|Application ||WB, IHC-P, FC, E|
|Calculated MW||47077 Da|
|Antigen Region||373-402 aa|
|Other Names||G1/S-specific cyclin-E1, CCNE1, CCNE|
|Target/Specificity||This CCNE1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 373-402 amino acids from the C-terminal region of human CCNE1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||CCNE1 Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Essential for the control of the cell cycle at the G1/S (start) transition.|
|Tissue Location||Highly expressed in testis and placenta. Low levels in bronchial epithelial cells|
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Provided below are standard protocols that you may find useful for product applications.
Cyclin E1 belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. Cyclin E1 forms a complex with and functions as a regulatory subunit of CDK2, whose activity is required for cell cycle G1/S transition. Cyclin E1 accumulates at the G1-S phase boundary and is degraded as cells progress through S phase. Overexpression of Cyclin E1 has been observed in many tumors, which results in chromosome instability, and thus may contribute to tumorigenesis. This protein was found to associate with, and be involved in, the phosphorylation of NPAT protein (nuclear protein mapped to the ATM locus), which participates in cell-cycle regulated histone gene expression and plays a critical role in promoting cell-cycle progression in the absence of pRB.
Ausserlechner, M.J., et al., Leukemia 19(6):1051-1057 (2005).
Wingate, H., et al., J. Biol. Chem. 280(15):15148-15157 (2005).
Honda, R., et al., EMBO J. 24(3):452-463 (2005).
Brzezinski, J., et al., Clin. Cancer Res. 11(3):1037-1043 (2005).
Hayami, R., et al., Cancer Res. 65(1):6-10 (2005).
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