Apoptosis - Intrinsic (Mitochondrial) Antibody Sampler Pack

Apoptosis - Intrinsic (Mitochondrial) Antibody Sampler Pack

The Apoptosis - Intrinsic (Mitochondrial) Antibody Sampler Pack from Assay Genie brings together 8 rigorously validated antibodies spanning the key nodes of this pathway, supplied in a convenient 20µL trial size. It lets researchers screen an entire signalling axis in a single, cost-effective pack — validated for applications including ELISA, IF/ICC, IHC-P, IP, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

The intrinsic, or mitochondrial, apoptotic pathway integrates intracellular stress signals such as DNA damage, growth factor withdrawal, and oncogenic stress into a committed decision to die. The pathway is governed by the BCL-2 family of proteins, whose opposing pro-survival and pro-death members set the threshold for mitochondrial outer membrane permeabilization. Anti-apoptotic guardians including Bcl-2 and Bcl-xL sequester the pro-apoptotic effectors and restrain cell death, while the multidomain effectors Bax and Bak oligomerize within the outer mitochondrial membrane to form pores once their inhibition is relieved. The BH3-only protein Bad acts as a sensitizer; when dephosphorylated it displaces effectors from Bcl-2 and Bcl-xL, tipping the balance toward permeabilization. Once Bax and Bak generate pores, Cytochrome c is released from the intermembrane space into the cytosol, where it nucleates assembly of the apoptosome together with Apaf-1 and dATP. This platform recruits and activates the initiator protease Caspase-9, which in turn cleaves and activates downstream executioner caspases. The appearance of Cleaved Caspase-3 marks irreversible commitment to apoptosis, driving the proteolysis of structural and regulatory substrates that produce the morphological hallmarks of programmed cell death. In cancer, this axis is frequently subverted: overexpression of Bcl-2 or Bcl-xL, loss of pro-apoptotic effectors, and attenuated Cytochrome c release allow malignant cells to evade death and resist chemotherapy and radiation. These dependencies have become therapeutic targets, exemplified by BH3-mimetic drugs that neutralize Bcl-2, restoring effector function and apoptotic signaling. Quantifying the relative abundance, phosphorylation state, and processing of these regulators provides a mechanistic readout of how close a cell sits to its apoptotic threshold. This pack brings together validated antibodies against Bcl-2, Bax, Bak, Bcl-xL, Bad, Cytochrome c, Caspase-9, and Cleaved Caspase-3 for studying the intrinsic mitochondrial apoptosis pathway.