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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.
Activation of cdk4 triggers NAFLD (show TSC2 ELISA Kits).
results showed that fascaplysin inhibited ovarian cancer cell proliferation, invasion and migration, as well as inducing S arrest and cell apoptosis. Treatment with fascaplysin also suppressed CDK4, cyclin D1 (show CCND1 ELISA Kits), Bcl-2 (show BCL2 ELISA Kits), and VEGFA (show VEGFA ELISA Kits) expression at protein levels
The first preclinical study evaluates the response to CDK4/6 inhibition in endometrial malignancies driven by PTEN deficiency, and it reveals an important role of cyclin D-CDK4/6 activity in their development.
Our results show that combined exogenous expression of hTERT and mutant CDK4 is an effective method to generate single-cell-derived Cancer-associated fibroblasts (CAFs) clones. This provides an innovative and suitable approach to investigate the heterogeneous function and phenotype of CAFs
these findings support that PIKE (show AGAP2 ELISA Kits) amplification or overexpression coordinately acts with CDK4 to drive glioblastoma tumorigenesis.
Specific E2Fs also have prognostic value in breast cancer, independent of clinical parameters. We discuss here recent advances in understanding of the RB-E2F (show E2F1 ELISA Kits) pathway in breast cancer. We also discuss the application of genome-wide genetic screening efforts to gain insight into synthetic lethal interactions of CDK4/6 inhibitors in breast cancer for the development of more effective combination therapies.
p16 in combination with MDM2 (show MDM2 ELISA Kits) and CDK4 immunohistochemistry may help in the differential diagnosis of atypical lipomatous tumor/well-differentiated liposarcoma and dedifferentiated liposarcoma.
conclude that p16 is highly sensitive for retroperitoneal DDL. However, the lack of specificity limits the diagnostic utility compared with the more established markers MDM2 (show MDM2 ELISA Kits) and CDK4
CDK4 overexpression is associated with cancer.
High CDK4 expression is associated with Melanoma.
The in vitro cultivation of cumulus cells was associated with cell proliferation and that Cx43 (show GJA1 ELISA Kits) and Cdk4 gene expression was upregulated after in vitro cultivation, resulting in significantly higher protein levels.
This novel mechanism explains how CDK4 promotes anabolism by blocking catabolic processes (FAO) that are activated by AMPK (show PRKAA1 ELISA Kits).
PD 0332991 (PD), an FDA (show FDA ELISA Kits)-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 (show SOD2 ELISA Kits).
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 (show CDK2 ELISA Kits) and Cdk4 play important overlapping roles in homeostatic and stress hematopoiesis, which need to be considered when using broad-spectrum cyclin-dependent kinase (show CDK1 ELISA Kits) 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 (show CDK2 ELISA Kits) is dispensable for tumorigenesis in these neuroendocrine cell types.
Cdk4 and Cdk6 (show CDK6 ELISA Kits) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (show CDK6 ELISA Kits) 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.
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 (show NRF1 ELISA Kits) and consequent induction of Tfam (show TFAM ELISA Kits) 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 (show MRPL12 ELISA Kits) 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