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Validated All-in-One™ qPCR Primer for CDK4(NM_000075.3) Search again
Product ID:
HQP054656
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CMM3, PSK-J3
Gene Description:
cyclin dependent kinase 4
Target Gene Accession:
NM_000075.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene is a member of the Ser/Thr protein kinase family. This protein is highly similar to the gene products of S. cerevisiae cdc28 and S. pombe cdc2. It is a catalytic subunit of the protein kinase complex that is important for cell cycle G1 phase progression. The activity of this kinase is restricted to the G1-S phase, which is controlled by the regulatory subunits D-type cyclins and CDK inhibitor p16(INK4a). This kinase was shown to be responsible for the phosphorylation of retinoblastoma gene product (Rb). Mutations in this gene as well as in its related proteins including D-type cyclins, p16(INK4a) and Rb were all found to be associated with tumorigenesis of a variety of cancers. Multiple polyadenylation sites of this gene have been reported. [provided by RefSeq].
Gene References into function
- Rarity of CDK4 germline mutations in familial melanoma.
- Reversal of growth suppression by p107 via direct phosphorylation by cyclin D1/cyclin-dependent kinase 4
- Results show that Tax directly interacts with CDK4. The Tax/CDK complex represents an active holoenzyme which capably phosphorylates the Rb protein in vitro and is resistant to repression by the inhibitor p21(CIP).
- ultraviolet-B-induced cell cycle arrest in A431 cells is mediated by cyclin-dependent kinase 4 downregulation
- Keratinocytes engineered to express cdk4(R24C) and hTERT but not p53DD did not exhibit an extended life span.
- Sequential extension of proliferative lifespan in human fibroblasts is induced by over-expression of CDK4 or 6 and loss of p53 function.
- data identify a new role for oncogenic Ras in CDK4 regulation and highlight the functional importance of CDK4 suppression in preventing uncontrolled growth
- Cdk4 binds to p16INK4A and causes its phosphorylation
- Interferon gamma reduces the activity of Cdk4 and Cdk2, inhibiting he G1 cell cycle in human hepatocellular carcinoma cells.
- Cdk4-overexpressing cells divide in an apparently normal regulated fashion, are able to respond to changes in calcium levels, and fully differentiate . These results suggest that the differentiation pathways in Cdk4-overexpressing cells remain intact
- Data provide evidence of a role for MDM2 and CDK4 in the pathogenesis of carcinosarcoma.
- increases of cyclin D1, cyclin-dependent kinase 4, cyclin E, cyclin A, and Wee1 play an important role in the development of hepatocellular carcinoma from cirrhosis
- Cells overexpressing cdk4 or cyclin D1 exhibited nuclear features characteristic of apoptosis.
- DNA mutation analysis of the CDK4 gene in many types of neoplasms reveal it is very rare. Random mutagenisis the CDK4 gene showed that most of the mutations that disrupted interactions with p16(INK4) also knocked out the activity of CDK4.
- significant difference in their biochemical properties between CDK4/cyclin D1 and CDK2/cyclin A affecting regulation of cellular RB function
- susceptibility to skin tumor formation by forced expression of CDK4
- Data suggest that cyclin dependent kinase 4 is involved in the development of tobacco-mediated oral carcinogenesis, and that c-myc expression is absent in normal and high in later stages of oral cancer development.
- cyclin-dependent kinase (CDK)2, -4, and -6 were down-regulated from the myelocytes/metamyelocytes stages and onward
- CDK4 binding to cyclin D1 is stimulated by Cdc37
- cyclin D1/Cdk4 complexes are regulated by calcium/calmodulin-dependent protein kinase I
- Cdk2 and Cdk4 phosphorylate human Cdt1 and induce its degradation
- CDK4, MDM2, SAS and GLI genes are amplified in leiomyosarcoma, alveolar and embryonal rhabdomyosarcoma
- A novel Cdk4 docking motif has been defined within a stretch of 19 amino acids from the C-terminal domain of the Rb protein that are essential for Cdk4 binding.
- Transcriptional regulation of the CDK4 promotor is compared in normal breast cell lines vs breast cancer cell lines.
- When expressed in transgenic mice, total CDK4 protein expression was increased by up to 5-fold, with a concomitant increase in CDK4 activity.
- Expression levels of CDK4 predict the cellular effects ofmTOIR inhibitors in ovarian carcinoma.
- This suggests that dysregulation of CCND2 and CDK4 plays a specific role in WT tumorigenesis.
- CDK4 melanoma families known to date have a substitution of amino acid 24.
- Breast cancer patients might benefit from inhibiting CDK4 kinase.
- there is a novel function for CDK4-cyclin D3 activity in S and G(2) phase that is critical for G(2)/M progression and the fidelity of mitosis
- the subtype 2 receptor-mediated antiproliferative effect of SRIH on TT cell proliferation may be exerted through a decrease in cyclin D1 and cdk4 levels
- Mantle cell lymphoma should be very sensitive to targeted therapy aimed at functional inhibition of the cyclin D1/CDK4 complex.
