is restricted to vascular smooth muscle and SRF-I expression is restricted to the embryo. Transfection of SRF-L and SRF-M into C2C12 cells showed that both forms are transactivators of the promoter of the smooth-muscle-specific gene SM22α, whereas SRF-I acted as a dominant negative form of SRF.


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