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“We estimated that a solar panel’s carbon footprint is about twice as high when made in China and used in Europe, compared to those locally made and used in…
The Eastern Himalayas are home to more than 360 different songbird species, most of which are to be found nowhere else on the planet.
An individual ant searching for food walks in random ways, biologists found. Yet the collective foraging behaviour of ants goes well beyond that, as a…
A new research study from Brigham and Women's Hospital (BWH) that compares low-dose oral estrogen and low-dose non-hormonal venlafaxine hydrochloride extended…
The co-stimulatory CD40-CD40L dyad is crucial in the development and progression of immune responses and chronic inflammatory diseases, such as atherosclerosis, obesity and multiple sclerosis. However, long-term antibody-mediated inhibition of CD40L or CD40 is not clinically feasible as it results in thromboembolic events and severe immune suppression. More downstream inhibition of the CD40L-CD40 pathway is therefore preferable, especially tumor necrosis factor receptor-associated factors (TRAFs) recruited by CD40. Here we created a set of inhibitors that selectively block CD40-TRAF6 interactions. The rest of the CD40 cascade is left unaffected preventing unwanted immune-suppressive side effects. Therefore, our new inhibitors offer promising candidates as therapeutic agents for the treatment of chronic inflammatory diseases, such as atherosclerosis, obesity and multiple sclerosis.
Experiments at the University of Bonn have shown that the expression of MED15, a subunit of the trans-criptional co-regulator Mediator, correlates with the proliferative activity of cells. MED15 is essential for TGF-ß-signaling and control of cholesterol/lipid homeostasis. The protein shows low frequency in androgen-sensitive prostate cancer and lacks expression in benign prostatic tissue.