Phospho-CCNE1-Thr395 Rabbit Polyclonal Antibody
No Size Price Availability  
ARP898P-61 50ul 1500.00 In Stock
ARP898P-61 100ul 2000.00 In Stock
  • Details
  • FAQs
  • Manual
Source: Rabbit Gene Id: 898
Isotype: IgG Swiss Prot: P24864
purity: Affinity purification
Background:
The protein encoded by this gene 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. This cyclin forms a complex with and functions as a regulatory subunit of CDK2, whose activity is required for cell cycle G1/S transition. This protein accumulates at the G1-S phase boundary and is degraded as cells progress through S phase. Overexpression of this gene 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. Two alternatively spliced transcript variants of this gene, which encode distinct isoforms, have been described. Two additional splice variants were reported but detailed nucleotide sequence information is not yet available. [provided by RefSeq
Reactivity Human
Tested applications WB IHC
Clonality Polyclonal Antibody
Calculated MW 48 kDa
Recommended Dilutions
WB 1:500-1:2000
IHC 1:50-1:200
Immunogen A synthetic peptide derived from human CCNE1 around the phosphorylation site of Threonine 395
Storage Store at -20°C or -80°C in PBS with 0.02% sodium azide and 50% glycerol. Avoid freeze/thaw cycles.
Synonym CCNE
This product is for research use only, not for diagnostic or therapeutic use!

backtop
QQ
service center
Contact Us