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High CDK6 Expression is associated with Oral Squamous Cell Carcinomas.
The results indicate that C-glycosyl flavone may exert induction of apoptosis, cell cycle arrest and inhibition of angiogenesis via CDK6. Thus, targeting CDK6 using C-glycosyl flavone may serve as a novel therapeutic approach for the treatment of breast, hepatic and colon cancers.
the miR494/CDK6 axis has a significant tumorsuppressive effect on osteosarcoma.
High CDK6 expression is associated with bladder carcinoma.
Results suggest that dysregulation and activation of the cell cycle proteins CDK4 (show CDK4 Proteins)/CDK6-CCND1 (show CCND1 Proteins)-phospho-RB1 (show RB1 Proteins) axis is associated with higher proliferative index in neuroendocrine tumors (NETs).
Ongoing trials of doublet and triplet targeted therapies containing ribociclib seek to identify optimal CDK4/6 (show CDK4 Proteins)-based targeted combination regimens for various tumor types and advance the field of precision therapeutics in oncology
Transfection of cells with ClC-3 (show CLCN3 Proteins) siRNA decreased the expression of cyclin D1 (show CCND1 Proteins), cyclin dependent kinase 4 (show CDK4 Proteins) and 6, and increased the expression of cyclin dependent kinase (show CDK1 Proteins) inhibitors (CDKIs), p21 (show CDKN1A Proteins) and p27 (show PAK2 Proteins). Pretreatments of cells with p21 (show CDKN1A Proteins) and p27 (show PAK2 Proteins) siRNAs depleted the inhibitory effects of ClC-3 (show CLCN3 Proteins) siRNA on the expression of CDK4 (show CDK4 Proteins) and CDK6, but not on that of cyclin D1 (show CCND1 Proteins)
miRNA-195 was associated with tumor malignancy grade and might be involved in the development and progression of OVC. In addition, CDK6 was predicted to be a target gene of miRNA-195 and obviously increased in both OVC and OSCC.
Palbociclib induces activation of AMPK (show PRKAA1 Proteins) and inhibits hepatocellular carcinoma in a CDK4/6 (show CDK4 Proteins)-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 .
data indicate that Gli3 (show GLI3 Proteins) controls the onset of cortical neurogenesis by determining the levels of Cdk6 expression, thereby regulating neuronal output and cortical size.
These results indicate that p18 (show CDKN2C Proteins) blocks reprogramming by targeting Cdk4/6 (show CDK4 Proteins)-mediated cell cycle regulation.
CDK6 kinase activity negatively regulates the conversion of fat-storing cells into fat-burning cells by suppressing RUNX1 (show RUNX1 Proteins), and may be a therapeutic target for the treatment of obesity and related metabolic diseases
Cdk6 interacts with a number of proteins involved in cytoskeleton organization. Cdk6 regulates the transcription of a panel of genes involved in actin (de-)polymerization.
PD 0332991 (PD), an FDA-approved selective inhibitor of cyclin-dependent kinase 4/6 (CDK4/6 (show CDK4 Proteins)), prevents radiation-induced lethal intestinal injury in mice. Treating mice with PD or a structurally distinct CDK4/6 (show CDK4 Proteins) inhibitor prior to radiation blocked proliferation and crypt apoptosis and improved crypt regeneration.
CDK6-mediated suppression of CD25 (show IL2RA Proteins) is required for initiation of T-ALL by activated Notch1 (show NOTCH1 Proteins). . Pharmacologic inhibition of CDK6 kinase induces CD25 (show IL2RA Proteins) and RUNX1 (show RUNX1 Proteins) expression, cell cycle arrest and apoptosis in mouse and human T-ALL.
Fbxo7 (show FBXO7 Proteins)-deficient immature thymocytes failed to undergo expansion in the thymus due to a lack of Cdk6 activity, while mature T cells showed enhanced proliferative capacity upon T-cell receptor engagement due to reduced p27 (show CDKN1B Proteins) levels. These studies reveal differential cell cycle regulation by Fbxo7 (show FBXO7 Proteins) at different stages in T-cell development.
Taken together, our results suggested that microRNA-33 enhanced the replicative senescence of MEFs potentially by suppressing CDK6 expression.
Data show that E11/glycoprotein 38 (show PDPN Proteins)(GP38 (show PDPN Proteins)) was up-regulated upon SEMA3A (show SEMA3A Proteins) stimulation, and cyclin-dependent kinase 6 (CDK6) was down-regulated in a time-dependent manner.
Notch3 (show NOTCH3 Proteins) transcription and growth of lymphoma cells was dependent on CDK6.
the T-1075C SNP of bovine CDK6 is significantly associated with body length and heart girth
The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK family members are highly similar to the gene products of Saccharomyces cerevisiae cdc28, and Schizosaccharomyces pombe cdc2, and are known to be important regulators of cell cycle progression. This kinase is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression and G1/S transition. The activity of this kinase first appears in mid-G1 phase, which is controlled by the regulatory subunits including D-type cyclins and members of INK4 family of CDK inhibitors. This kinase, as well as CDK4, has been shown to phosphorylate, and thus regulate the activity of, tumor suppressor protein Rb. Expression of this gene is up-regulated in some types of cancer. Multiple alternatively spliced variants, encoding the same protein, have been identified.
cyclin-dependent kinase 6
, cell division protein kinase 6-like
, cell division protein kinase 6
, serine/threonine-protein kinase PLSTIRE
, CR2 protein kinase