These antibodies are critical for detecting UNC45A in cancer biology studies, particularly in breast, ovarian, and cervical cancers .
UNC45A antibodies have enabled breakthroughs in understanding its roles in:
Silencing UNC45A via siRNA inhibits breast cancer cell growth in vitro and tumor growth in vivo (Fig. 1E–G) .
UNC45A localizes to centrosomes, where it regulates checkpoint kinase 1 (ChK1) activation and centrosomal separation .
Depletion of UNC45A induces metaphase arrest, cytokinesis failure, and mitotic catastrophe due to disrupted NEK7 expression .
UNC45A promotes myosin II folding and stress fiber assembly, with knockout cells showing defective contractile actomyosin bundles .
It destabilizes microtubules (MTs) and is overexpressed in paclitaxel-resistant ovarian cancers .
High UNC45A expression is observed in proliferative cells of the mouse ovaries, fallopian tube cilia, and neurons (Fig. 1B–C, 5A–G) .
In human cancers, UNC45A correlates with tumor grade and chemoresistance .
UNC45A localizes to the nucleus and enhances glucocorticoid receptor (GR)-mediated transcription of NEK7, a mitotic kinase essential for centrosome homeostasis (Fig. 2A, Table S1) .
UNC45A co-purifies with γ-tubulin and Hsp90β in centrosomal fractions (Fig. 2B–D) .
Loss of UNC45A reduces ChK1 phosphorylation (S345) and centrosomal retention, leading to multi-nucleation (Fig. 4A–D) .
UNC45A is a promising target for solid tumors, as its inhibition triggers apoptosis in HeLa and MDA-MB-231 cells in vivo (Fig. 1G–J) .