Abstract
Fas/APO-1(CD95) ligation activates programmed cell death, a cellular process that plays an important role in the maturation of the host immune response. We show that activation of a specific MAP kinase kinase (MKK), MKK6b, is necessary and sufficient for Fas-induced apoptosis of Jurkat T cells. MKK6b activation occurs downstream of an interleukin-1 converting enzyme-like (ICE-like) protease(s), while execution of the apoptotic pathway by MKK6b requires both ICE- and CPP32-like proteases. Surprisingly, the p38 MAP kinase protein, a known substrate of MKK6b, does not participate in Fas/MKK6b-mediated apoptosis. These findings indicate a divergence of the MKK6b signaling pathways, one of which activates p38 and leads to regulation of gene expression, and one of which activates the ICE/Cad-3 family of proteases and leads to cell death. These studios represent a demonstration of an apoptotic pathway that is comprised of both the ICF/Ced-3 family of proteases and MAP kinase kinase 6.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 739-749 |
| Number of pages | 11 |
| Journal | Immunity |
| Volume | 6 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jan 1 1997 |
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ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases
Cite this
Apoptosis signaling pathway in T cells is composed of ICE/Ced-3 family proteases and MAP kinase kinase 6b. / Huang, Shuang; Jiang, Yong; Li, Zhuangjie; Nishida, Eisuke; Mathias, Patricia; Lin, Shengcai; Ulevitch, Richard J.; Nemerow, Glen R.; Han, Jiahuai.
In: Immunity, Vol. 6, No. 6, 01.01.1997, p. 739-749.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Apoptosis signaling pathway in T cells is composed of ICE/Ced-3 family proteases and MAP kinase kinase 6b
AU - Huang, Shuang
AU - Jiang, Yong
AU - Li, Zhuangjie
AU - Nishida, Eisuke
AU - Mathias, Patricia
AU - Lin, Shengcai
AU - Ulevitch, Richard J.
AU - Nemerow, Glen R.
AU - Han, Jiahuai
PY - 1997/1/1
Y1 - 1997/1/1
N2 - Fas/APO-1(CD95) ligation activates programmed cell death, a cellular process that plays an important role in the maturation of the host immune response. We show that activation of a specific MAP kinase kinase (MKK), MKK6b, is necessary and sufficient for Fas-induced apoptosis of Jurkat T cells. MKK6b activation occurs downstream of an interleukin-1 converting enzyme-like (ICE-like) protease(s), while execution of the apoptotic pathway by MKK6b requires both ICE- and CPP32-like proteases. Surprisingly, the p38 MAP kinase protein, a known substrate of MKK6b, does not participate in Fas/MKK6b-mediated apoptosis. These findings indicate a divergence of the MKK6b signaling pathways, one of which activates p38 and leads to regulation of gene expression, and one of which activates the ICE/Cad-3 family of proteases and leads to cell death. These studios represent a demonstration of an apoptotic pathway that is comprised of both the ICF/Ced-3 family of proteases and MAP kinase kinase 6.
AB - Fas/APO-1(CD95) ligation activates programmed cell death, a cellular process that plays an important role in the maturation of the host immune response. We show that activation of a specific MAP kinase kinase (MKK), MKK6b, is necessary and sufficient for Fas-induced apoptosis of Jurkat T cells. MKK6b activation occurs downstream of an interleukin-1 converting enzyme-like (ICE-like) protease(s), while execution of the apoptotic pathway by MKK6b requires both ICE- and CPP32-like proteases. Surprisingly, the p38 MAP kinase protein, a known substrate of MKK6b, does not participate in Fas/MKK6b-mediated apoptosis. These findings indicate a divergence of the MKK6b signaling pathways, one of which activates p38 and leads to regulation of gene expression, and one of which activates the ICE/Cad-3 family of proteases and leads to cell death. These studios represent a demonstration of an apoptotic pathway that is comprised of both the ICF/Ced-3 family of proteases and MAP kinase kinase 6.
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UR - http://www.scopus.com/inward/citedby.url?scp=0030812347&partnerID=8YFLogxK
U2 - 10.1016/S1074-7613(00)80449-5
DO - 10.1016/S1074-7613(00)80449-5
M3 - Article
VL - 6
SP - 739
EP - 749
JO - Immunity
JF - Immunity
SN - 1074-7613
IS - 6
ER -