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CDK4 inhibits RB1. 122 / 136
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"Importantly, CDK4-induced Rb inactivation dramatically restored the defective transformation of MIF-deficient DKO cells (Figure 3E) ."
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"Cell cycle arrest is initiated and maintained through the p53/p21 pathway and/or the p16 pathway, which prevent CDK4- and CDK6- mediated inactivation of retinoblastoma protein (Rb) to block cell cycle progression [2, 3]."
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"The activities of cyclin dependent kinase 2 (Cdk2) and cyclin dependent kinase 4 (Cdk4) are greatly reduced, due to the increased expression of the Cdk inhibitor proteins p21, and p16, causing Rb to be present in its hypophosphorylated form."
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"We confirmed that CDK4 siRNA efficiently abolished p-Rb as well as CDK4 mRNA and protein expression (XREF_FIG)."
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"These results are consistent with a model in which the only requirement of cdk4 in MCF-7 cell proliferation is to inactivate pRb family members XREF_BIBR, XREF_BIBR."
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"As p16 functions as a CDK inhibitor, cell cycle progression from G1 to S phase requires the activation of CDK4 and CDK6, which inactivate the retinoblastoma (Rb) tumor-suppressor protein by phosphorylation [52]."
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"Levels of the cyclin-dependent kinase inhibitors (CDKIs) p18, p21 and p27 were shown to be increased in all treated RMS cell lines but no CDK4 inhibition or hypophosphorylation of the Rb protein suggesting that ATRA-induced differentiation was not sufficient to induce cell cycle arrest in RMS cells."
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"The cyclin D–CDK4 complex phosphorylates and inactivates the Rb."
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"Since CDK4-dependent Rb inactivation contributes to subsequent CDK2 activation in late G 1 (due to induction of cyclins E and A), we also determined the effect of Mcm7-depletion on CDK2 activity."
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"The prevailing perspective on the role of CDKs is that CDK4 and CDK6, in conjunction with D-type cyclins, impede the retinoblastoma (Rb) protein pathway to trigger the transition from the G1 to S phases of the cell cycle [6]."
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"p16 is a cyclin dependent kinase inhibitor of CDK4 and CDK6, which activates the negative cell cycle regulator retinoblastoma protein (pRB)."
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"In particular a high fraction of tumors exhibit amplification of the p53 negative regulators MDM2, 4 and WIP1, as well as CDK4 which negatively regulates Rb."
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"p16 blocks cell cycle progression by inhibiting the expression of CDK4/CDK6, which prevent the activation of pRB."
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"During the G 1 phase, Rb proteins are inactivated by sequential phosphorylation mediated by various Cdks, mainly the D-type cyclin dependent Cdk4 and Cdk6 and the E-type cyclin dependent Cdk2."
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"Intriguingly, the knockdown of both CDK4 and CDK6, but not CDK2, allowed RB to become the most hypophosphorylated form and converted the SN38 sensitive cells to a resistant state."
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"CDK4 inhibition can induce Rb positive cells to exit the cell cycle into a non proliferative state, however, this can take the form of either quiescence, which is readily reversible, or senescence, which is more stable."
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"CDKN2A inhibits CDK4 and CDK4 inhibits RB1 in the RB signaling pathway."
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"Cyclin D1 and cyclin dependent kinase-4 (CDK4) phosphorylate and inhibit RB to induce proliferation."
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"In complexes with D-type cyclins, the cyclin-dependent kinase-4 (CDK4) phosphorylates and inactivates RB1 [ xref , xref ]."
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"Several proteins from the KEGG cellular senescence pathway, such NFKB1, MAP2K1, RASSSF5, MRE11A, and RAD50, were upregulated in the low-mortality-risk group, whereas CDK4, which, when bound to Cyclin D inhibits Rb, was downregulated (Figure 3F)."
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"Likewise, Rb inactivation by CDK4 also induced upregulation of target genes in both genotypes (Supplemental Figure S4C)."
