Search

Hematopoietic stem cells (HSCs) exit the bone marrow and enter the bloodstream in a circadian rhythm, according to a report in Nature (doi:10.1038/nature06685). If the findings hold true in people, [...]

Author(s): Allison Alcivar Bone marrow cells lodged throughout the body seed the development of metastases in mice, report Rosandra Kaplan and colleagues (Nature 438, 820-827). What's more, blocking a signal [...]

Author(s): Allison Alcivar Normal cells will commit suicide if they lose strong attachments to neighboring cells or extracellular matrix. Cancer cells overcome this checkpoint and grow in an anchorage-independent manner. [...]

The article discusses several pharmaceutical research highlights. Calprotectin, a protein spewed out by neutrophils, sucks up zinc and manganese, which help spur bacterial growth. A topical gel containing antisense DNA against a single target reduces the formation of scar tissue and expedites the repair of wounds. Researchers have pinpointed a target for the treatment of psychosis, a complex of two receptors that reacts to antipsychotics and to hallucinogenic drugs.

The article focuses on several results of research related to medicine. A synthetic metabolite of the amino acid tryptophan reverses paralysis in a mouse model of multiple sclerosis. A dampened immune response leaves alcoholics susceptible to lung infections and pneumonia. The myc oncoprotein is switched on and off by ubiquitination, according to a new report. A mouse model uncovers a twist to the molecular basis of a toxic ironoverload disorder. Dampening production of nitric oxide seems to protect against brain pathology and prolong lifespan in a mouse model of Alzheimer disease.

The pathogenesis of mucosa-associated lymphoid tissue (MALT) lymphomas is associated with independent chromosomal translocations that lead to the upregulation of either BCL10 or MALT1 or the generation of a fusion protein, cIAP2-MALT1. While both BCL10 and MALT1 are critically involved in antigen receptor-mediated NF-B activation, the role of cIAP2 is not clear. Here we show that cIAP2 is a ubiquitin ligase (E3) of BCL10 and targets it for degradation, inhibiting antigen receptor-mediated cytokine production. cIAP2-MALT1 lacks E3 activity, and concomitantly, the BCL10 protein is stabilized in MALT lymphomas harboring this fusion. Furthermore, BCL10 and cIAP2-MALT1 synergistically activate NF-B. These results reveal cIAP2 as an inhibitor of antigenic signaling and implicate its dysfunction in MALT lymphomas. [ABSTRACT FROM AUTHOR]