Talk:Glutamate dehydrogenase 1
|WikiProject Molecular and Cell Biology||(Rated B-class, Low-importance)|
Any proposed treatments for this yet? Maybe glutamine supplementation? —Preceding unsigned comment added by Interestedperson (talk • contribs) 01:59, 14 August 2008 (UTC) Can someone help explain the glutamate connection to this? —Preceding unsigned comment added by Interestedperson (talk • contribs) 02:02, 14 August 2008 (UTC)
tricks to remember activators and inhibitors
The enzyme cause catabolism of amino acids (a.a.), which provide energy precursors. But it also stimulate insulin secretion: so
1- ADP means low energy -> need catabolism -> activator
If low -> need catabolism BUT risk for direct enzyme stimulation (due to co-stimulation of insulin) so directly inhibit, leaving the activation to be done indirectly via ADP-rybosilation cause this inhibitory mechanism (when relaxed) it stimulate the enzyme, but no longer stimulation of TRPM2 receptor, which is another insulin secretor: antagonize insulin secretion stimulation.
If intermediate ATP : no risk, directly stimulate the enzyme
If very high: we have enough energy, no catabolism.
3- zinc found in food, so probabely he have energy enough -> no catabolism needed -> inhibitor
4- palmitoyl coA: seems fat derivative, fat=food : same as in no. 3
5- a.a. : we will have much a.a. : degrade some (differ from energy cause)
6- NADH : enough energy -> inhibit catabolism
Potentially a grave mistake: sub-cellular location !
here you suppose it present in Mitochondrion matrix, Mitochondrion, & cytoplasm.
But I have read that it present only in Mitochondrion matrix.
however: I must admit that the same website where I found that, was also listing the other sites below under a category (go-cellular component): which I understood as simple reference links for studying these cellular locations.