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"Mechanistically, CDK4 phosphorylates and functionally inactivates the retinoblastoma (Rb) protein, which results in uninhibited cell cycle progression from G1 to S phase and restoring native cell cycle regulation by CDK4 inhibition could prevent uncontrolled proliferation."
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"In our study, we focused on CCDN1 and CDK4, as the cyclinD1-CDK4 dimer normally inhibits the pRb protein allowing the E2F transcription factor to transcribe the genes necessary for entry into the S phase, while in an HPV-mediated infection E7 binds to pRb thus modifying the normal control of the cell cycle [58, 59]."
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"CDK4 kinase phosphorylates and inhibits the Rb protein, enabling the cell cycle progression [ xref , xref ]."
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"p14 ARF mediates growth arrest by stabilizing the tumor suppressor p53 [ xref ], whereas p16 induces cellular senescence by preventing the inactivation of the retinoblastoma protein (pRB) by the cyclin dependent kinases cdk4 and cdk6 [ xref , xref ], a step otherwise required for cell cycle progression."
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"p16 interacts with CDK4 and inhibits its activity, while CDK4 associates with cyclin D1 to inactivate pRB resulting in cell cycle progression."
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"MDM2 , which represses p53, has been shown to be amplified in human sarcomas ( Leach et al., 1993 ) while CDK4 , complexing with other cyclins, inhibits the retinoblastoma protein and releases cells f[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In particular a high fraction of tumors exhibit amplification of the p53 negative regulators MDM2, 4 and WIP1, and CDK4 which is also known to negatively regulate Rb."
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"The MDM2 gene product binds and inactivates p53 protein, whereas the CDK4 gene product is a cyclin dependent kinase and possibly inactivates Rb function."
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"Cyclin D1 and CDK4 phosphorylate and inactivate Rb during the G1/S transition, thereby allowing cell cycle progression to occur [ xref ]."
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"Palbociclib, an inhibitor of CDK4 and CDK6, restores cell cycle checkpoints independently of Rb."
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"Cdk4 and Cdk2 can inactivate Rb family members, including p107, by phosphorylation."
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"CDK4 and 6 negatively regulate Rb activity through phosphorylation and inactivation of this tumor suppressor protein; therefore, it is possible that only tumors containing Rb-proficient cells may be sensitive to CDK4 and 6 inhibition."
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"Rb negative tumors were expected to be resistant to abemaciclib treatment, since CDK4 and 6 inhibitors inhibit upstream of Rb; however, abemaciclib effects were not associated with Rb expression status."
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"Progression from G 1 to S relies on both Cdk4 and Cdk2 : Cdk4 and cyclin D is required to inactivate the Rb family of proteins at the restriction point, whereas Cdk2 and cyclin E is required not only [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"According to the prevailing model, the major role of CDK4 and CDK6 is to inactivate pRB."
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"CDK4 inhibits RB1, and CDKN2B inhibits CDK4 in the RB signaling pathway."
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"Cyclin D1 and Cdk4 complex inhibits Rb by partial phosphorylation, decreasing its association with E2F transcription factor and allowing E2F regulated activation of downstream gene transcription [XREF_BIBR, XREF_BIBR]."
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"Moreover, in this context, E2F1 transcriptional activity is regulated by glucose and insulin through the CDK4 dependent inactivation of the pRB protein."
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"Inhibition of CDK4 and CDK6 acts to restore the tumour suppressor role of Rb and promote cell cycle arrest."
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"CDK4 and its close homolog CDK6 form heterodimers with D-type cyclins, and CDK4/6-mediated deactivation of the retinoblastoma (RB) tumor suppressor is critical for cell-cycle progression [40]."
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"Subsequent studies have demonstrated that overexpression of cyclin D1 or cdk4, instead of HPV E6/E7, effectively inhibited Rb activity and might be an alternative method of overcoming premature senescence in primary epithelial cells of other origins."
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"Similarly, p16 can inhibit CDK4 and prevent CDK4-mediated inactivation of RB to block cell cycle progression in G1 phase [34]."
