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CDK2 depletion arrested tumor growth of acute myeloid leukemia (AML) cells in nude mice and extended survival in both AML cell line and PDX-AML cells derived xenograft mouse models.
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Cdk2, the kinase responsible for the G1 to S phase transition, is also required in multiciliated cells to initiate motile ciliogenesis.
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study suggests that hepatocellular carcinoma initiation specifically depends on CcnE1 and Cdk2, while HCC progression requires expression of any E-cyclin, but no Cdk2.
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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.
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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.
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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.
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CDK2 serves as an important nexus linking primary beta-cell dysfunction to progressive beta-cell mass deterioration in diabetes
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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
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Testosterone is the positive regulator of hepatocyte cell cycle via cyclin E/cdk2 promoting hepatocarcinogenesis.
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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.
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RingoA is an important activator of Cdk2 at meiotic telomeres.
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Foxo3 circular RNA retards cell cycle progression via forming ternary complexes with p21 and CDK2.
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Results identify phosphorylation of CDK2 at tyrosine 160 as a gate-keeping mechanism for hepatocyte proliferation.
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Sox2 phosphorylation by Cdk2 promotes the establishment but not the maintenance of the pluripotent state.
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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.
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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.
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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.
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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.
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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
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Results show that CDK2 phosphorylates Thr-156 in GATA3.