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Characterization of XIAP-deficient mice
H Harlin1, S B Reffey, C S Duckett
1Committee on Immunology, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Molecular and Cellular Biology
|April 21, 2001
Summary
Mice lacking X-linked inhibitor of apoptosis protein (XIAP) showed no defects in apoptosis. However, levels of related proteins c-IAP1 and c-IAP2 increased, suggesting a compensatory mechanism for XIAP loss.
Area of Science:
- Cell Biology
- Molecular Biology
- Immunology
Background:
- The inhibitor of apoptosis protein (IAP) family regulates programmed cell death.
- X-linked IAP (XIAP) inhibits apoptosis by binding caspases.
- XIAP expression is regulated at multiple levels.
Purpose of the Study:
- To investigate the in vivo function of XIAP.
- To determine the effects of XIAP deficiency on apoptosis.
- To explore compensatory mechanisms within the IAP family.
Main Methods:
- Homologous gene targeting to generate XIAP-deficient mice.
- Histopathological analysis of XIAP-deficient and wild-type mice.
- Assessment of caspase-dependent and -independent apoptosis induction in cells.
Main Results:
- XIAP-deficient mice were viable with no apparent histopathological differences.
- No defects in apoptosis induction were observed in cells from XIAP-deficient mice.
- XIAP deficiency led to increased protein levels of c-IAP1 and c-IAP2.
Conclusions:
- XIAP is not essential for normal development or apoptosis induction in mice.
- A compensatory mechanism upregulates other IAP family members upon XIAP loss.
- Increased c-IAP1 and c-IAP2 may compensate for XIAP deficiency.