This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population in which the ANKS1B gene has been disrupted in HeLa cells. The polyclonal format provides a heterogeneous pool of edited alleles, enabling rapid functional assessment of gene loss without the need for single-cell cloning. The resulting loss-of-function model is suitable for investigating ANKS1B-dependent cellular processes in a well-established human cell line background. No specific editing mechanism or clonal derivation is implied; the population derives from pooled transfection and selection.
The host cell line, HeLa, is a human cervical adenocarcinoma epithelial line originally derived in 1951 from a 31-year-old African-American woman. These cells are HPV-18 positive and have been immortalized, making them a robust model for cancer biology, signal transduction, and general cell physiology. HeLa cells offer high transfection efficiency and rapid proliferation, facilitating the generation and expansion of knockout populations for biochemical and imaging-based studies.
ANKS1B (also known as AIDA-1) encodes a multidomain scaffold protein that plays a critical role in synaptic plasticity and intracellular signaling. It directly binds the amyloid precursor protein intracellular domain (AICD), a fragment generated by gamma-secretase cleavage of APP, and modulates downstream signaling cascades, including the ERK/MAPK pathway. ANKS1B interacts with DISC1, NMDA receptor subunits, and other neuronal proteins, and is regulated by upstream factors such as BDNF signaling, neuronal activity, and AICD itself. Downstream targets include ERK1/2 and synaptic AMPA receptors. Thus, ANKS1B functions as a molecular hub linking AICD to MAPK1/3 activation and synaptic protein regulation.
In HeLa cells, ANKS1B expression is relevant to non-neuronal AICD-mediated transcriptional regulation. Disruption of ANKS1B may alter the transcriptional activity of AICD, thereby affecting cell proliferation, survival, and possibly migratory behavior. This model allows researchers to dissect the scaffolding functions of ANKS1B in a simplified cellular environment that lacks the complexity of neuronal networks, while still retaining core APP processing machinery. Consequently, it provides a tractable system to examine the consequences of ANKS1B loss on MAPK/ERK signaling and AICD-dependent gene expression.
Typical applications include Western blotting and RT-qPCR for confirming reduced ANKS1B expression, cell proliferation and migration assays to probe functional outcomes, and luciferase reporter assays for quantifying AICD transcriptional activity. Researchers can employ this polyclonal population to study APP signaling in non-neuronal contexts, evaluate ANKS1B??s role in cancer cell biology, or screen for modulators of AICD-driven transcription. For further technical details, pricing, or custom services, please contact Ascent Research.