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"The pRB cell cycle regulatory cascade is frequently perturbed in neoplasia by overexpression of a component of the pRB phosphorylating cyclin D1 and CDK4 complex or by inactivation of pRB or the CDK4 inhibitors p16 and p15."
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"6 Cyclin D1-bound CDK4 catalytically inactivates RB, which induces cells to progress past the G1/S checkpoint."
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"PRb, which controls the G1-S checkpoint of the cell cycle, was inhibited by the CCND1-CDK4 complex in the promotion of passage via the G1 phase."
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"CDKN2A inhibits CDK4 and CDK4 inhibits RB1 in the RB signaling pathway."
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"Cyclin D1 and CDK4 phosphorylate and inactivate Rb during the G1/S transition, thereby allowing cell cycle progression to occur [6]."
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"The recently reported antiproliferative action of selected estrone-16-oxime ethers was explained by the mRNA-level induction of tumor suppressor p16 and the repression of retinoblastoma protein and cy[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"CDK4 inhibits RB1, and CDKN2B inhibits CDK4 in the RB signaling pathway."
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"Moreover, in this context, E2F1 transcriptional activity is regulated by glucose and insulin through the CDK4-dependent inactivation of the pRB protein."
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"Interestingly, extra copies of chromosome 20 were also observed in a recent study in which bronchial epithelial cells were immortalized by co-expression of hTERT and wild-type cdk4, which would also b[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Of note, both RB versions were able to repress E2F transcription in the absence of stress ( Figure S3 B) and were inactivated by CDK4 overexpression ( Figure S3 C), indicating that the RB mutant does [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Furthermore, the p16 INK4a -driven inhibition of CDK4 and CDK6 promotes changes in cell morphology independent of Rb, suggesting additional kinase targets may contribute to the activity of p16 INK4a."
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"The cyclin D1-CDK4 complex inactivates Rb to promote G1/S transition and cell proliferation."
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"Besides, we found CDK4 and MDM2 amplifications with upregulated phospho-Rb in the recurrent tumor and its xenografts, suggesting the multiple deregulated cell cycle mechanisms to support tumor progression and facilitate xenograft formation in the present case.Although the overall prognostic significance is still controversial [37], a large-scale study demonstrated that in addition to CDKN2A/B deletion, CDK4 amplification, which also deregulates Rb pathway, was associated with poor prognosis in IDH-mutant astrocytoma [3, 27]."
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"CDK2 and CDK4 modulate cell cycle progression by inducing Rb dependent repression of E2F mediated transcription (XREF_FIG A and B)."
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"CDK4 and CDK6 suppress the downstream inhibition of pRB, allowing the progression from G1 to S phase of the cell cycle."
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"CDK4 inactivates pRB and pRB may be required during OIS to induce a closed chromatin state that represses expression of genes that are required for cell proliferation ( xref )."
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"E2F1 transcriptional activity is regulated by glucose and insulin through the CDK4 dependent inactivation of the pRB protein."
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"The authors suggest that one reason for this is the ability of deregulated cdk4 to fully inactivate pRb as a consequence of eroded phosphorylation site specificity in tumor cells."
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"Our data showed that L. hatsudake extracts downregulated cyclin D1 mRNA expression due to RT-qPCR assay in HCT116 cancer cells, and the decreased expression of cyclin D1 reduced the binds to CDK4 and CDK6, which inhibited RB in releasing transcription factor E2F and reduced proliferation-related gene expressions [28]."
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"Cell cycle arrest is initiated and maintained through the p53/p21 pathway and/or the p16 pathway, which prevent CDK4- and CDK6- mediated inactivation of retinoblastoma protein (Rb) to block cell cycle progression [2, 3]."
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"When CDK4 and CDK6 form complexes with cyclin D, they phosphorylate and inactivate the retinoblastoma protein (Rb1), leading to the release of the E2F transcription factor, which in turn allows the cell cycle to progress from the G1 to S phase [54,55]."
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"Cycling cells progressing through G1 normally accumulate cyclin D, which partners with cyclin-dependent kinase 4 (CDK4) or CDK6 to inhibit retinoblastoma-associated protein (Rb; also known as RB1) and enable S-phase entry ."
