Tuesday, February 4, 2014

TRPM7 (and PLBC)

It is potentially a dangerous gene when mutated (TRPM)
Its autophosphorylation capacity makes it a potential DRIVER gene...
And it is an Ion Channel and therefore has direct implications on cellular depolarisation
Use of Calcium as a co-factor put it center to all function calcium does. It's importance in Traumatic Brain Injury cannot be undermined.  It seemed to be at the center of neuronal death.  It also may impact the NFAT...  
1. Its implication of Alzheimer needs assessment
2. Its role in the endothelium leads to
"Defects in this gene have been associated to magnesium deficiency in human microvascular endothelial cells.[3]" wikipedia



3.It also has a significant relation with P38 or MAPK and therefore  reaches ATF2, C-MYC,PAX6 and P53
And again through P38, this gene impact the epigenic event commanded by ELK1, ETS1 and MK2 by which it reach the CREB, RAR, and the NFkB/P65.

4.Through the PLBC, it reaches the Inositiol based pathway.
5.  It is unclear if it participates in Micro-vascular disease seen on so many Brain MRI in elderly, raising the issue of whether this will be a biomarker for this silent disease and whether Aspirin is the best course.
6.?Disruption here is accompanied by disturbance of calcium in blood, or dysfunction of Parathyroid?

Focusing on P38!

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