A human Mad protein acting as a BMP-regulated transcriptional activator

Article Abstract:

Human Smad1 gene is a homologue of the Mothers against decapentaplegic and Sma genes, and induces transcription in the presence of the cytokine, bone-morphogenetic-protein 4 (BMP4). The GAL4-Smad1 gene construct activates transcription. BMP4-signals increase transcription and act through the BMP-receptor types I and II. The transcription activity is due to the C-terminal region in the absence of the N-terminal region. Smad1 encoded protein is involved in BMP signaling as its overexpression in the Xenopus embryo animal cap induces ventralization of the mesoderm.

Author: Liu, Fang, Harland, Richard M., Hata, Akiko, Massague, Joan, Baker, Julie C., Doody, Jacqueline, Carcamo, Juan
Physiological aspects, Genetic regulation, Gene expression, Cytokines

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Opposing BMP and EGF signalling pathways converge on the TGF-beta family mediator Smad1

Article Abstract:

Cell proliferation, apoptosis and differentiation is controlled and regulated by bone morphogenetic proteins (BMPs), TGF-beta and related factors, which are involved in signalling networks. Such signalling involves the antagonistic or synergistic interaction of different pathways. The mechanisms concerned with such agonistic interplay is ill understood. A study of the tumour-suppressor SMAD protein SMAD1, which moderates BMP signals, shows that it is a target of growth-factor signalling via the Erk MAP pathway. Details of the study are presented.

Author: Massague, Joan, Doody, Jacqueline, Kretzschmar, Marcus
Proteins

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Inhibition of transforming growth factor-beta/SMAD signalling by the interferon-gamma/STAT pathway

Article Abstract:

Transforming growth factor-beta (TGF-beta) and interferon-gamma (IFN-gamma) have opposing effects on cellular functions. TGF-Beta signals via a receptor serine kinase that activates transcription factors Smads 2 and 3, while the IFN-gamma receptor mediates activation of transcription factor Stat1. A basis for the integration of TGF-Beta and IFN-gamma signals is presented, suggesting a mechanism of transmodulation between STAT and SMAD.

Author: Massague, Joan, Doody, Jacqueline, Ulluoa, Luis

User Contributions:

Comment about this article or add new information about this topic:

CAPTCHA


Subjects list: Research, Genetic transcription, Transcription (Genetics), Transforming growth factors
This website is not affiliated with document authors or copyright owners. This page is provided for informational purposes only. Unintentional errors are possible.