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"When CDK4 and CDK6 form complexes with cyclin D, they phosphorylate and inactivate the retinoblastoma protein (Rb1), leading to the release of the E2F transcription factor, which in turn allows the cell cycle to progress from the G1 to S phase [54,55]."
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"Thus, the dual role of Rb in regulating cell proliferation and differentiation is mediated by its phosphorylation status. xref Both cyclin D1-CDK4 and cyclin E-CDK2 phosphorylate Rb during the G1/S cell cycle progression, and cyclin D1-CDK4 specifically phosphorylates Rb at Serine 780 in vitro in human fibroblasts. xref We previously reported that sepsis inhibits cyclin-dependent kinase inhibitor p21 expression due to increases in the NFI-A protein. xref P21 inhibits the cyclin D1-CDK4 protein complex, which facilitates cell cycle arrest and promotes cell differentiation. xref , xref In this study, knockdown of cyclin D1 or CDK4 in sepsis Gr1 + CD11b + cells inhibited Rb phosphorylation at Serine 780 ( xref ), Rb knockdown displaced C/EBPβ from the miR promoters and simultaneously induced C/EBPα binding ( xref ) and abolished the miR promoter-driven reporter gene expression ( xref )."
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"Rb itself is inactivated through phosphorylation by the Cyclin D1 and CDK4 complex, liberating E2F to promote cell entry into S phase."
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"These four genes are members of the RB signaling pathway (as annotated in xref ) involved in G1/S progression (by Bonferonni-corrected hypergeometric test): CDKN2A and CDKN2B inhibits CDK4, which in turn inhibits RB1."
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"Cyclin D binds to CDK4, forming the active cyclin D–CDK4 complex, the cyclin D–CDK4 complex phosphorylates and inactivates the Rb."
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"6 Cyclin D1-bound CDK4 catalytically inactivates RB, which induces cells to progress past the G1/S checkpoint."
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"Cdk4 and Cdk2 can inactivate Rb family members, including p107, by phosphorylation."
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"This observation is consistent with the fact that while active, RB1 sequesters and represses the E2F1 transcription factor, which is liberated when CDK4 phosphorylates and inactivates RB1."
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"CDKN2B inhibits CDK4, CDK4 inhibits RB1."
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"CDK4 activation inhibits the retinoblastoma protein, promoting cell cycle progression, and is usually associated with tumor suppressor CDKN2A (p16INK4A) deletion, furthering melanoma cell survival [121]."
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"Cyclin-dependent kinase 2 (CDK2) and cyclin-dependent kinase 4 (CDK4) regulate RB hyper-phosphorylation status and prevent RB from binding with E2F transcription factors, thereby promoting cell cycle progression [28]."
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"The cyclin D1 and CDK4 complex inactivates Rb to promote G1/S transition and cell proliferation."
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"The resulting cyclin D1-CDK4 complex inhibits retinoblastoma protein, thus facilitating the transcription of S-phase genes [ xref ]."
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"These four genes are members of the RB signaling pathway involved in G1/S progression (by Bonferonni corrected hypergeometric test) : CDKN2A and CDKN2B inhibits CDK4, which in turn inhibits RB1."
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"CDK4, a cell cycle regulator, suppresses the retinoblastoma protein RB1 to stimulate cell cycle progression and the expression of a battery of genes, including MDM2."
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"To investigate the requirement for p53 and Rb activity in senescence-associated OPN regulation, we ectopically expressed a well-characterized dominant negative p53 cDNA (p53-DD) ( xref ) or a cDNA expressing a fusion protein consisting of a mutant form of cyclin dependent kinase 4 R24C (Cdk4) and cyclin D1 (DK) that inhibits Rb ( xref ) ( xref )."
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"p16 is so named because it is a specific inhibitor of CDK4 and CDK6 [57], two nearly identical cyclin dependent kinases, which inactivate the retinoblastoma (RB1) tumor suppressor [20]."
