epitope corresponding to phosphorylated Ser 380 of PTEN of human origin
Modification
Phosphoralated
Modification Notes
As human tumors progress to advanced stages, one genetic alteration that occurs at high frequency is a loss of heterozygosity (LOH) at chromosome 10q23. Mapping of homozygous deletions on this chromosome led to the isolation of the PTEN gene, also designated MMAC1 (for mutated in multiple advanced cancers) and TEP1. This candidate tumor suppressor gene exhibits a high frequency of mutations in human glioblastomas and is also mutated in other cancers, including sporadic brain, breast, kidney and prostate cancers. PTEN has been associated with Cowden disease, an autosomal dominant cancer predisposition syndrome. The PTEN gene product is a putative protein tyrosine phosphatase that is localized to the cytoplasm, and it shares extensive homology with the cytoskeletal proteins tensin and auxilin. Gene transfer studies have indicated that the phosphatase domain of PTEN is essential for growth suppression of glioma cells. PTEN contains five major phosphorylation sites and these are all located in the C-terminal 50–amino acid tail region (Ser370, Ser380, Thr382, Thr383, and Ser385) and have been implicated in controlling PTEN activity.
Key Feature
Clonality
Polyclonal
Isotype
IgG
Host Species
Rabbit
Tested Applications
IFIHC
recommended for detection of Ser 380 phosphorylated PTEN of mouse, rat and human origin by IF and IHC(P):
Species Reactivity
HumanMouseRat
Concentration
1mg/ml
Purification
Affinity purified
Target Information
Alternative Names
epitope corresponding to phosphorylated Ser 380 of PTEN of human origin
Tissue Specificity
epitope corresponding to phosphorylated Ser 380 of PTEN of human origin