RINGO/Speedy proteins, a family of non-canonical activators of CDK1 and CDK2

González, Laura; Nebreda, Ángel R.

doi:10.1016/j.semcdb.2020.03.010

Cited by 14 publications

(5 citation statements)

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“…Spy1/RINGO proteins bind to and activate Cdk1 and Cdk2 in a cyclin-independent manner, thereby promoting cell cycle progression (Gonzalez and Nebreda, 2020). However, they have not been previously implicated in transcriptional regulation.…”

Section: Distinct Transcriptional Activities Within Tf Familiesmentioning

confidence: 99%

Identification and functional characterization of transcriptional activators in human cells

Alerasool

Lin

et al. 2022

Molecular Cell

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Section: Distinct Transcriptional Activities Within Tf Familiesmentioning

confidence: 99%

Identification and functional characterization of transcriptional activators in human cells

Alerasool

Lin

et al. 2022

Molecular Cell

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“…It is widely known that cell cycle progression is a complex process governed by cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors and cell cycle is frequently dysregulated in neoplasia due to alterations in oncogenes that indirectly affect the cell cycle. Of note, in both ICGC and TCGA databases, the cell cycle-related genes we examined including CCNA2, 56 CCNB1, 57 CDC20, 58 CDC23, 59 CDC25A, 60 CDK1, CDK2, 61 CDK4, CDK7, 62 CHEK1, CHEK2, 63 E2F1, E2F3, E2F4, E2F5 64 showed a trend of overexpression in the high-risk group. Our current research showed that OLA1|CLEC3B levels demonstrated strong correlations with a variety of cell cycle-related molecules including CDK1, CCNB1, CDK4, CCNB2, CDC25A, CDC20, CDK2, CHEK1, E2F5, CDK7, CDC23, E2F3, E2F4, E2F1, CHEK2, CCNA2 from TCGA cohorts and CDC20, CCNB1, CDK1, CCNB2, E2F5, CDK4, CDC25A, CHEK1, CCNA2, E2F1, E2F3, CDK2, CDK7, CHEK2, E2F4 from ICGC cohort.…”

Section: Discussionmentioning

confidence: 99%

Combined OLA1 and CLEC3B Gene Is a Prognostic Signature for Hepatocellular Carcinoma and Impact Tumor Progression

Chen,

Zeng,

Chen

et al. 2024

Technol Cancer Res Treat

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Hepatocellular carcinoma (HCC), partly because of its complexity and high heterogeneity, has a poor prognosis and an extremely high mortality rate. In this study, mRNA sequencing expression profiles and relevant clinical data of HCC patients were gathered from different public databases. Kaplan–Meier survival curves as well as ROC curves validated that OLA1|CLEC3B was an independent predictor with better predictive capability of HCC prognosis compared to OLA1 and CLEC3B separately. Further, the cell transfection experiment verified that knockdown of OLA1 inhibited cell proliferation, facilitated apoptosis, and improved sensitivity of HCC cells to gemcitabine. In this study, the prognostic model of HCC composed of OLA1/CLEC3B genes was constructed and verified, and the prediction ability was favorable. A higher level of OLA1 along with a lower level of CEC3B is a sign of poor prognosis in HCC. We revealed a novel gene pair OLA1|CLEC3B overexpressed in HCC patients, which may serve as a promising independent predictor of HCC survival and an approach for innovative diagnostic and therapeutic strategies.

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“…Phosphorylation of the A-loop is not required to activate CDK2 when it is bound to RINGO/Speedy family members -meiosis-specific proteins that only encode a single cyclin-box fold (CBF). 41,42 Here, the A-loop is pulled out of the active site to form a platform that is structurally distinct from that seen in Thr160-phosphorylated CDK2 (pCDK2)-cyclin A but is compatible with peptide substrate recognition and catalysis (Fig. 1B).…”

Section: Recent Progress In Cdk Structure-function Studiesmentioning

confidence: 99%