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"p16 is known to arrest cells in G1 phase of cell cycle by inhibiting CDK4 and CDK2 proteins which in turn down-regulate retinoblastoma (RB) and E2F factors [ 181 ]."
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"The RB regulatory pathway is very commonly disrupted during tumorigenesis, by activation of cyclin D1 or Cdk4, or by elimination of the Cdk4 antagonist, p16, or RB itself."
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"Intuitively, any genomic alteration, including CDKN2A deletion, CDK4 amplification, and RB1 mutations, can inactivate RB, resulting in cell proliferation."
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"Deletion of p18 (Ink4c) (p18), an inhibitor of CDK4 and CDK6, functionally inactivates the RB pathway, stimulates mammary luminal stem cell (LSC) proliferation, and leads to spontaneous luminal tumor development."
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"Activation of p16INK4a inhibits cell cycle progression and promotes senescence by preventing the inactivation of Rb by CDK4 or CDK6 [ xref ]."
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"By contrast, assessment of the CDK4 and cyclin D1 complex and measurement of its kinase activity are entirely congruent with the proliferative response, and suggest that CDK4 compensated for diminished CDK2 activity to inactivate pRb and promote cell cycle progression (XREF_FIG)."
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"Cyclin D1 and CDK4 phosphorylate and inactivate Rb during the G1/S transition, thereby allowing cell cycle progression to occur [6] ."
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"Activation of p16INK4a inhibits cell cycle progression and promotes senescence by preventing the inactivation of Rb by CDK4 or CDK6 [186]."
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"CDK4 phosphorylates and inactivates Rb protein."
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"The retinoblastoma protein (RB) enforces arrest in G /G , but can be inactivated through phosphorylation by CDK4 or CDK6 acting in concert with D-cyclins."
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"The retinoblastoma protein (RB) enforces arrest in G /G , but can be inactivated through phosphorylation by CDK4 or CDK6 acting in concert with D-cyclins."
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"We hypothesize that in such cases, posttranslational inhibition of pRB by ecDNA-amplified CDK4 may be so extreme that it results in a pRb null-like state, leading to reciprocal p16 overexpression."
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"38 Another study found that, in patients with AA, loss of both wild-type copies of the tumor suppressor genes CDKN2A, CDKN2B, and RB1 or gene amplification of CDK4, disrupting the Rb1 pathway, were sh[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The activities of cyclin dependent kinase 2 (Cdk2) and cyclin dependent kinase 4 (Cdk4) are greatly reduced, due mostly to the increased expression of the Cdk inhibitor (CKI) proteins p21 CIP1 and WAF[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"E2F1 transcriptional activity is regulated by glucose and insulin through the CDK4-dependent inactivation of the pRB protein (Annicotte et al, xref )."
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"Aberrant cell cycle entry in post-mitotic neurons results in abnormal up-regulation of CDK4 that inactivates retinoblastoma protein (Rb) through phosphorylation resulting in activating E2 promoter-bin[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"CDK4 and CDK6 inhibited by DNA damage detection cannot inactivate RB, which allows RB to bind to E2F and further suppress the activity of E2F, thereby leading to cell cycle arrest [16]."
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"We used a panel of DLBCL cell lines derived from patients with relapsed and refractory disease; all lines have decreased or absent p53 activity and CNAs of cell cycle components including CDKN2A, CCND3, CDK4, CDK6, CDK2 and/or copy loss of RB1 (XREF_SUPPLEMENTARY)."
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"Further reinforcing this notion were experiments utilizing supra-physiologic overexpression of D-type cyclins and Cdk4 and Cdk6 that inactivated Rb and drove cells into S phase."
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"We also noticed that CDK4 siRNA transfection could abrogate the phosphorylated levels of downstream Rb molecule in CS-1 and SW1353 cells significantly."
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"Despite the traditional association of senescence with the G0 phase, one known mechanism of senescence begins with the tumor suppressor p16 Ink4a (CDKN2A), which inhibits Rb inactivation by CDK4 and CDK6, leading to failure to transition from G1 phase into S phase [ xref , xref ]."
