Secretory carrier membrane proteins interact and regulate trafficking of the organellar (Na+,K+)/H+ exchanger NHE7.

The mammalian (Na(+),K(+))/H(+) exchanger NHE7 resides chiefly in the trans-Golgi network (TGN) and post-Golgi vesicles where it is thought to contribute to organellar pH homeostasis. However, the mechanisms that underlie the targeting and regulation of NHE7 are unknown. To gain insight into these processes, yeast two-hybrid methodology was used to screen a human brain cDNA library for proteins that interact with the cytoplasmic C-terminus of NHE7.

The p53-stabilizing compound, CP-31398, does not enhance chemosensitivity in human melanoma cells.

Background: Malignant melanoma is a life-threatening disease with a poor prognosis due to its capacity for rapid metastasis and resistance to radio- and chemo-therapy. A pharmacological compound, CP-31398, was recently found to be able to stabilize wild-type p53 and rescue mutant p53 to enhance its transcriptional activity and suppress tumor growth in mice. Since many chemotherapeutic drugs induce p53-dependent apoptosis, we sought to investigate if CP-31398 would enhance chemosensitivity in human melanoma cells by stabilizing p53.

The 19-kDa Mycobacterium tuberculosis protein induces macrophage apoptosis through Toll-like receptor-2.

Macrophages infected with Mycobacterium tuberculosis undergo increased rates of apoptosis. Important objectives are to define the microbial factors that cause apoptosis, the mechanisms involved and the impact on infection. The 19-kDa M.

The p53 stabilizing compound CP-31398 induces apoptosis by activating the intrinsic Bax/mitochondrial/caspase-9 pathway.

p53 is considered the guardian of the genome and has a number of biological functions, including cell cycle arrest, DNA repair, and apoptosis. In a recent study by Foster and colleagues, the pharmacological compound CP-31398 was found to stabilize wild-type p53 to enhance its transcriptional activity and inhibit tumor growth in mice. We hypothesize that CP-31398 induces apoptosis by stabilizing the p53 protein and activating the mitochondrial-mediated pathway.