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The activation of c-Met/TrkA-B pathways is a novel mechanism involved in therapeutic resistance of GBM to CDK4/6 inhibition.
MiR-384 repressed tumorigenesis by regulating CDK6 in ccRCC and predicted good prognosis for ccRCC.
It is likely that CDK4/6 inhibitors will have a broader impact than their expected induction of cell cycle arrest in the treatment of human cancers
A tumor-suppressive role of miR-1296-5p through the translational repression of oncogenic CDK6 and EGFR in gastric cancer.
CDK6 3'UTR polymorphisms are associated with susceptibility to cervical cancer in Uyghur females.
CDK6 was identified as a target of miR-29c. CDK6 knockdown attenuated the effects of miR-29c inhibition on paclitaxel cytotoxicity in breast cancer cells.
The expression of let7b was negatively correlated with the expression of HOST2 and CDK6 in tumor tissues.
Combination treatment with MTOR and CDK4/6 inhibitors had potent activity across a large number of patient-derived models of PDAC underscoring the potential clinical efficacy.
Results suggested that UCA1 acted as sponge of miR-298 and enhanced the level of CDK6 in adrenocortical cancer (AC) cells regulating the cell cycle progression of ACC cells.
CDK6 is a validated target of miR-107 and was downregulated upon miR-107 overexpression.
In human medulloblastoma, misactivation of Hh signaling was associated with high levels of CDK6, pointing to CDK6 as a direct transcriptional target of the Hh pathway. These results suggest that CDK6 antagonists may be a promising therapeutic approach for Hh-associated medulloblastoma in humans.
Targeting of glutamine addiction and overcoming of CDK4/CDK6 antineoplastic drug resistance in human esophageal squamous cell carcinoma has been reported.
miR-9 induces cell arrest and apoptosis of oral squamous cell carcinoma via CDK 4/6 pathway.
High CDK6 expression is associated with Cellular Proliferation and Invasion in Glioma.
Acetylated FOXO3a recognizes the BD2 domain of BRD4, recruits the BRD4/RNAPII complex to the CDK6 gene promoter, and induces its transcription.
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.
The authors' findings establish a firm molecular link of multiaggressiveness among SCP3, NANOG, cyclin D1, and CDK4/6 and identify CDK4/6 inhibitors as actionable drugs for controlling SCP3(high) immune-refractory cancer. These findings reveal cyclin D1-CDK4/6 inhibition as an effective strategy for controlling SCP3high immune-refractroy cancer.
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
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