Klc2, the light chain of kinesin-1, mediates cargo binding and regulates kinesin-1 motility, which is crucial for the microtubule-based intracellular transport system [3]. It is involved in various cellular processes related to the movement of vesicles and organelles along microtubules. The study of Klc2 in genetic models, especially KO mouse models, has been valuable for understanding its functions.

In Klc2-deficient C57BL/6 J mice, low-frequency sensorineural hearing loss occurs as early as 1 month of age. This deficiency leads to abnormal mitochondrial transport and down-regulation of the GABAA receptor family, indicating Klc2's essential role in cochlear hair cell function [1].

In zebrafish (Danio rerio), knockdown and overexpression of klc2 result in a mild to severe curly-tail phenotype, suggesting its role in neuromuscular disorders [2].

In non-small cell lung cancer (NSCLC), down-regulation of KLC2 can increase radiosensitivity by activating the P53 pathway, while KLC2 forms a positive feedback loop with HuR to promote radioresistance [4].

In conclusion, Klc2 is essential for functions like cochlear hair cell function, potentially in neuromuscular processes, and in influencing radiosensitivity in NSCLC. Studies using KO mouse models and other genetic models have been instrumental in revealing Klc2's functions in these specific disease-related biological processes, highlighting its importance in understanding sensorineural hearing loss, neuromuscular disorders, and NSCLC radiotherapy.