Cardiotrophin 1
Today, Cardiotrophin 1 is a topic of great relevance and interest to a wide variety of people. Whether due to its impact on society, its influence on popular culture or its importance in the professional field, Cardiotrophin 1 has become a recurring topic of conversation around the world. With its variety of facets and its ability to generate debate, Cardiotrophin 1 remains an ever-evolving topic that continues to capture the audience's attention and curiosity. In this article, we will explore in detail different aspects of Cardiotrophin 1, its impact and its relevance today.
| cardiotrophin 1 | |||||||
|---|---|---|---|---|---|---|---|
| Identifiers | |||||||
| Symbol | CTF1, CT1, CT-1 | ||||||
| NCBI gene | 1489 | ||||||
| HGNC | 2499 | ||||||
| OMIM | 600435 | ||||||
| RefSeq | NM_001330 | ||||||
| UniProt | Q16619 | ||||||
| Other data | |||||||
| Locus | Chr. 16 p11.2-16p11.1 | ||||||
| |||||||
Cardiotrophin-1 (CT-1) is a cytokine. It is a cardiac hypertrophic factor of 21.5 kDa and a protein member of the IL-6 cytokine family.
Pathology
CT-1 is associated with the pathophysiology of heart diseases, including hypertension, myocardial infarction, valvular heart disease, and congestive heart failure.
Mode of action
The protein exerts its cellular effects by interacting with the glycoprotein 130 (gp130)/leukemia inhibitory factor receptor beta (LIFR) heterodimer. In addition, CT-1 activates phosphatidylinositol 3-kinase (PI-3 kinase) in cardiac myocytes and enhances transcription factor NF-κB DNA -binding activities.
CT-1 is highly expressed in the heart, skeletal muscle, prostate and ovary and to lower levels in lung, kidney, pancreas, thymus, testis and small intestine. [1]
References
- ^ "Recombinant human Cardiotrophin 1 protein (ab9838)". www.abcam.com. Retrieved 2017-08-09.
External links
- cardiotrophin+1 at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- Irving, Michael (August 8, 2017). "The protein that can make your heart think you exercise". newatlas.com. Retrieved 2017-08-09.
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