Mouse Anti-CDK4 Recombinant Antibody (CBT3483) (V2LY-0625-LY1702)

Cyclin Dependent Kinase 4

Ser/Thr-kinase component of cyclin D-CDK4 (DC) complexes that phosphorylate and inhibit members of the retinoblastoma (RB) protein family including RB1 and regulate the cell-cycle during G1/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complexes and the subsequent transcription of E2F target genes which are responsible for the progression through the G1 phase. Hypophosphorylates RB1 in early G1 phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex.

Adipose tissue development Source: Ensembl
Animal organ regeneration Source: Ensembl
Cell division Source: UniProtKB-KW
Cellular response to insulin stimulus Source: Ensembl
Cellular response to interleukin-4 Source: Ensembl
Cellular response to ionomycin Source: Ensembl
Cellular response to lipopolysaccharide Source: Ensembl
Cellular response to phorbol 13-acetate 12-myristate Source: Ensembl
Circadian rhythm Source: Ensembl
G1/S transition of mitotic cell cycle Source: BHF-UCL
Granulocyte differentiation Source: Reactome
Lens development in camera-type eye Source: Ensembl
Negative regulation of cell cycle arrest Source: UniProtKB
Negative regulation of G1/S transition of mitotic cell cycle Source: Reactome
Positive regulation of apoptotic process Source: Ensembl
Positive regulation of cell cycle Source: Reactome
Positive regulation of cell population proliferation Source: BHF-UCL
Positive regulation of cell size Source: Ensembl
Positive regulation of fibroblast proliferation Source: BHF-UCL
Positive regulation of G2/M transition of mitotic cell cycle Source: UniProtKB
Positive regulation of translation Source: Ensembl
Protein phosphorylation Source: BHF-UCL
Regulation of cell cycle Source: GO_Central
Regulation of gene expression Source: BHF-UCL
Regulation of insulin receptor signaling pathway Source: Ensembl
Regulation of lipid biosynthetic process Source: Ensembl
Regulation of lipid catabolic process Source: Ensembl
Regulation of multicellular organism growth Source: Ensembl
Regulation of transcription initiation from RNA polymerase II promoter Source: Reactome
Response to drug Source: UniProtKB
Response to hyperoxia Source: Ensembl
Response to lead ion Source: Ensembl
Response to testosterone Source: Ensembl
Response to toxic substance Source: Ensembl
Signal transduction Source: Ensembl

Nucleus; Nucleus membrane; Cytoplasm. Cytoplasmic when non-complexed. Forms a cyclin D-CDK4 complex in the cytoplasm as cells progress through G1 phase. The complex accumulates on the nuclear membrane and enters the nucleus on transition from G1 to S phase. Also present in nucleoli and heterochromatin lumps. Colocalizes with RB1 after release into the nucleus.

Melanoma, cutaneous malignant 3 (CMM3): A malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.

Phosphorylation at Thr-172 is required for enzymatic activity. Phosphorylated, in vitro, at this site by CCNH-CDK7, but, in vivo, appears to be phosphorylated by a proline-directed kinase. In the cyclin D-CDK4-CDKN1B complex, this phosphorylation and consequent CDK4 enzyme activity, is dependent on the tyrosine phosphorylation state of CDKN1B. Thus, in proliferating cells, CDK4 within the complex is phosphorylated on Thr-172 in the T-loop. In resting cells, phosphorylation on Thr-172 is prevented by the non-tyrosine-phosphorylated form of CDKN1B.