The caspase-activated DNase: apoptosis and beyond
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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The caspase-activated DNase : apoptosis and beyond. / Larsen, Brian D; Sørensen, Claus S.
I: F E B S Journal, Bind 284, Nr. 8, 04.2017, s. 1160-1170.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - The caspase-activated DNase
T2 - apoptosis and beyond
AU - Larsen, Brian D
AU - Sørensen, Claus S
N1 - © 2016 Federation of European Biochemical Societies.
PY - 2017/4
Y1 - 2017/4
N2 - Organismal development and function requires multiple and accurate signal transduction pathways to ensure that proper balance between cell proliferation, differentiation, inactivation, and death is achieved. Cell death via apoptotic caspase signal transduction is extensively characterized and integral to this balance. Importantly, the view of apoptotic signal transduction has expanded over the previous decades. Subapoptotic caspase signaling has surfaced as mechanism that can promote the adoption of a range of cellular fates. An emerging mechanism of subapoptotic caspase signaling is the activation of the caspase-activated DNase (CAD) through controlled cleavage of the inhibitor of CAD (ICAD). CAD-induced DNA breaks incite a DNA damage response, frequently invoking p53 signaling, that transduces a change in cell fate. Cell differentiation and senescence are fates demonstrated to arise from CAD-induced DNA breaks. Furthermore, an apparent consequence of CAD activity is also emerging, as a potential source of oncogenic mutations. This review will discuss the mechanisms underlying CAD-induced DNA breaks and highlight how CAD activity promotes diverse cell fates.
AB - Organismal development and function requires multiple and accurate signal transduction pathways to ensure that proper balance between cell proliferation, differentiation, inactivation, and death is achieved. Cell death via apoptotic caspase signal transduction is extensively characterized and integral to this balance. Importantly, the view of apoptotic signal transduction has expanded over the previous decades. Subapoptotic caspase signaling has surfaced as mechanism that can promote the adoption of a range of cellular fates. An emerging mechanism of subapoptotic caspase signaling is the activation of the caspase-activated DNase (CAD) through controlled cleavage of the inhibitor of CAD (ICAD). CAD-induced DNA breaks incite a DNA damage response, frequently invoking p53 signaling, that transduces a change in cell fate. Cell differentiation and senescence are fates demonstrated to arise from CAD-induced DNA breaks. Furthermore, an apparent consequence of CAD activity is also emerging, as a potential source of oncogenic mutations. This review will discuss the mechanisms underlying CAD-induced DNA breaks and highlight how CAD activity promotes diverse cell fates.
KW - Review
KW - Journal Article
U2 - 10.1111/febs.13970
DO - 10.1111/febs.13970
M3 - Review
C2 - 27865056
VL - 284
SP - 1160
EP - 1170
JO - F E B S Journal
JF - F E B S Journal
SN - 1742-464X
IS - 8
ER -
ID: 179349914