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Cyclin-dependent kinase 6

CDK6, Cyclin-Dependent Kinase 6
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. [provided by RefSeq, Nov 2009] (from NCBI)
Top mentioned proteins: PCNA, CDK4, CDK2, p21, p27
Papers using CDK6 antibodies
Cyclin E and its low molecular weight forms in human cancer and as targets for cancer therapy.
Gartel Andrei L., In PLoS ONE, 2002
... the polyclonal antibodies against EGFR, pEGFR, cyclin A, cyclin B, cyclin D, cyclin E, and CDK6 were obtained from Santa Cruz Biotechnology.
Inhibitory effects of progesterone on plasma membrane fluidity and tumorigenic potential of ovarian epithelial cancer cells.
Navarro Alfons, In PLoS ONE, 2002
... Cyclin D1 and CDK6 antibodies were from Cell Signaling Technology (Danvers, MA) ...
Papers on CDK6
Phosphorylated retinoblastoma protein is a potential predictive marker of irinotecan efficacy for colorectal cancer.
Sakai et al., Kyoto, Japan. In Int J Oncol, Feb 2016
Intriguingly, the knockdown of both CDK4 and CDK6, but not CDK2, allowed RB to become the most hypophosphorylated form and converted the SN38-sensitive cells to a resistant state.
Axon guidance molecule Semaphorin3A is a novel tumor suppressor in head and neck squamous cell carcinoma.
Song et al., Nanjing, China. In Oncotarget, Feb 2016
Both genetic and recombinant SEMA3A protein inhibited cell proliferation and colony formation and induced apoptosis, accompanied by decreased cyclin E, cyclin D, CDK2, CDK4 and CDK6 and increased P21, P27, activated caspase-5 and caspase-7.
Overexpression of Cell Cycle Proteins of Peripheral Lymphocytes in Patients with Alzheimer's Disease.
Kim et al., Seoul, South Korea. In Psychiatry Investig, Jan 2016
The cell cycle proteins CDK2, CDK4, CDK6, cyclin B, and cyclin D were measured in peripheral lymphocytes.
Cyclin-Dependent Kinases as Coregulators of Inflammatory Gene Expression.
Kracht et al., Gießen, Germany. In Trends Pharmacol Sci, Jan 2016
This process involves the cytokine-induced recruitment of CDK6 to the nuclear chromatin fraction where it associates with transcription factors of the NF-κB, STAT, and AP-1 families.
Endocrine resistance in breast cancer - An overview and update.
Dixon et al., Washington, D.C., United States. In Mol Cell Endocrinol, Jan 2016
Encouraging evidence that drug combinations with CDK4/CDK6 inhibitors can extend recurrence free survival may yet translate to improvements in overall survival.
Targeting CDK4 and CDK6: From Discovery to Therapy.
Shapiro et al., London, United Kingdom. In Cancer Discov, Jan 2016
UNASSIGNED: Biochemical and genetic characterization of D-type cyclins, their cyclin D-dependent kinases (CDK4 and CDK6), and the polypeptide CDK4/6 inhibitor p16(INK4) over two decades ago revealed how mammalian cells regulate entry into the DNA synthetic (S) phase of the cell-division cycle in a retinoblastoma protein-dependent manner.
METTL13 is downregulated in bladder carcinoma and suppresses cell proliferation, migration and invasion.
Man et al., Shenyang, China. In Sci Rep, Dec 2015
Further research suggested that METTL13 negatively regulates cell proliferation in bladder cancer and reinstates G1/S checkpoint via the coordinated downregulation of CDK6, CDK4 and CCND1, decreased phosphorylation of Rb and subsequent delayed cell cycle progression.
FDA Approval: Palbociclib for the Treatment of Postmenopausal Patients with Estrogen Receptor-Positive, HER2-Negative Metastatic Breast Cancer.
Cortazar et al., White Oak, United States. In Clin Cancer Res, Dec 2015
On February 3, 2015, the FDA granted accelerated approval to palbociclib (IBRANCE, Pfizer Inc.), an inhibitor of cyclin-dependent kinases 4 and 6 (CDK4 and CDK6), for use in combination with letrozole for the treatment of postmenopausal women with estrogen receptor (ER)-positive, HER2-negative advanced breast cancer as initial endocrine-based therapy for their metastatic disease.
