Anti-Cyclin D1

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Cyclin D1, also known as CCND1, belongs to the highly conserved cyclin family whose members are characterized by a dramatic periodicity in protein abundance throughout the cell cycle. CCND1 encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma protein and promotes progression through the G1-S phase of the cell cycle. Amplification or overexpression of the protein plays pivotal roles in the development of a subset of human cancers including parathyroid adenoma, breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer. The gene is overexpressed in breast cancers and is required for oncogene-induced tumorigenesis. Brisken et al. (2003) found that prolactin (PRL, 176760) induced IGF2 (147470) mRNA and IGF2 induced cyclin D1 protein expression in mouse mammary epithelial cultures. They also concluded that IGF2 is a mediator of prolactin-induced alveologenesis and that prolactin, IGF2, and Cyclin D1 are components of a developmental pathway in mammary gland. Protein function: Regulatory component of the cyclin D1-CDK4 (DC) complex that phosphorylates and inhibits members of the retinoblastoma (RB) protein family including RB1 and regulates the cell-cycle during G(1)/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complex and the subsequent transcription of E2F target genes which are responsible for the progression through the G(1) phase. Hypophosphorylates RB1 in early G(1) phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also substrate for SMAD3, phosphorylating SMAD3 in a cell-cycle-dependent manner and repressing its transcriptional activity. Component of the ternary complex, cyclin D1/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex. Exhibits transcriptional corepressor activity with INSM1 on the NEUROD1 and INS promoters in a cell cycle-independent manner. [The UniProt Consortium]