- cyclin D1/Cdk4 converts FOXM1c from an almost inactive form into a strong transactivator in G1-phase, i.e., just at the time point at which the transcriptional activity of FOXM1 is required for stimulation of the G1/S-transition
- The data shows the expression and purification of an Hsp90-Cdc37-Cdk4 complex, defining its stoichiometry, and determining its 3D structure by single-particle electron microscopy.
- significant cytoplasmic mislocalization of ordinarily nuclear RB in cells harboring Cdk4 mutations
- Overexpression of p16 and CDK4 in the cytoplasm, as well as loss expression of p16 in the nucleus might be important in the evolution of colorectal carcinoma from adenoma and, of adenoma from normal epithelia.
- findings confirm CDK4 overexpression is a frequent phenomenon in laryngeal carcinoma, which occurs at transcriptional level but not related to gene amplification or mutation, & suggest cooperation with CCND1 may be involved in laryngeal tumor progression
- Sensitization towards TRAIL was due to the transcriptional downregulation of survivin
- CDK4 delays senescence by kinase-dependent and p16INK4a-independent mechanisms.
- study reports the largest genetic analysis to date of melanoma susceptibility genes (CDKN2A and CDK4) among melanoma patients from Latvia and describe the seventh CDK4-positive melanoma family, worldwide, identified so far
- Over expression of H179Y-mutant p53 promoted G1 to S phase transition with enlarged cell size and increased cyclin A1 and Cdk4 expression in HELF cells.
- a new role for YY1 as both an inducer of p53 instability in smooth muscle cells, and an indirect repressor of p21WAF1/Cip1 transcription, p21WAF1/Cip1-cdk4-cyclin D1 assembly and intimal thickening.
- CDK4 and c-Myc is generally expressed in benign and malignant pancreatic endocrine tumors, and regardless of MEN1 mutational status
- Data suggest that calcineurin may regulate the kinase activity of CDK4 in a cell cycle-dependent manner and may be an important component of the negative regulation of CDK4.
- In conclusion, we recommend that the evaluation of MDM2-CDK4 amplification using FISH or Q-PCR be used to supplement IHC analysis when diagnosis of adipose tissue tumors is not possible based on clinical and histologic information alone.
- CDK4 is a modulator of TRAIL-induced apoptosis pathway
- Variants are associated with multiple primary cutaneous melanomas in a Norwegian population.
- serum starvation induces G1 arrest through suppression of Skp2-dependent CDK2 activity and Skp2-independent CDK4 activity in human SK-OV-3 ovarian cancer cells
- Genomic aberrations of CDK4 in neuroblastoma indicate that dysregulation of the G(1) entry checkpoint is an important cell cycle aberration in this pediatric tumor.
- Loss of p16/Rb protein expression and overexpression of cyclin D1/CDK4 were observed in 49%/40% and 37%/37% of gastric carcinomas, respectively.Cyclin D1 and CDK4 overexpession was inversely associated with lymph node metastasis and depth of invasion.
- No evidence for linkage to melanoma susceptibility genes for both CDKN2A and CDK4.
- co-overexpression of KIT/CDK4 is a potential mechanism of oncogenic transformation in some BRAF/NRAS wild-type melanomas
- These results demonstrate that ERKs and JNKs are responsible for the decrease of cyclin D1 and CDK4 expression levels in human embryonic lung fibroblasts induced by silica.
- The present data support a role for p27 in the assembly of D-type cyclin-Cdk complexes and indicate that both cyclin D1-Cdk4-p27 assembly and kinase activation are regulated by p27 phosphorylation.
- CDK4/6 activity is important in regulating the expression of these critical mediators of DNA replication
- These studies identify the activating phosphorylation of CDK4 as a common target of opposite cell cycle regulations by cyclic AMP.
- The present study has shown an absence of CDK4 mutations in Slovenian population of familial melanoma patients (37%)
- a pattern of translocalization suggests a spatial separation of the cyclin D-Cdk complex from pRb and DNA in the nucleus to regulate the G1-S transition
- TsA markedly down-regulated the expression of cyclin D1 and CDK4, up-regulated the expression of p21WAF1 and p53 and induced cell cycle arrest at the G1 phase in MCF10A-ras cells
- Proliferation parameters of differentiating cells correlate with the activity and structure of cyclin A/E-CDK2 but not of cyclin D-CDK4/6-p27 complexes.
- These results highlight the prognostic value of CDK4 amplification and of simultaneous EGFR-p53 alterations in the clinical outcome of patients with primary GBM.
- either p57Kip2 "apice" or p27Kip1 "apice" inhibitors bound to cyclin D1/cdk4 complex, thus, suggesting that they cooperated to inhibit the activity of cyclin D1/cdk4.