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CDK6 inhibition and MiR-320c overexpression attenuated IL-1beta-induced increases in expression of inflammatory products such as iNOS and MMP13 and decreased the expression of anabolic products such as COL2A1 and aggrecan.
Our data suggested that miR-29a could play an important role in inhibiting proliferation and motility of cancerous Schwann cells, and may suppress tumor growth through upregulation of CDK6.
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/CDK6-CCND1-phospho-RB1 axis is associated with higher proliferative index in neuroendocrine tumors (NETs).
Molecular dynamics simulations showed that the free energy barrier of the transition from open to closed state decreased ~47.2% after Thr177 phosphorylation, increasing the flexibility around the ATP-binding pocket. Binding preferences of 10 different inhibitors to open or closed state were also investigated.
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
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 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 .
CDK4/6 inhibition suppressed cell cycle progression of ER+/HER2- brreast cancer models.
Proliferating tumor stem cells with high telomerase expression are suitable targets for CDK4/6 inhibitor, palbociclib.
Results show that miR-218-5p is increased in bone metastases and promotes breast cancer cell proliferation by activating wnt signaling.
Ribociclib (an oral, highly specific cyclin-dependent kinase 4/6 inhibitor) inhibits tumor growth.
Upregulation of CDK6 may be an important mechanism in overcoming fulvestrant-mediated growth inhibition in breast cancer cells.
Combined PI3Kalpha and CDK4/6 inhibition significantly improved disease control in human xenograft models compared with either monotherapy.
in ovarian cancer cells, DOT1L regulates the transcription of G1 phase genes CDK6 and CCND3 through H3K79 dimethylation
The downregulation of Cdkn1a and the upregulation of Cdk6.
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.
data indicate that Gli3 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 blocks reprogramming by targeting Cdk4/6-mediated cell cycle regulation.
CDK6 kinase activity negatively regulates the conversion of fat-storing cells into fat-burning cells by suppressing RUNX1, 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), 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.
CDK6-mediated suppression of CD25 is required for initiation of T-ALL by activated Notch1. . Pharmacologic inhibition of CDK6 kinase induces CD25 and RUNX1 expression, cell cycle arrest and apoptosis in mouse and human T-ALL.
Fbxo7-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 levels. These studies reveal differential cell cycle regulation by Fbxo7 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(GP38) was up-regulated upon SEMA3A stimulation, and cyclin-dependent kinase 6 (CDK6) was down-regulated in a time-dependent manner.
Notch3 transcription and growth of lymphoma cells was dependent on CDK6.
CDK6 is an important regulator of stem cell activation and an essential component of a transcriptional complex that suppresses Egr1 in hematopoietic and leukemic stem cell activation
Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.
Cdk6/Ccnd1 overexpression inhibits chondrocyte maturation and enhances G1/S transition by phosphorylating pRb; the chondrocytes then undergo p53-dependent apoptosis
p107 retinoblastoma protein is regulated by Cdk6/Ccnd1 in growth plates.
A chrysin derivative suppresses skin cancer growth by inhibiting cyclin-dependent kinases.
Cdk6 deficiency prevents the expansion of neuronally committed precursors by lengthening G(1) phase duration, reducing concomitantly the production of newborn neurons
a mechanism for LPS signaling which involves a decrease in miR-107 leading to an increase in 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