Intraflagellar transport protein 88 homolog (IFT88)

Intraflagellar transport protein 88 homolog (**IFT88**) is a core component of the **intraflagellar transport-B (IFT-B) complex**, required for the formation and maintenance of cilia and flagella in eukaryotic cells[1][3]. As a member of the tetratricopeptide repeat (TPR) family, IFT88 mediates assembly of macromolecular complexes that shuttle structural and signaling proteins along ciliary and flagellar axonemes, primarily by interacting with other IFT-B proteins such as IFT52 and IFT70, and with motor proteins like kinesin-2 for anterograde movement[3][4][6]. IFT88 is indispensable for ciliogenesis; its absence results in failure to form functional cilia and flagella, underlying a range of **ciliopathies** such as polycystic kidney disease and congenital anosmia[1][2][5]. Beyond ciliary roles, IFT88 regulates cell cycle progression, ensuring proper spindle orientation and planar cell polarity in dividing cells[1][2]. Mutations or silencing of IFT88 disrupt essential signaling pathways within the cilium, leading to defects in organ development, neural function, and tissue homeostasis, particularly affecting kidney, cartilage, and neural tissue[1][5][6]. Animal models and cell studies demonstrate that loss of IFT88 impairs cilia length and function, confirming its status as a critical structural and regulatory protein but not a classical druggable target[4]. IFT88 serves as a molecular marker in experimental studies for ciliary diseases and is commonly used to investigate the mechanism of ciliogenesis and centrosome-cilia cross-talk in development and disease[1][3][4][6].

Other names

PolarisTG737TTC10TPR repeat protein 10hTg737D13S1056EMGC26259Recessive polycystic kidney disease protein Tg737 homologTetratricopeptide repeat protein 10DAF19Testicular tissue protein Li 93Tetratricopeptide repeat domain 10

Not applicable; there are no drugs currently known to act on IFT88