Antibodies That Detect a Novel Tumor Supressor (BIN1) Implicated in Human Carcinomas and Apoptosis

Inventor(s)
Tech ID
PG01RR
Background

Wistar researchers have developed polyclonal and monoclonal antibodies (PAb 99Pst and MAbs 99D through 99I) that bind to BIN1, a novel tumor suppressor protein that interacts with and inhibits the oncogenic activity of the MYC oncoprotein. BIN1 is functionally deleted in carcinomas of the breast, colon, lung, liver and cervix and has been implicated in programmed cell death (apoptosis). Apoptosis is an active process of physiological cell suicide that is critical to normal tissue homeostasis but that does not function properly in tumor cells. Work aimed at defining the genetic control of apoptosis and understanding its dysfunction in cancer has centered on the MYC oncoprotein, because it can promote either cell proliferation or apoptosis. Wistar scientists theorize that BIN1 may activate or facilitate apoptosis, thereby overcoming MYC's malignant growth activity. The antibodies generated by Wistar scientists are useful for research aimed at understanding the role of the BIN1 protein in the genetic events associated with apoptosis.

Origin

Anti-99Pst is derived from rabbits immunized with a recombinant BIN1 polypeptide fused to glutathione s-transferase. 99D-I are secreted by hybridomas derived from mice immunized with recombinant BIN1 polypeptide fused to glutathione s-transferase. Isotypes are IgG1 (E, G, H) and IgG2b(D, E).

Reactivity

The polyclonal antibody recognizes BIN1 and at least one additional BIN1-related protein. This antibody does not appear to recognize the murine BIN1 polypeptide and therefore appears to be human-specific. The monoclonal antibodies are specific for BIN1 but recognize proteins from human, murine, rat, and avian cells. The epitope recognized by 99F, 99G, 99H, and 99I has been mapped to a 10-residue region of BIN1. Two other epitopes mapping outside of this region are recognized by the three other antibodies.

Intellectual Property Status

United States patent has been allowed.