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Human CDK2 Protein expressed in Wheat germ - ABIN1348934
Bockstaele, Kooken, Libert, Paternot, Dumont, de Launoit, Roger, Coulonval: Regulated activating Thr172 phosphorylation of cyclin-dependent kinase 4(CDK4): its relationship with cyclins and CDK "inhibitors". in Molecular and cellular biology 2006
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The authors demonstrated that the CDK2-PAK4 kinase signature may be a useful prognostic indicator and potential target for non-small cell lung cancers, and also proposed that poor outcome subgroup stratified by this classifier may benefit from the recently developed CDK2 and PAK4 inhibitors.
Cyclin-dependent kinase 1 (CDK1) and CDK2 have opposing roles in regulating interactions of splicing factor 3B1 with chromatin
Data suggest that MCM4 phosphorylation by CDK2 plays role in DNA replication licensing system MCM4/MCM6/MCM7; this phosphorylation interferes with MCM complex function by lowering stability of MCM complex; MCM4 is highly phosphorylated in S phase. (MCM = minichromosome maintenance complex [hexamer of components 4/6/7]; CDK2 = cyclin-dependent kinase-2)
Data suggest that SNAI1 is a key regulator of FGF2-dependent mesenchymal transition in corneal endothelium, with ZEB1 regulating type I collagen expression and CDK2 regulating cell proliferation. (SNAI1 = snail family transcriptional repressor-1; FGF2 = fibroblast growth factor-2; ZEB1 = zinc finger E-box binding homeobox-1 protein; CDK2 = cyclin dependent kinase-2)
Results indicate that although PIN1 increases p27 levels, it also attenuates p27's inhibitory activity on CDK2 and thereby contributes to increased G1-S phase transitions and cell proliferation.
CDK2 mutation is not associated with non-obstructive azoospermia.
Proteomics and phosphoproteomics analyses identified CDK2 as a driver of resistance to both BRAF and Hsp90 inhibitors and its expression is regulated by the transcription factor MITF upon XL888 treatment of melanoma cells.
identified a new phosphorylation-based substrate recognition mechanism of PTPN12 by CDK2, which orchestrated signaling crosstalk between the oncogenic CDK2 and HER2 pathways
CDK2 gene is a strong candidate gene for type-2 diabetes. CDK2 gene is located in a risk area composed of 4 blocks in strong LD around the type-2 diabetes SNP rs2069408. CDK2 overexpression inhibits the association of insulin receptor to the microtubule components, tubulin alpha and tubulin beta. Physical association of the insulin receptor complex with CDK2 is inhibited by the expression of tyrosine phosphatase PTPLAD1.
ATM and CDK2 control the chromatin remodeling activity of CSB in the regulation of double strand break repair pathway choice.
Among these genes, STAT3 and CDK2 were significantly associated with recurrence. Further study suggested that inhibition of CDK2 reduced invasion of Pca cell lines. The invasion ability was rescued after reintroduction of CDK2.
The roles of the CDK2/SIRT5 axis in gastric cancer.
CDK2 may have key functions in neuroblastoma progression by regulating the expression of neoplastic genes.
The authors show that human Cyclin-Dependent-Kinases (CDKs) target the RAD9 subunit of the 9-1-1 checkpoint clamp on Thr292, to modulate DNA damage checkpoint activation. Thr292 phosphorylation on RAD9 creates a binding site for Polo-Like-Kinase1 (PLK1), which phosphorylates RAD9 on Thr313.
this study suggests that CDK2 and CDK9 are potential therapeutic targets in Neuroblastoma (NB) and that abrogating CDK2 and CDK9 activity by small molecules like dinaciclib is a promising strategy and a treatment option for NB patients
LINC00958 acts as an oncogenic gene in the gliomagenesis through miR-203-CDK2 regulation, providing a novel insight into glioma tumorigenesis.
These compounds bind CDK2/ Cyclin A, inhibit its kinase activity, compete with substrate binding, but not with ATP, and dock onto the T-loop of CDK2. The best compound also binds CDK4 and CDK4/Cyclin D1, but not CDK1.
CDK2 contributes to S81-AR phosphorylation and transactivation while CDK4 was not shown to be involved in this process.
Our findings provide a rationale for clinical use of Bcl-2 family inhibitors in combination with CDK2 inhibitors for treatment of Mcl-1-dependent colorectal tumours associated with expression of Bcl-2, Bcl-XL and Bcl-w proteins. In addition, we have shown potential of CDK2 inhibitors for treatment of tumours expressing R273H mutant p53.
Analysis of genomic data from TCGA demonstrated coamplification of CCNE1 and AKT2 Overexpression of Cyclin E1 and AKT isoforms, in addition to mutant TP53, imparted malignant characteristics in untransformed fallopian tube secretory cells, the dominant site of origin of high-grade serous ovarian cancer
Cdk2, the kinase responsible for the G1 to S phase transition, is also required in multiciliated cells to initiate motile ciliogenesis.
study suggests that hepatocellular carcinoma initiation specifically depends on CcnE1 and Cdk2, while HCC progression requires expression of any E-cyclin, but no Cdk2.
