Recombinant Human CEND1 protein (His tag N-Terminus)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CEND1 also known as cell cycle exit and neuronal differentiation 1 is a protein with a mass of approximately 16 kDa. Researchers have identified its expression specifically in neural precursor cells of the central nervous system. CEND1 plays a role in controlling neuronal differentiation by interacting with cell cycle regulators. This function highlights its importance in the development of the nervous system and its involvement in maintaining the balance between proliferation and differentiation in neurons.

Biological function summary

CEND1 facilitates neuronal outgrowth and maturation without forming part of a larger multiprotein complex. It acts directly on governing neuronal progenitor cell fate promoting differentiation over proliferation. Researchers have found CEND1 to affect cell cycle arrest in neuronal populations steering progenitor cells towards post-mitotic states essential for healthy neural tissue maturation. The presence of CEND1 in neurogenesis stages establishes it as an important player in the shaping of the neuronal landscape in the brain.

Pathways

Several cell cycle-related pathways involve CEND1 in regulating the transition from proliferation to differentiation in neural progenitors. It interacts with key proteins such as p27^Kip1 and cyclin-dependent kinases. These interactions are important in coordinating neurogenesis and neuronal pathway specification. CEND1 ensures proper function and cooperation with other elements of the neurogenic program including pathways like Notch signaling to regulate the temporal and spatial aspects of neuronal differentiation.

Research has linked CEND1 to neurodevelopmental conditions such as microcephaly and certain forms of epilepsy. Malfunctions or dysregulation of CEND1 can result in impaired neuronal differentiation leading to disturbed neural circuit formation. In these contexts CEND1 interacts with proteins like p53 which governs cell cycle arrest and apoptosis offering insights into how disrupted CEND1 expression contributes to the pathophysiology of these neurological disorders. Understanding these relationships provides potential therapeutic targets for correcting or mitigating such conditions.