Antisense inhibition of human Smad1 expression

Chemistry: molecular biology and microbiology – Animal cell – per se ; composition thereof; process of... – Method of regulating cell metabolism or physiology

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435 6, 435 911, 435325, 435366, 435455, 536 231, 536 2431, 536 2433, 536 245, C12Q 168, C12N 1500, C07H 2104

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active

060135220

ABSTRACT:
Antisense compounds, compositions and methods are provided for modulating the expression of Smad1. The compositions comprise antisense compounds, particularly antisense oligonucleotides, targeted to nucleic acids encoding Smad1. Methods of using these compounds for modulation of Smad1 expression and for treatment of diseases associated with expression of Smad1 are provided.

REFERENCES:
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Crooke, S.T. Ch1, "Antisense Research & Application" Springer, pp. 1-50.
Branch TIBS 23:45-50, Feb. 1998.
Heldin et al., TGF-beta signalling from cell membrane to nucleus through SMAD proteins, Nature, 1997, 390:465-471.
Kretzschmar et al., Opposing BMP and EGF signalling pathways converge on the TGF-beta family mediator Smadl, Nature, 1997, 389:618-622.
Kretzschmar et al., SMADs: mediators and regulators of TGF-beta signaling, Curr. Opin. Genet. Dev., 1998, 8:103-111.
Liu et al., A human Mad protein acting as a BMP-regulated transcriptional activator [see comments], Nature, 1996, 381:620-623.
Wrana, TGF-beta receptors and signalling mechanisms, Miner. Electrolyte Metab., 1988, 24:120-130.
Yamamoto et al., Smad1 and smad5 act downstream of intracellular signalings of BMP-2 that inhibits myogenic differentiation and induces osteoblast differentiation in C2C12 myoblasts, Biochem. Biophys. Res. Commun., 1997, 238:574-580.

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