Dynlrb1, also known as Dynein Light Chain Roadblock-Type 1, is an essential component of the dynein complex. The cytoplasmic dynein motor complex, of which Dynlrb1 is a part, is crucial for transporting essential signals and organelles from the cell periphery to the perinuclear region, thus being vital for the survival and function of highly polarized cells like neurons [1]. It is also involved in multiple signaling pathways and may play a role in axonal transport of lysosomes and retrograde signaling endosomes [1].

Homozygous Dynlrb1 null mice are not viable and die during early embryonic development [1]. Heterozygous or adult knockdown animals display reduced neuronal growth, and selective depletion of Dynlrb1 in proprioceptive neurons compromises their survival [1]. Conditional depletion of Dynlrb1 in sensory neurons causes deficits in several signaling pathways, including β -catenin subcellular localization, and severely impairs the axonal transport of lysosomes and retrograde signaling endosomes [1]. In addition, knockdown of Dynlrb1 in human CRC cells reduces cell migration, suggesting its role in cancer cell invasion [2].

In conclusion, Dynlrb1 is essential for dynein-mediated transport and neuronal survival. Studies using Dynlrb1 knockout mouse models have revealed its critical role in early embryonic development, neuronal growth and survival, as well as in certain signaling pathways. The findings also hint at its potential involvement in neurodegenerative diseases and cancer cell invasion, providing valuable insights into the underlying biological mechanisms and potential disease-related functions.