CDK4 and CDK6 interact with c-Myb in human cells. The c-Myb protein has been linked to the regulation of proliferation 7, 8 and can interact with cyclin D1. 37 We used coimmunoprecipitation assays to test whether c-Myb also formed stable complexes with cyclin-dependent kinases (CDKs) in animal cells. As a first approach, we used a ...

This review discusses the role that CDK4 plays in cell cycle control, normal development and tumorigenesis as well as the current status and utility of approved small molecule CDK4/6 inhibitors that are currently being used as cancer therapeutics. Keywords: CDK4/6, cancer, cell cycle, targeted therapy, checkpoint inhibitor.

Inhibition of CDK2 and CDK4/6 functions has been found to suppress the growth of triple negative breast cancer cells (TNBC), which manifests itself in loss of expression of the RB protein, or high expression of cyclin E, which are thought to confer resistance to treatment with CDK4/6 inhibitors.

Feb 2, 2018 · We show here that: i) the growth of Ph+ ALL cell lines and primary cells is highly dependent on MYB-mediated transcriptional upregulation of CDK6, cyclin D3, and BCL2 and ii) restoring their expression in MYB-silenced Ph+ ALL cells …

May 4, 2014 · In human cells, c-Myb protein interacts with and is regulated by Cyclin D1 and CDK4 or CDK6, suggesting that regulation of c-Myb activity may play a role in the G1/S transition . In contrast, c-Myb has also been shown to directly regulate the promoter of the Cyclin B1 gene, which is involved in G2/M phase transition [ 55 ].

CDK4 overexpression is a predictive biomarker for resistance to conventional chemotherapy in patients with osteosarcoma. Cell size homeostasis is maintained by CDK4-dependent activation of p38 MAPK. CDK4/6 inhibition blocks cancer metastasis through a USP51-ZEB1-dependent deubiquitination mechanism.

Jul 1, 2014 · MYB-related protein B (B-MYB/MYBL2), a member of the myeloblastosis family of transcription factors, has recently emerged as a potential candidate for regulating entry into senescence. Here, we review the evidence which indicates that loss of B-MYB expression has an important role in causing senescence growth arrest.

May 29, 2024 · To assess how CDK4/6 activity promotes multiciliated cell differentiation, we examined the expression of early multiciliated cell transcription factors, MYB and FOXJ1, in CDK4/6 inhibited cells.

The pathway starts with inappropriate activation of cyclin dependent kinase 4 (Cdk4) in neurons which leads to hyper-phosphorylation of the pRb family member p130. This in turn results in dissociation of p130 and its associated chromatin modifiers Suv39H1 and HDAC1 from the transcription factor E2F4.

Nov 1, 2005 · E2F transcription factors are transformed from activators to inhibitors of gene expression by interacting with retinoblastoma family members. Growth factor-induced activation of cyclinD1 causes cdk4-dependent phosphorylation of retinoblastoma proteins which can no longer bind to E2F, which becomes free to activate transcription.