Identified a telomere localization domain on Speedy A covering the distal N terminus and the Cdk2-binding Ringo domain, and this domain is essential for the localization of Speedy A to telomeres.
CDK2 phosphorylates polyQ-AR specifically at Ser(96). Phosphorylation of polyQ-AR by CDK2 increased protein stabilization and toxicity and is negatively regulated by the adenylyl cyclase/protein kinase A signaling pathway in spinobulbar muscular atrophy.
Ad-p21 inhibits RNV in OIR. A potential underlying mechanism for this may be that overexpression of p21 arrests the cell cycle at the G1- to S-phase transition via inhibition of CDK2 activity.
CDK2 serves as an important nexus linking primary beta-cell dysfunction to progressive beta-cell mass deterioration in diabetes
data indicate that the essential meiotic functions of Cdk2 depend on its kinase activity, without which the generation of haploid cells is disrupted, resulting in sterility of otherwise healthy animals
Testosterone is the positive regulator of hepatocyte cell cycle via cyclin E/cdk2 promoting hepatocarcinogenesis.
This approach allowed us to determine the identity of cyclin E protein partners, as well as phosphorylation substrates of cyclins E (cyclin E1and cyclin E2)and its associated kinase, Cdk2, in different mouse organs.
RingoA is an important activator of Cdk2 at meiotic telomeres.
Foxo3 circular RNA retards cell cycle progression via forming ternary complexes with p21 and CDK2.
Results identify phosphorylation of CDK2 at tyrosine 160 as a gate-keeping mechanism for hepatocyte proliferation.
Sox2 phosphorylation by Cdk2 promotes the establishment but not the maintenance of the pluripotent state.
Our data indicate that Cdk2 and Cdk4 play important overlapping roles in homeostatic and stress hematopoiesis, which need to be considered when using broad-spectrum cyclin-dependent kinase inhibitors for cancer therapy.
ablation of the kinase CDK2 alters the nuclear envelope in mouse spermatocytes, and that the proteins SUN1, KASH5 (also known as CCDC155) and lamin C2 show an abnormal cap-like distribution facing the centrosome.
CDK4 is a critical downstream target of MEN1-dependent tumor suppression and is required for tumorigenic proliferation in the pituitary and pancreatic islet, whereas CDK2 is dispensable for tumorigenesis in these neuroendocrine cell types.
Our results highlight an important role for p-CDK2(39) in influencing silencing of the sex chromosomes during male meiosis by interacting with gamma-H2AX.
abnormal pairing and synapsis of homologous chromosomes, heterologous chromosome associations, unrepaired double-strand DNA breaks, disruptions in telomeric structure and defects in cyclin-dependent-kinase 2 localization
Results show that CDK2 phosphorylates Thr-156 in GATA3.
Loss of Cdk2 and cyclin A2 impairs cell proliferation and tumorigenesis.
intestinal clock controls the expression of key cell cycle regulators, such as cdc2, wee1, p21, PCNA and cdk2, but only weakly influences cyclin B1, cyclin B2 and cyclin E1 expression.
PI3-kinase and Akt participate in insulin stimulation of p34cdc2 activation in zebrafish oocyte with phosphodiesterase 3 as a potential downstream target.
an essential role for UHRF1 phosphorylation by cyclin-dependent kinase 2/cyclin A2 during early vertebrate development
cyclin D1, CDK2 and CDK4 are expressed in both caruncular and intercaruncular cells derived from both nonpregnant, and artificially inseminated cows on days 30 and 60 of gestation
evidence that cyclin A1-associated activity is a mediator of apoptosis and that cyclin A1/Cdk2 is sufficient to induce apoptosis
our results indicate that an ATM-P53-P21 DNA damage checkpoint is intact in the absence of CDK2; however, CDK2 is important for proper repair of the damaged DNA by either directly or indirectly influencing DNA repair-related gene expression.
The protein encoded by this gene is a member of the Ser/Thr protein kinase family. This protein kinase is highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2. It is a catalytic subunit of the cyclin-dependent protein kinase complex, whose activity is restricted to the G1-S phase, and essential for cell cycle G1/S phase transition. This protein associates with and regulated by the regulatory subunits of the complex including cyclin A or E, CDK inhibitor p21Cip1 (CDKN1A) and p27Kip1 (CDKN1B). Its activity is also regulated by its protein phosphorylation. Two alternatively spliced variants and multiple transcription initiation sites of this gene have been reported.
cdc2-related protein kinase
, cell devision kinase 2
, cell division protein kinase 2
, p33 protein kinase
, cyclin dependent kinase 2-alpha
, cyclin-dependent kinase 2
, CDC2 homolog Eg1 protein kinase
, Cell division protein kinase 2