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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 (show CDK4 Proteins) inhibition suppressed cell cycle progression of ER+/HER2 (show ERBB2 Proteins)- brreast cancer models.
Proliferating tumor stem cells with high telomerase expression are suitable targets for CDK4/6 (show CDK4 Proteins) inhibitor, palbociclib.
Results show that miR (show MLXIP Proteins)-218-5p is increased in bone metastases and promotes breast cancer cell proliferation by activating wnt (show WNT2 Proteins) signaling.
Ribociclib (an oral, highly specific cyclin-dependent kinase 4/6 (show CDK4 Proteins) inhibitor) inhibits tumor growth.
Upregulation of CDK6 may be an important mechanism in overcoming fulvestrant-mediated growth inhibition in breast cancer cells.
Combined PI3Kalpha (show PIK3CA Proteins) and CDK4/6 (show CDK4 Proteins) inhibition significantly improved disease control in human xenograft models compared with either monotherapy.
in ovarian cancer cells, DOT1L (show DOT1L Proteins) regulates the transcription of G1 phase genes CDK6 and CCND3 (show CCND3 Proteins) through H3K79 dimethylation
the MYU/hnRNP-K (show HNRNPK Proteins)/CDK6 pathway functions downstream of Wnt/c (show WNT7B Proteins)-Myc (show MYC Proteins) signaling and plays a critical role in the proliferation and tumorigenicity of colon cancer cells.
metabolic function of cyclin D3 (show CCND3 Proteins)-CDK6 kinase in cancer cell survival
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.
CDK6 is an important regulator of stem cell activation and an essential component of a transcriptional complex that suppresses Egr1 (show EGR1 Proteins) in hematopoietic and leukemic stem cell activation
Cdk4 (show CDK4 Proteins) and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4 (show CDK4 Proteins).
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