Microtubule plus-end (MT plus-end) (MT plus-end)

The microtubule plus-end is the highly dynamic extremity of a microtubule polymer where beta-tubulin subunits are exposed. It serves as the primary site for the addition and loss of tubulin heterodimers, a process known as dynamic instability, which is essential for cellular processes such as mitotic spindle formation, intracellular trafficking, and maintaining cell polarity [1][2]. This region is regulated by a specialized group of proteins called plus-end tracking proteins (+TIPs), such as End-binding protein 1 (EB1), which coordinate microtubule interactions with other cellular structures and organelles [3]. In oncology, the microtubule plus-end is a critical therapeutic target; drugs like taxanes (e.g., paclitaxel) bind to the interior or the ends to stabilize the polymer and prevent depolymerization, while vinca alkaloids (e.g., vincristine) bind to the plus-end to inhibit polymerization [4][5]. Both mechanisms ultimately disrupt the mitotic spindle, leading to cell cycle arrest at the M-phase and subsequent apoptosis [4]. Beyond cancer, dysregulation of microtubule dynamics at the plus-end is implicated in various neurodegenerative disorders, such as Alzheimer's disease, and developmental defects known as tubulinopathies [6]. Sources: [1] Akhmanova A, et al. (2008) Nat Rev Mol Cell Biol; [2] Desai A, et al. (1997) Annu Rev Cell Dev Biol; [3] Galjart N. (2010) Curr Opin Cell Biol; [4] Jordan MA, et al. (2004) Nat Rev Cancer; [5] Dumontet C, et al. (2010) Nat Rev Drug Discov; [6] Tischfield MA, et al. (2010) Cell.

Other names

Plus-end of microtubuleFast-growing microtubule endBeta-tubulin exposed end

Microtubule-targeting agents (MTAs) bind to tubulin subunits at the microtubule plus-end to either stabilize the polymer or inhibit polymerization, disrupting dynamic instability and inducing mitotic arrest [4][5].