4.6 Article

Transcription variants of the prostate-specific PrLZ gene and their interaction with 14-3-3 proteins

Journal

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.08.165

Keywords

PrLZ gene; Prostate-specific gene; Alternative splicing; Protein interaction; 14-3-3; Mammalian two-hybrid assay

Funding

  1. [R21CA112330]
  2. [PC040578]
  3. [CA132388]
  4. [CA98912-02]

Ask authors/readers for more resources

We have reported isolation and characterization of the prostate-specific and androgen-regulated PrLZ gene abnormally expressed in prostate cancer. PrLZ is a potential biomarker for prostate cancer and a candidate oncogene promoting cell proliferation and survival in prostate cancer cells. A full delineation of the PrLZ gene and its gene products may provide clues to the mechanisms regulating its expression and function. In this report, we identified three additional exons in the PrLZ gene and recognized five transcript variants from alternative splicing that Could be detected by RT-PCR and Western blotting. Structural comparison demonstrated that the PrLZ proteins are highly conserved among species. PrLZ contains multiple potential sites for interaction with other proteins. We used mammalian two-hybrid assays to demonstrate that PrLZ isoforms interact with 14-3-3 proteins, and multiple sites in the PrLZ may be involved in the interaction. Alternative splicing may contribute to abnormally enhanced PrLZ levels in Prostate cancer, and interaction with 14-3-3 proteins may be a mechanism by which PrLZ promotes Cell Proliferation and Survival during prostate cancer development and progression. This information is a Valuable addition to the investigation of the oncogenic properties of the PrLZ gene. (C) 2009 Elsevier Inc. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available