Deans' stroke musings: New function of MK2 in protecting cells from the cytotoxic effect of TNF

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, October 2, 2017

New function of MK2 in protecting cells from the cytotoxic effect of TNF

But is this other blocking of TNF better?

Developing drugs to reduce brain impairment after stroke -CAL-101 to block TNF December 2015.

The latest here:

New function of MK2 in protecting cells from the cytotoxic effect of TNF

29 September 2017 Ghent University

Identification of a novel cell death checkpoint in the TNF signalling pathway
The group of Prof. Mathieu Bertrand (VIB/UGent) reveals a new function of MK2 in protecting cells from the cytotoxic effect of TNF.
Tumor necrosis factor (TNF) is a proinflammatory cytokine that plays a very important role in orchestrating the immune response. Nevertheless, inappropriate signalling by TNF can also be detrimental and implicated in a variety of human inflammatory diseases, such as rheumatoid arthritis, inflammatory bowel disease and psoriasis. The pathogenic role of TNF in inflammatory conditions has long been thought to result from the ability of TNF to induce expression of a wide panel of proinflammatory mediators, but more recent studies have demonstrated that binding of TNF to its cognate receptor also promotes inflammation by inducing cell death, in the form of apoptosis and necrosis. Interfering with cell death induction therefore emerges as a promising therapeutic approach for the treatment of inflammatory conditions.
The research team of Prof. Bertrand (VIB/UGent), in the unit headed by Prof. Vandenabeele, is investigating the molecular mechanisms that protect the cells from death, and which are dysregulated in pathologic conditions. In the current issue of Nature Cell Biology, the group of Prof. Bertrand reveals the existence of a new cell death checkpoint in the TNF pathway. Dondelinger, Delanghe and colleagues show that MK2 protects the cells from death by inactivating the kinase RIPK1 through phosphorylation. Importantly, they show that this protective mechanism is affected in some inflammatory conditions and consequently results in cell death. This cell death can however be completely prevented by pharmacological inhibition of RIPK1. Together with other studies, this work highlights the promising therapeutic potential of RIPK1 kinase inhibitor for the treatment of inflammatory diseases.
https://www.nature.com/ncb/journal/vaop/ncurrent/full/ncb3608.html

Full bibliographic information“MK2 phosphorylation of RIPK1 regulates TNF-mediated cell death”
Dondelinger, Delanghe et al. Nature Cell Biology 2017.