Abstract
Apoptosis, programmed cell death, eliminates injured or harmful cells. It can mediate its response through the actions of death ligands including TRAIL. TRAIL, a member of TNF superfamily, induces apoptosis of transformed cells through the action of death domain receptors DR-4 and DR5. It directly induces apoptosis through an extrinsic pathway, which involves the activation of caspases. TRAIL also is able to prevent apoptosis through the actions of its decoy receptors DcR-1 and DcR-2. Various regulators of TRAIL include FADD, IAPs, Bcl-2s, p53, and FLIPs. TRAIL is present in cells involved in asthma including eosinophils, mast cells, fibroblasts, and airway epithelial cells. It is expressed in airway remodeling and may be linked with the pathways of transforming growth factor-beta1, which is thought to cause damage to the epithelium. The repair process of the epithelium is hindered as a result of increased apoptosis induced by TGF-β1, which overlaps with the pathways of TRAIL. Analogs of TRAIL could have therapeutical applications for asthma. TRAIL is also seen as the basis for a "miracle" drug for cancer because of its ability to selectively kill cancer cells.
| Original language | English |
|---|---|
| Pages (from-to) | 249-262 |
| Number of pages | 14 |
| Journal | Immunologic Research |
| Volume | 35 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jul 2006 |
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All Science Journal Classification (ASJC) codes
- Immunology
Cite this
Following the TRAIL to apoptosis. / Chaudhari, Bharti R.; Murphy, Richard F.; Agrawal, Devendra K.
In: Immunologic Research, Vol. 35, No. 3, 07.2006, p. 249-262.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Following the TRAIL to apoptosis
AU - Chaudhari, Bharti R.
AU - Murphy, Richard F.
AU - Agrawal, Devendra K.
PY - 2006/7
Y1 - 2006/7
N2 - Apoptosis, programmed cell death, eliminates injured or harmful cells. It can mediate its response through the actions of death ligands including TRAIL. TRAIL, a member of TNF superfamily, induces apoptosis of transformed cells through the action of death domain receptors DR-4 and DR5. It directly induces apoptosis through an extrinsic pathway, which involves the activation of caspases. TRAIL also is able to prevent apoptosis through the actions of its decoy receptors DcR-1 and DcR-2. Various regulators of TRAIL include FADD, IAPs, Bcl-2s, p53, and FLIPs. TRAIL is present in cells involved in asthma including eosinophils, mast cells, fibroblasts, and airway epithelial cells. It is expressed in airway remodeling and may be linked with the pathways of transforming growth factor-beta1, which is thought to cause damage to the epithelium. The repair process of the epithelium is hindered as a result of increased apoptosis induced by TGF-β1, which overlaps with the pathways of TRAIL. Analogs of TRAIL could have therapeutical applications for asthma. TRAIL is also seen as the basis for a "miracle" drug for cancer because of its ability to selectively kill cancer cells.
AB - Apoptosis, programmed cell death, eliminates injured or harmful cells. It can mediate its response through the actions of death ligands including TRAIL. TRAIL, a member of TNF superfamily, induces apoptosis of transformed cells through the action of death domain receptors DR-4 and DR5. It directly induces apoptosis through an extrinsic pathway, which involves the activation of caspases. TRAIL also is able to prevent apoptosis through the actions of its decoy receptors DcR-1 and DcR-2. Various regulators of TRAIL include FADD, IAPs, Bcl-2s, p53, and FLIPs. TRAIL is present in cells involved in asthma including eosinophils, mast cells, fibroblasts, and airway epithelial cells. It is expressed in airway remodeling and may be linked with the pathways of transforming growth factor-beta1, which is thought to cause damage to the epithelium. The repair process of the epithelium is hindered as a result of increased apoptosis induced by TGF-β1, which overlaps with the pathways of TRAIL. Analogs of TRAIL could have therapeutical applications for asthma. TRAIL is also seen as the basis for a "miracle" drug for cancer because of its ability to selectively kill cancer cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=33845872311&partnerID=8YFLogxK
U2 - 10.1385/IR:35:3:249
DO - 10.1385/IR:35:3:249
M3 - Review article
C2 - 17172650
AN - SCOPUS:33845872311
VL - 35
SP - 249
EP - 262
JO - Immunologic Research
JF - Immunologic Research
SN - 0257-277X
IS - 3
ER -