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"In the same way, astrocytic gliomas (including glioblastomas) also display non-random genetic alterations: 1) EGFR, CDK4, or MDM2 amplification; 2) inactivating mutations or deletions of TP53, RB1, p1[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The combination of CDK4 and cyclin D1 can cause the retinoblastoma tumour suppressor (Rb) protein to lose its blocking effect on cell cycle by phosphorylating the Rb protein and realizing the effect of promoting and transforming the cell cycle (Pines, 1995)."
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"Cycle inhibitory proteins p15 INK4b and p16 INK4a encoded by this locus are able to induce cell cycle arrest in G1 by inhibiting cyclin dependent kinases CDK4 and CDK6 which normally inactivate two tumour-suppressor pathways, Rb and p53."
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"The CKIs, p16, p15, p18 and p19, inhibit the activity of the CDKs CDK4 and CDK6, thereby preventing phopsphorylation of Rb, and G1 to S phase transition, and a mouse with a Cdk4 point mutation (Arg24Cys) that resulted in insensitivity to the CKIs, developed tumours of the pituitary, pancreas and testes."
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"Overexpression of CDK4 inhibits RB1 function, increasing cell signaling, and promoting cell cycle progression."
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"Furthermore, Chou and collaborators showed that inhibition of CDK4 with palbociclib significantly induces apoptosis in pancreatic tumour overexpressing Rb and also enhances the apoptotic effect of chemotherapeutic gemcitabine in patient derived xenografts in mice."
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"Cyclin D1 and Cdk4 complex inhibits Rb by appropriate phosphorylation andreduces its association with E2F transcription factor, leading tothe activation of downstream gene transcription [XREF_BIBR]."
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"During G1, Rb proteins are inactivated by sequential phosphorylation mediated by various Cdks, mainly the D-type cyclin dependent Cdk4 and Cdk6 and the E-type cyclin dependent Cdk2."
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"Multiple laboratory and clinical studies have confirmed that CDK4 suppresses the evolution of liposarcoma by negatively regulating the RB pathway (58)."
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"For example, CDK4/CDK6 inhibitor palbociclib reduces tumor growth by reducing retinoblastoma (RB) protein phosphorylation and cell cycle arrest, which induces G1/S phase transition."
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"Cyclin D1 and CDK4 phosphorylate and inactivate Rb during the G1/S transition, thereby allowing cell cycle progression to occur [XREF_BIBR]."
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"Cyclin D1/D3 promote CDK4 and CDK6 activities that stabilize the anti-senescence transcription factor FoxM1 and inhibit Rb, causing Rb release from E2F transcription factors that drive cell cycle progression (XREF_FIG)."
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"Nevertheless, in our follow-up experiments, we recapitulated the CDK4-RB interaction as RB (phosphorylated at Ser 780 and Ser 807) was suppressed by PD0332991 and by CDK4 directed siRNA (XREF_FIG)."
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"The mutually exclusive cyclin D1–Cdk4 and cyclin D2–Cdk4/6 pairing is able to inactivate the Rb protein, even in the presence of CKIs."
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"The effects of exogenous human telomerase reverse transcriptase expression, p53 knockdown, disruption of the pRb pathway by over-expression of CDK4 and reduced oxygen concentration on the lifespan of primary HCEC were evaluated."
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"The induction of p16 is consistent with p16 expression in some MYCN neuroblastomas (34) but is still surprising since p16 is expected to inhibit Cyclin D:CDK4/CDK6 kinases that inactivate pRB."
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"MDM2 and CDK4 effect cell cycle regulation through separate mechanisms: inactivation of p53 and RB1 respectively (8,10) ."
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"CDK4, a cell cycle regulator, suppresses the retinoblastoma protein RB1 to stimulate cell cycle progression and the expression of a battery of genes, including MDM2."
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"This induction could be strengthened by the addition of ectopic Cyclin D and Cdk4, which form a G1 Cyclin/Cdk complex to inhibit Rb and further convert repressive E2F complexes to activator complexes."
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