In Stock Cell Lines
Homo sapiens (Human)
Prostate
Adherent
The TUBB4A Knockout DU145 Cell Line is a CRISPR/Cas9-edited knockout model derived from androgen-independent prostate cancer cells, targeting the TUBB4A gene encoding tubulin beta-4A. This cell line enables functional studies of microtubule dynamics, mitotic spindle regulation, and cell migration in a metastatic prostate carcinoma background. TUBB4A interacts with microtubule-associated proteins (e.g., MAP2, tau) and motor complexes (kinesin-5, dynein) to control intracellular transport and division. Key applications include taxane sensitivity testing, mitotic progression analysis, migration assays, and investigation of beta-tubulin isotype-specific roles in tumorigenesis.
ATP11C Knockout K562 Polyclonal Cells
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AMPD2 Knockout HEK293T Polyclonal Cells
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AP2A1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG27279
C20orf27 Knockout MES-OV Polyclonal Cells
Cat. No. ARG41345
ISOC2 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28416
MAP4K2 Knockout Raji Polyclonal Cells
Cat. No. ARG1148
The TUBB4A Knockout DU145 Cell Line is a CRISPR/Cas9-edited human cell line derived from DU145 prostate carcinoma cells, featuring targeted disruption of TUBB4A. This gene encodes tubulin beta-4A chain, a core component of microtubules critical for mitosis, intracellular transport, and cell migration. The knockout model enables loss-of-function analysis of beta-tubulin isotype-specific functions in an androgen-independent prostate cancer background.
DU145 is a well-characterized, androgen-independent prostate cancer cell line originally isolated from a brain metastasis. It lacks functional androgen receptor signaling and exhibits a highly aggressive, metastatic phenotype. This line is widely used to study advanced prostate cancer mechanisms, including migration, invasion, and drug resistance, making it an ideal host for investigating microtubule-related processes.
TUBB4A heterodimerizes with alpha-tubulin to form microtubules, whose dynamics are modulated by microtubule-associated proteins (MAPs) like MAP1, MAP2, and tau, plus motor proteins including kinesin-5 and the dynein-dynactin complex. Plus-end tracking proteins (+TIPs) such as EB1 and CLIP-170 regulate stability. Activity is controlled downstream of cell cycle machinery, MAP kinase cascades, and p53, and is crucial for mitotic spindle assembly orchestrated by Aurora A kinase and PLK1. Tubulin folding cofactors TBCA?CE assist biogenesis. Disruption undermines spindle formation, chromosome segregation, trafficking, and migration.
In DU145 cells, TUBB4A knockout creates a model to examine microtubule-dependent drivers of tumor aggressiveness. Altered tubulin isotype expression can influence sensitivity to taxanes, and loss of TUBB4A is expected to impair mitosis and reduce migration. This system is relevant for oncology research into microtubule organization and therapeutic resistance, though TUBB4A mutations are also linked to leukodystrophy and dystonia.
Applications include western blotting and immunofluorescence to confirm knockout and visualize microtubule architecture, flow cytometry for cell cycle and apoptosis analysis, and migration/invasion assays to evaluate metastatic behavior. RNA-seq can profile transcriptomic changes, while co-immunoprecipitation maps altered tubulin interactomes. Drug sensitivity testing with microtubule-targeting agents (e.g., paclitaxel) aids in identifying synthetic lethal interactions. This model supports studies of beta-tubulin isotypes in cancer and novel target discovery. For further details, contact Ascent Research.