CDK6-a review of the past and a glimpse into the future: from cell-cycle control to transcriptional regulation.
Sexl et al., Vienna, Austria. In Oncogene, Nov 2015
UNASSIGNED: The G1 cell-cycle kinase CDK6 has long been thought of as a redundant homolog of CDK4.
Palbociclib in Hormone-Receptor-Positive Advanced Breast Cancer.
PALOMA3 Study Group et al., Melbourne, Australia. In N Engl J Med, Aug 2015
BACKGROUND: Growth of hormone-receptor-positive breast cancer is dependent on cyclin-dependent kinases 4 and 6 (CDK4 and CDK6), which promote progression from the G1 phase to the S phase of the cell cycle.
CDK6 levels regulate quiescence exit in human hematopoietic stem cells.
Dick et al., Toronto, Canada. In Cell Stem Cell, Apr 2015
We report here that quiescence exit kinetics are differentially regulated within human HSC subsets through the expression level of CDK6.
Whole genomes redefine the mutational landscape of pancreatic cancer.
Grimmond et al., Brisbane, Australia. In Nature, Mar 2015
A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence.
The history and future of targeting cyclin-dependent kinases in cancer therapy.
Knudsen et al., Dallas, United States. In Nat Rev Drug Discov, Feb 2015
In particular, cyclin-dependent kinases (CDKs) that promote transition through the cell cycle were expected to be key therapeutic targets because many tumorigenic events ultimately drive proliferation by impinging on CDK4 or CDK6 complexes in the G1 phase of the cell cycle.
Downregulation of cell cycle-related proteins in ovarian cancer line and cell cycle arrest induced by microRNA.
Ling et al., Yongchuan, China. In Int J Clin Exp Med, 2014
The cell cycle-related proteins CDK6 and CDC254 were downregulated.
Genetic screens in human cells using the CRISPR-Cas9 system.
Lander et al., Cambridge, United States. In Science, 2014
A screen for resistance to the nucleotide analog 6-thioguanine identified all expected members of the DNA mismatch repair pathway, whereas another for the DNA topoisomerase II (TOP2A) poison etoposide identified TOP2A, as expected, and also cyclin-dependent kinase 6, CDK6.
Knockdown of CDK6 enhances glioma sensitivity to chemotherapy.
Lu et al., Shanghai, China. In Oncol Rep, 2012
CDK6 is an important mediator of glioma resistance to chemotherapy.
Modification of the DNA damage response by therapeutic CDK4/6 inhibition.
Knudsen et al., Philadelphia, United States. In J Biol Chem, 2012
CDK4/6 inhibition can antagonize cytotoxic therapeutic strategies and increases utilization of error-prone DNA repair mechanisms that could contribute to disease progression.
MicroRNA-191 triggers keratinocytes senescence by SATB1 and CDK6 downregulation.
Candi et al., Roma, Italy. In Biochem Biophys Res Commun, 2012
miR-191 overexpression is sufficient to induce senescence in HEKn cells and that the direct targets, involved in this process, are the Special AT-rich Binding protein 1 (SATB1) and the Cyclin Dependent Kinase 6 (CDK6) mRNAs.
Inactivation of CDK/pRb pathway normalizes survival pattern of lymphoblasts expressing the FTLD-progranulin mutation c.709-1G>A.
Martín-Requero et al., Madrid, Spain. In Plos One, 2011
Inactivation of CDK6/pRb pathway normalizes survival pattern of lymphoblasts expressing the FTLD-progranulin mutation c.709-1G>A
[Relationship between miR-218 and CDK6 expression and their biological impact on glioma cell proliferation and apoptosis].
Wen et al., Tianjin, China. In Zhonghua Bing Li Xue Za Zhi, 2011
An aberrant decrease of miR-218 expression may lead to an increase of CDK6 expression and proliferative activity of giloma cells.
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