High impact information on ICK2

• Constitutive overexpression of KRP2 slightly above its endogenous level only inhibited the mitotic cell cycle-specific CDKA;1 kinase complexes, whereas the endoreduplication cycle-specific CDKA;1 complexes were unaffected, resulting in an increase in the DNA ploidy level [1].
• In accordance with this model, KRP2 protein levels increased in plants with reduced CDKB1;1 activity [1].
• We illustrate that KRP2 protein abundance is regulated posttranscriptionally through CDK phosphorylation and proteasomal degradation [1].
• KRP2 appears to regulate early lateral root initiation by blocking the G1-to-S transition and to be regulated transcriptionally by auxin [2].
• When overproduced, KRP2 dramatically inhibited cell cycle progression in leaf primordia cells without affecting the temporal pattern of cell division and differentiation [3].

Biological context of ICK2

• We conclude that KRP2 exerts a plant growth inhibitory activity by reducing cell proliferation in leaves, but, in contrast to its mammalian counterparts, it may not control the timing of cell cycle exit and differentiation [3].
• KRP1 and KRP2 might specifically be involved in the establishment of polyploidy [4].

Other interactions of ICK2

• Outside of this domain, ICK2 is distinct from ICK1, p27Kip1, and other proteins [5].

References