Linked Life Data

15715940

Source:http://linkedlifedata.com/resource/pubmed/id/15715940

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-2-17
pubmed:abstractText
Transforming Growth Factor (TGF)-beta family, including TGF-beta, bone morphorgenic protein (BMP), and activn, plays an important role in essential cellular functions such as proliferation, differentiation, apoptosis, tissue remodeling, angiognesis, immune responses, and cell adhesions. TGF-beta predominantly transmits the signals through serine/threonine receptor kinases and cytoplasmic proteins called Smads. Since the discovery of TGF-beta in the early 1980s, the dysregulation of TGF-beta /Smad signaling has been implicated in the pathogenesis of human diseases. Among signal transducers in TGF-beta/Smad signaling, inhibitory Smads (I-Smads), Smad6 and Smad7, act as major negative regulators forming autoinhibitory feedback loops and mediate the cross-talking with other signaling pathways. Expressions of I-Smads are mainly regulated on the transcriptional levels and post-translational protein degradations and their intracellular levels are tightly controlled to maintain the homeostatic balances. However, abnormal levels of I-Smads in the pathological conditions elicit the altered TGF-beta signaling in cells, eventually causing TGF-beta-related human diseases. Thus, exploring the molecular mechanisms about the regulations of I-Smads may provide the therapeutic clues for human diseases induced by the abnormal TGF-beta signaling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1225-8687
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-16
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Fine tuning and cross-talking of TGF-beta signal by inhibitory Smads.
pubmed:affiliation
Department of Pathology and Research Institute of Medical Science, Inha University College of Medicine, Incheon, Republic of Korea. parksh@inha.ac.kr
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't