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Expression of cells a mutant CDK4 (CDK4(R24C)) in beta-cells enhanced beta-cell replication. CDK4(R24C) also dampened compensatory beta-cell neogenesis in larvae and improved glucose tolerance in adult zebrafish.
miR-9 induces cell arrest and apoptosis of oral squamous cell carcinoma via CDK 4/6 pathway.
the present study is the first to demonstrate that miR-338-3p functions as a tumor suppressor in multiple myeloma (MM)through inhibiting CDK4. This finding implies that miR-338-3p is a potential therapeutic target for the treatment of MM.
CDK4 variants were not commonly found in Greek patients with familial melanoma.
CDK4 is a direct target of miR-142-3p.
Data indicate that PAQR4 has a tumorigenic effect on human breast cancers, and such effect is associated with a modulatory activity of PAQR4 on protein degradation of CDK4
MiR-340 overexpression inhibited tumor growth by regulating CDK4 expression. miR-340 functions as a tumor suppressor in non small cell lung cancer (NSCLC) cells and may provide a potential target of NSCLC treatment.
CDK4 and XPO1 are not altered in a rare undifferentiated sarcoma, making them therapeutic targets
while mTOR inhibitors restore endocrine sensitivity, CDK4/6 inhibitors may favor the emergence of estrogen receptor 1 (ESR1) mutations resulting in ligand-independent activity of the receptor
Inhibition of CDK4/6 is potentially a highly effective strategy for the treatment of SHH and MYC-amplified group 3 medulloblastoma.
SOX12 can increase the expression of CDK4 and IGF2BP1, which confer malignant phenotypes to Hepatocellular Carcinoma.
Study showed that CDK4 and BCAS2 may be target genes of miR-486 and levels of CDK4 and BCAS2 were both significantly higher in the esophageal cancer tissues and cell lines than levels in the normal tissues and cells.
Results suggest that dysregulation and activation of the cell cycle proteins CDK4/CDK6-CCND1-phospho-RB1 axis is associated with higher proliferative index in neuroendocrine tumors (NETs).
blocking CDK4 activity efficiently eliminated both normal and chemotherapy-resistant cancer cells in triple negative breast cancers, highlighting CDK4 as a promising novel therapeutic target for these aggressive breast tumors.
Amplification of gene CDK4 is associated with lung adenocarcinoma.
PD-L1 protein abundance is regulated by cyclin D-CDK4 and the cullin 3-SPOP E3 ligase via proteasome-mediated degradation
Ongoing trials of doublet and triplet targeted therapies containing ribociclib seek to identify optimal CDK4/6-based targeted combination regimens for various tumor types and advance the field of precision therapeutics in oncology
Transfection of cells with ClC-3 siRNA decreased the expression of cyclin D1, cyclin dependent kinase 4 and 6, and increased the expression of cyclin dependent kinase inhibitors (CDKIs), p21 and p27. Pretreatments of cells with p21 and p27 siRNAs depleted the inhibitory effects of ClC-3 siRNA on the expression of CDK4 and CDK6, but not on that of cyclin D1
Palbociclib induces activation of AMPK and inhibits hepatocellular carcinoma in a CDK4/6-independent manner
The combination of ribociclib, a dual inhibitor of cyclin-dependent kinase (CDK) 4 and 6, and the ALK inhibitor ceritinib demonstrated higher cytotoxicity and synergy scores (P = 0.006) in cell lines with ALK mutations as compared with cell lines lacking mutations or alterations in ALK .
Results showed that CDK4 expression was up-regulated in colorectal carcinoma and suggested that cdc37 increased the stability of CDK4 to activate RB1 which ultimately promotes G1-S transition.
The in vitro cultivation of cumulus cells was associated with cell proliferation and that Cx43 and Cdk4 gene expression was upregulated after in vitro cultivation, resulting in significantly higher protein levels.
CDK4/CDK6-dependent activation of DUB3 regulates cancer metastasis through SNAIL1.
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.
These results indicate that p18 blocks reprogramming by targeting Cdk4/6-mediated cell cycle regulation.
Activation of cdk4 triggers NAFLD.
This novel mechanism explains how CDK4 promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK.
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.
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.
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
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.
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.
Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.
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.
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
CDK4 deficiency markedly accelerated lymphoma development in the Emu-Myc transgenic model of B lymphoma
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.
A chrysin derivative suppresses skin cancer growth by inhibiting cyclin-dependent kinases.
UCH-L1 physically interacts with CDK1, CDK4, and CDK5, enhancing their kinase activity.
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.
Data demonstrate the induction of neurogenic divisions in the absence of critical mediators of G1/S transition-Cdk2 and Cdk4, and highlight their evolutionary importance in the determination of cortical thickness.
CCND1 mRNA expression is increased by FGF9 in bovine theca cells and granulosa cells.
The results indicate that the precise regulation of neuronal Cdk4 activity is important to limit mitochondrial reactive oxygen species production and prevent neurodegeneration.
CDK4 activity regulates mitobiogenesis by the activation of NRF-1 and consequent induction of Tfam and mitochondrial ribossomal transcription.
Delg and cyclin D/Cdk4 have roles in nutritional control of mitochondrial biogenesis in the Drosophila adipose tissue
Cyclin D-cdk4 is not a master regulator of cell multiplication in Drosophila embryos
mRpL12 is required for CycD/Cdk4-induced cell growth
Our data suggest that the growth-specific function of CycD/Cdk4 is conserved from arthropods to mammals.
The protein encoded by this gene is a member of the Ser/Thr protein kinase family. This protein is highly similar to the gene products of S. cerevisiae cdc28 and S. pombe cdc2. It is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression. The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). This kinase was shown to be responsible for the phosphorylation of retinoblastoma gene product (Rb). Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. Multiple polyadenylation sites of this gene have been reported.
cell division protein kinase 4
, cyclin dependent kinase 4
, serine/threonine kinase
, Cell division protein kinase 4
, Cyclin-dependent kinase 4/6
, cyclin-dependent kinase 4
, protein kinase-like 53C