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The authors' findings establish a firm molecular link of multiaggressiveness among SCP3, NANOG, cyclin D1, and CDK4/6 and identify CDK4/6 inhibitors as actionable drugs for controlling SCP3(high) immune-refractory cancer. These findings reveal cyclin D1-CDK4/6 inhibition as an effective strategy for controlling SCP3high immune-refractroy cancer.
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DNA Damage Response in Proliferating Muller Glia in the Mammalian Retina.
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CDK4/CDK6-dependent activation of DUB3 regulates cancer metastasis through SNAIL1.
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Study examined proliferation rates of cortical progenitor cells in mice lacking individual cdk proteins or combinations thereof. Results provide evidence that concomitant loss of cdk4 and cdk6 leads to reduced proliferation rates specifically in basal progenitor cells in both the dorsal and ventral forebrain. Cdk4-/-;Cdk6-/- double mutant progenitor cells in the dorsal telencephalon exhibit accelerated cell cycle exit.
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These results indicate that p18 blocks reprogramming by targeting Cdk4/6-mediated cell cycle regulation.
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Activation of cdk4 triggers NAFLD.
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This novel mechanism explains how CDK4 promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK.
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PD 0332991 (PD), an FDA-approved selective inhibitor of cyclin-dependent kinase 4/6 (CDK4/6), prevents radiation-induced lethal intestinal injury in mice. Treating mice with PD or a structurally distinct CDK4/6 inhibitor prior to radiation blocked proliferation and crypt apoptosis and improved crypt regeneration.
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The results demonstrate a unique CDK4-mediated mitochondrial communication that allows cells to sense environmental genotoxic stress and boost mitochondrial homeostasis by enhancing phosphorylation and activation of MnSOD.
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a crucial role of RXRa in suppression of UVB-induced melanomas in the context of driver mutations such as activated CDK4(R24C/R24C) or oncogenic NRAS(Q61K) and altered expression of p53 and PTEN
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Our data indicate that Cdk2 and Cdk4 play important overlapping roles in homeostatic and stress hematopoiesis, which need to be considered when using broad-spectrum cyclin-dependent kinase inhibitors for cancer therapy.
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CDK4 is a critical downstream target of MEN1-dependent tumor suppression and is required for tumorigenic proliferation in the pituitary and pancreatic islet, whereas CDK2 is dispensable for tumorigenesis in these neuroendocrine cell types.
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Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.
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CDK4 seems to be expressed as multiple proteins that respond differently to different shRNAs, and have previously unrecognized functions at the S-G 2/M phases of the cell cycle via mechanisms independent of binding to CCND and RB.
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insulin activates cyclin D1-cyclin-dependent kinase 4 (Cdk4), which, in turn, increases GCN5 acetyltransferase activity and suppresses hepatic glucose production independently of cell cycle progression
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CDK4 deficiency markedly accelerated lymphoma development in the Emu-Myc transgenic model of B lymphoma
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Cdk4- and Arf-mutant mice exhibited similar profiles, the Trp53(F/F) ::Tyr-Cre(ER)::Tyr-NRAS melanomas were strikingly different, showing relative down-regulation of melanocyte-related genes, and up-regulation of genes related to neural differentiation.
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A chrysin derivative suppresses skin cancer growth by inhibiting cyclin-dependent kinases.
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UCH-L1 physically interacts with CDK1, CDK4, and CDK5, enhancing their kinase activity.
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Hesperetin prevented the xenograft growth by down-regulating the expression of cyclin D1, CDK4 and Bcl-xL and up-regulating p57Kip2 expression in MCF-7 cells.