Cyclin Y, a novel membrane‐associated cyclin, interacts with PFTK1

Jiang, Mei; Gao, Yankun; Yang, Tao; Zhu, Xueliang; Chen, Jiangye

doi:10.1016/j.febslet.2009.06.010

Cited by 77 publications

(84 citation statements)

References 27 publications

(44 reference statements)

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“…20 Like CDK16, ectopically expressed CDK14 is cytoplasmic unless co-expressed with CCNY, which targets it to the plasma membrane. 23 PFTK2/CDK15 is very poorly characterized, and little is known about its expression and regulation. Evolutionarily, CDK15 seems to be of a newer origin, since most animal species have only one PFTAIRE, which is more similar to CDK14 ( Table 1).…”

Section: From Orphans To Eccentric Family Membersmentioning

confidence: 99%

“…In shorter lived complexes, a constitutively unstable component is stabilized by incorporation into multiprotein complexes, which makes CDK activity dependent on complex assembly. Another way to generate short-lived complexes is to that CCNY binding to PFTAIRE kinases is regulated by phosphorylation, 23 although serine153 is conserved. One explanation for this difference could be that Ser119, which is responsible for 14-3-3 binding, is not conserved between the two kinases.…”

Section: Pctaires Interact With Ccnymentioning

confidence: 99%

“…In contrast to CDK2, the kinase domains of CDK14 and 16 are not sufficient for CCNY binding, but require also the N-terminal extensions. 9,23 In CDK16, the N-terminal domain has another important regulatory function, which was first identified by showing that bacterially expressed recombinant CDK16 harboring a non-phosphorylatable alanine at position 153 had higher kinase activity after incubation with brain extracts than wild-type CDK16. 62 We found that phosphorylation of S153, which is embedded within a PKA consensus motif, prevents CCNY binding.…”

Section: Functions Of Pctaires and Pftairesmentioning

confidence: 99%

“…8 This interaction involves the typical CDK-cyclin domains, such as the cyclin fold domain in CCNY and the "PFTAIRE" motif in CDK14, but also, additional regions outside the CDK domain. 23 CCNY activates and recruits CDK14 to the cell membrane to phosphorylate the WNT co-receptor LRP5/6. 8,23 Thus, PCTAIREs and PFTAIREs share the same activator, and their co-expression in many murine and human tissues suggests functional redundancy.…”

Section: Ccny Is a Promiscuous Cyclinmentioning

confidence: 99%

“…23 CCNY activates and recruits CDK14 to the cell membrane to phosphorylate the WNT co-receptor LRP5/6. 8,23 Thus, PCTAIREs and PFTAIREs share the same activator, and their co-expression in many murine and human tissues suggests functional redundancy. In contrast to PCTAIRE kinases, there is no evidence a "PCTGIRE" sequence kinase that exhibits 40% identity to the kinase domain of CDK16.…”

Section: Ccny Is a Promiscuous Cyclinmentioning

confidence: 99%

See 4 more Smart Citations

Orphan kinases turn eccentric

2012

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Section: From Orphans To Eccentric Family Membersmentioning

confidence: 99%

Section: Pctaires Interact With Ccnymentioning

confidence: 99%

Section: Functions Of Pctaires and Pftairesmentioning

confidence: 99%

Section: Ccny Is a Promiscuous Cyclinmentioning

confidence: 99%

Section: Ccny Is a Promiscuous Cyclinmentioning

confidence: 99%

See 3 more Smart Citations

Orphan kinases turn eccentric

2012

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CDK6 is activated by the atypical cyclin I to promote E2F‐mediated gene expression and cancer cell proliferation

et al. 2023

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Cyclin-dependent kinases (CDKs), together with their cyclin partners, are the master cell cycle regulators. Remarkably, the cyclin family was extended to include atypical cyclins, characterized by distinctive structural features, but their partner CDKs remain elusive. Here, we conducted a yeast two-hybrid screen to identify new atypical cyclin-CDK complexes. We identified 10 new complexes, including a complex between CDK6 and cyclin I (CCNI), which was found to be active against retinoblastoma protein. CCNI upregulation increased the proliferation of breast cancer cells in vitro and in vivo, with a magnitude similar to that seen upon cyclin D upregulation, an effect that was abrogated by CDK6 silencing or palbociclib treatment. In line with these findings, CCNI downregulation led to a decrease in cell number and a reduction in the percentage of cells reaching S phase. Finally, CCNI upregulation correlated with the high expression of E2F target genes in large panels of cancer cell lines and tissue samples from breast cancer patients. In conclusion, we unveil CCNI as a new player in the pathways that activate CDK6, enriching the wiring of cell cycle control.

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Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

Zhao

et al. 2018

Journal Cellular Physiology

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Recently, increasing numbers of long noncoding RNAs (lncRNAs) have been found to be aberrantly expressed in various cancers. However, the roles of lncRNAs in hepatocellular carcinoma (HCC) progression is largely unknown. In our current study, we identified that long intergenic nonprotein‐coding RNA 707 (LINC00707) was remarkably elevated in HCC cells, indicating that LINC00707 was involved in HCC development. Subsequently, LINC00707 was significantly decreased in HepG2 and Huh7 cells. The in vitro functional assays demonstrated that knockdown of LINC00707 significantly reduced HCC cell proliferation, induced cell apoptosis, and blocked the cell cycle progression. In addition, HCC cell migration and invasion was also greatly inhibited by downregulation of LINC00707. Increasing evidence has indicated that lncRNAs can act as molecular sponges of microRNAs. Currently, we observed that microRNA‐206 (miR‐206) was dramatically inhibited in HCC cells and LINC00707 can modulate HCC development through sponging miR‐206. The binding correlation between LINC00707 and miR‐206 was confirmed by dual‐luciferase reporter assay, RNA pull down and RNA immunoprecipitation assay in our study. Moreover, cyclin‐dependent kinase 14 (CDK14) was predicted as a target of miR‐206 and we found that miR‐206 suppressed CDK14 levels in HCC cells. Finally, in vivo assays were used and it was proved that silence of LINC00707 can restrain HCC development through modulating miR‐206 to upregulate CDK14. In conclusion, it was implied that LINC00707 can lead to HCC progression through sponging miR‐206 and modulating CDK14.

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Cyclin Y, a novel membrane‐associated cyclin, interacts with PFTK1

Cited by 77 publications

References 27 publications

Orphan kinases turn eccentric

Orphan kinases turn eccentric

CDK6 is activated by the atypical cyclin I to promote E2F‐mediated gene expression and cancer cell proliferation

Retracted: LINC00707 contributes to hepatocellular carcinoma progression via sponging miR‐206 to increase CDK14

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