Cellular Senescence Antibody Sampler Pack

Cellular Senescence Antibody Sampler Pack

The Cellular Senescence 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 ChIP, ELISA, IF/ICC, IHC-P, IP, WB — before committing to full-size vials. Each antibody is also available individually in a full 100µL size.

Cellular senescence is a state of stable, essentially irreversible cell-cycle arrest triggered by telomere attrition, oncogene activation, DNA damage, and other stresses. It acts as a potent barrier to tumorigenesis by withdrawing damaged or oncogene-bearing cells from the proliferative pool, yet senescent cells persist metabolically active and can paradoxically promote tissue dysfunction and tumor progression through their secretory phenotype. The arrest is enforced principally by two tumor suppressor axes. The CDK inhibitor p16 INK4A blocks CDK4/6 activity to maintain the retinoblastoma protein Rb in its active, hypophosphorylated state, where Rb represses E2F-driven proliferative genes and stably locks cells out of the cycle. In parallel, the p53 pathway induces the CDK inhibitor p21 to establish and reinforce arrest in response to damage signals. A hallmark of the senescent nucleus is the loss of the nuclear lamina protein Lamin B1, whose downregulation accompanies chromatin reorganization and is a reliable senescence marker. Senescent cells also acquire a senescence-associated secretory phenotype, releasing inflammatory mediators such as IL-6 and the alarmin HMGB1, which relocalizes from the nucleus to the extracellular space; this secretome reinforces arrest locally but can remodel the tissue microenvironment, promote inflammation, and in some settings drive proliferation and immune evasion of neighboring tumor cells. Stress kinase signaling through p38 MAPK contributes to both arrest establishment and the secretory program. In cancer, senescence underlies therapy-induced growth arrest but also contributes to relapse and age-associated tumor risk, motivating senolytic strategies. Profiling these effectors distinguishes genuine senescence from quiescence and characterizes the secretory program. This pack brings together validated antibodies against p16 INK4A, p21, p53, Lamin B1, Rb, HMGB1, IL-6, and p38 MAPK for studying cellular senescence.