DNA Damage Response Antibody Sampler Pack

DNA Damage Response Antibody Sampler Pack

The DNA Damage Response 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, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

The DNA damage response is a coordinated signaling network that detects genomic lesions, halts cell-cycle progression, and orchestrates repair, thereby safeguarding genome integrity. The response is anchored by two apical kinases: ATM, which is activated chiefly by DNA double-strand breaks and whose autophosphorylation is detected as Phospho-ATM, and ATR, which responds primarily to single-stranded DNA and replication stress. These kinases phosphorylate a cascade of effectors to transmit and amplify the damage signal. One of the earliest events at double-strand breaks is phosphorylation of the histone variant H2AX to generate gamma-H2AX, which spreads across megabase domains flanking the lesion and serves as a platform for recruiting repair and signaling factors. The mediator 53BP1 accumulates at these sites and influences the choice between repair pathways, while the tumor suppressor BRCA1 promotes high-fidelity homologous recombination. The transducer kinases Chk1, activated principally downstream of ATR, and Chk2, activated downstream of ATM, propagate checkpoint signaling to arrest the cell cycle and stabilize stalled replication forks, providing time for repair or, when damage is irreparable, triggering apoptosis or senescence. Defects in this network are central to carcinogenesis: loss of ATM, BRCA1, or checkpoint function generates genomic instability that fuels tumor evolution, yet these same deficiencies create therapeutic vulnerabilities, most prominently the synthetic-lethal sensitivity of BRCA1-deficient tumors to PARP inhibitors and the targeting of ATR and Chk1 in replication-stressed cancers. Quantifying the activation and recruitment of these factors provides a mechanistic readout of damage burden, checkpoint engagement, and repair capacity. This pack brings together validated antibodies against ATM, Phospho-ATM, ATR, Chk1, Chk2, gamma-H2AX, BRCA1, and 53BP1 for studying the DNA damage response.