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Apoptosis

Latest questions in this category.

30 questions

Anoikis is apoptosis triggered by

The extrinsic pathway is initiated by binding of death ligands such as FasL or TNF to their cognate death receptors. Receptor clustering recruits adaptor proteins and caspase-8, forming the death-inducing signaling complex. Anoikis is a specialized form of apoptosis triggered by loss of integrin-mediated attachment to the extracellular matrix, thereby preventing survival of detached cells.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

The extrinsic apoptotic pathway is initiated by

The extrinsic pathway is initiated by binding of death ligands such as FasL or TNF to their cognate death receptors. Receptor clustering recruits adaptor proteins and caspase-8, forming the death-inducing signaling complex. Anoikis is a specialized form of apoptosis triggered by loss of integrin-mediated attachment to the extracellular matrix, thereby preventing survival of detached cells.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

Smac/DIABLO promotes apoptosis by

XIAP is a potent inhibitor of caspases-3, -7 and -9. The mitochondrial protein Smac/DIABLO, released during MOMP, binds XIAP and neutralizes its inhibitory activity, thereby facilitating full activation of the caspase cascade. This dual control—release of both cytochrome c and Smac—ensures robust commitment to apoptosis once mitochondria are permeabilized. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

Which protein directly inhibits caspase-3, -7, and -9?

XIAP, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

The apoptosome is composed of

Mitochondrial outer-membrane permeabilization (MOMP) releases cytochrome c into the cytosol. Cytochrome c binds Apaf-1, inducing formation of the heptameric apoptosome that recruits and activates caspase-9. Active caspase-9 then propagates the cascade by cleaving executioner caspases. MOMP is therefore the point of no return for the intrinsic apoptotic pathway. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

Cytochrome c released from mitochondria binds to

Mitochondrial outer-membrane permeabilization (MOMP) releases cytochrome c into the cytosol. Cytochrome c binds Apaf-1, inducing formation of the heptameric apoptosome that recruits and activates caspase-9. Active caspase-9 then propagates the cascade by cleaving executioner caspases. MOMP is therefore the point of no return for the intrinsic apoptotic pathway. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

MOMP stands for

Mitochondrial outer-membrane permeabilization (MOMP) releases cytochrome c into the cytosol. Cytochrome c binds Apaf-1, inducing formation of the heptameric apoptosome that recruits and activates caspase-9. Active caspase-9 then propagates the cascade by cleaving executioner caspases. MOMP is therefore the point of no return for the intrinsic apoptotic pathway. Careful

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

The intrinsic apoptotic pathway is triggered primarily by

DNA damage and cellular stress, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

During apoptosis, exposure of phosphatidylserine requires

Apoptosis is an orderly, energy-dependent form of programmed cell death that eliminates cells without provoking inflammation. Characteristic morphological features include cell shrinkage, chromatin condensation (pyknosis), nuclear fragmentation (karyorrhexis), membrane blebbing and formation of apoptotic bodies that display phosphatidylserine as an “eat-me” signal for phagocytes. Rapid clearance of these bodies prevents release of intracellular contents and subsequent inflammation.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

In healthy cells, phosphatidylserine is maintained in the inner leaflet by

Apoptosis is an orderly, energy-dependent form of programmed cell death that eliminates cells without provoking inflammation. Characteristic morphological features include cell shrinkage, chromatin condensation (pyknosis), nuclear fragmentation (karyorrhexis), membrane blebbing and formation of apoptotic bodies that display phosphatidylserine as an “eat-me” signal for phagocytes. Rapid clearance of these bodies prevents release of intracellular contents and subsequent inflammation.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

DNA laddering during apoptosis occurs due to cleavage at

Linker DNA between nucleosomes, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

Caspase-3 activation leads to DNA fragmentation by activating

CAD (caspase-activated DNase), is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)