1. Western blotting: ~1 g/mL 2. ELISA Other applications were not tested.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
PBS, 50 % glycerol
Konservierungsmittel
Azide free
Lagerung
-20 °C
Informationen zur Lagerung
Store at -20 C (For long term storage: -70 C).
Sherr: "Cancer cell cycles." in: Science (New York, N.Y.), Vol. 274, Issue 5293, pp. 1672-7, (1997) (PubMed).
Welch, Wang: "A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle." in: Cell, Vol. 75, Issue 4, pp. 779-90, (1993) (PubMed).
Nevins: "E2F: a link between the Rb tumor suppressor protein and viral oncoproteins." in: Science (New York, N.Y.), Vol. 258, Issue 5081, pp. 424-9, (1992) (PubMed).
Hu, Dyson, Harlow: "The regions of the retinoblastoma protein needed for binding to adenovirus E1A or SV40 large T antigen are common sites for mutations." in: The EMBO journal, Vol. 9, Issue 4, pp. 1147-55, (1990) (PubMed).
Retinoblastoma protein (Rb), the tumor suppressor product of the retinoblastoma susceptibility gene, is a 110 kDa protein that functions as a negative regulator of the cell cycle by arresting cells in the G1 phase and halting inappropriate cell proliferation. At the transcriptional level, Rb protein exerts its growth suppressive function by binding to transcription factors including E2F1, PU1, ATF2, UBF, Elf-1 and c-Abl. Loss of Rb function leads to uncontrolled cell growth and tumor development and is found in all retinoblastomas and in a variety of other human malignancies. The ability of Rb protein to inhinbit transcription and cell cycle progression is inactivated by hosphorylation, which is catalyzed by the cyclin-dependent protein kinases.