Response to Thum et al.

Journal of Clinical Investigation

Volumn 121, Issue 2, 2011, Pages 462-463

  Patrick, David M ^a   Kauppinen, Sakari ^b   Van Rooij, Eva ^c   Olson, Eric N ^a  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

^b Santaris Pharma AS   (Denmark)

^c miRagen Therapeutics Inc   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIMICRORNA 21 OLIGONUCLEOTIDE; MICRORNA 21; MOLECULAR THERAPY AGENT; TAMOXIFEN; UNCLASSIFIED DRUG;

ALLELE; DRUG EFFICACY; GENE DELETION; HEART DISEASE; HEART FUNCTION; HEART MUSCLE FIBROSIS; HEART VENTRICLE HYPERTROPHY; HUMAN; LETTER; NONHUMAN; NORTHERN BLOTTING; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; TRANSGENE;

EID: 79551506921     PISSN: 00219738     EISSN: 15588238     Source Type: Journal    
DOI: 10.1172/JCI46108     Document Type: Letter

References (4)

1. Thum T, et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signaling in fibroblasts. Nature. 2008;456(7224):980-984.
2. Patrick DM, et al. Stress-dependent cardiac remodeling occurs in the absence of miR-21 in mice. J Clin Invest. 2010;120(11):3912-3916.
3. Hatley ME, et al. Modulation of K-Ras-dependent lung tumorigenesis by microRNA-21. Cancer Cell. 2010;18(3):282-293.
4. van Rooij E, Sutherland LB, Qi X, Richardson JA, Hill J, Olson EN. Control of stress-dependent cardiac growth and gene expression by a microRNA. Science. 2007;316(5824):575-579. (Pubitemid 46683138)