May 18, 2005

RIP3 beta and RIP3 gamma, two novel splice variants of receptor-interacting protein 3 (RIP3), downregulate RIP3-induced apoptosis

Biochemical and Biophysical Research Communications
Yonghui YangMian Wu


Receptor-interacting protein 3 (RIP3) is an apoptosis inducing member of the RIP family. Here we report two novel splice variants of human RIP3, designated RIP3 beta and RIP3 gamma respectively. Unlike full-length RIP3, both variants possess a truncated N-terminal kinase domain and a distinct and shorter C terminus, and therefore abrogate nucleocytoplasmic shuttling and apoptosis-inducing activity. Transient expression of either variant was found to downregulate RIP3-mediated apoptosis. Importantly, real-time PCR analysis reveals that the ratio of RIP3 gamma to RIP3 is significantly increased in colon and lung cancers relative to their matched normal tissues, indicating that RIP3 gamma might be a major splice form associated with tumorigenesis.

Mentioned in this Paper

Real-Time Polymerase Chain Reaction
Nested Transcripts
Flow Cytometry
Tumor Suppressor Genes
Apoptosis, Intrinsic Pathway
Western Blotting
Proteins, Recombinant DNA
Tissue Specificity

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.


Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Alternative splicing

Alternative splicing a regulated gene expression process that allows a single genetic sequence to code for multiple proteins. Here is that latest research.