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CDK6
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CDK6 is a protein kinase that regulates cell cycle progression and differentiation. It interacts with D-type cyclins and phosphorylates Rb and NPM1. It is involved in various diseases and pathways, and has multiple aliases and identifiers.
CDK6 is an enzyme that regulates cell cycle progression and differentiation. It interacts with cyclins D and inhibitors of CDK4 and phosphorylates pRb, E2F and other proteins involved in transcription and proliferation.
Cyclin-dependent kinases 4 and 6 (CDK4 and CDK6) and their activating partners, D-type cyclins, link the extracellular environment with the core cell-cycle machinery. Constitutive activation of cyclin D-CDK4/6 represents the driving force of ...
The activity of CDK6 is controlled by interaction with several partners including cyclins and INK4 proteins, which have been shown to mainly bind to the amino-terminal lobe. We analyzed the impact of CDK6's C-terminus on its functions in a leukemia model, revealing a central role in promoting proliferation.
The regulation and function of cyclin‐dependent kinase 6 (CDK6)‐ and cyclin‐dependent kinase 4 (CDK4)‐cyclin complexes are commonly altered with enhanced kinase activity found in hematopoietic malignancies, breast cancer and melanoma making CDK4 and ...
当受到有丝分裂信号刺激时，细胞周期蛋白D (cyclin D)与CDK4或者CDK6发生相互作用。 被激活的cyclin D-CDK4/6复合物磷酸化 视网膜母细胞瘤相关蛋白 (retinoblastoma-associated protein, Rb),进而使转录抑制复合物Rb-E2F解聚，释放E2F转录因子。
Dysregulation of cyclin-dependent kinase 4 (CDK4) and CDK6, regulators of the cell cycle, favours the growth and survival of several cancer types. Owing to this, CDK4 and CDK6 inhibitors were ...
CDK6 is a novel predictive and prognosis biomarker correlated with immune infiltrates in multiple human neoplasms, including small cell lung carcinoma. Title: CDK6 is a novel predictive and prognosis biomarker correlated with immune infiltrates in multiple human neoplasms, including small cell lung carcinoma.
Herein, we describe the complex role of CDK6, balancing quiescence, proliferation, self-renewal, and differentiation in activated HSCs. Mouse HSCs expressing kinase-inactivated CDK6 show enhanced long-term repopulation and homing, whereas HSCs lacking CDK6 have impaired functionality.
The activity of CDK6 is controlled by interaction with several partners including cyclins and INK4 proteins, which have been shown to mainly bind to the amino-terminal lobe. We analyzed the impact of CDK6's C-terminus on its functions in a leukemia model, revealing a central role in promoting proliferation.