Just a generic question, what is the average half-life of a typical membrane protein? If you have a review off hand that could be sent to me, that would be greatly appreciated.
Your question is indeed generic and relates to many issues. What organism, which organelle, which type of membrane protein (with or without posttranslational modification) etc..
One interesting example that touches your question is the presence of a protein quality control system (and by failed quality subsequent degradation which obviously influences the half-life):
Related recent understanding and use of toxins in the regulated degradation process is interesting when thinking about half-life of (membrane) proteins:
https://www.mdpi.com/1422-0067/20/6/1307
More concrete example (and the influence of a specific mutation) is:
I have found that connexin and tight junction proteins are not present in humans (please see files; HepG2 fucoidan and JMBT alopecia). This seems to be due to Species differences.
Humans (Caco-2) transports fucoidan (sulphated poly-L-Fucose) actively via the active transport system, but not via tight junction and/or phagocytosis (please see file; JCB Fucoidan transport).
Membrane proteins seem to be labile as compared to soluble proteins (please see files; Purify Brain Lipoamidase and brain-BIN pig). Importance of turnover or half-life of bacterial membrane proteins has firstly indicated by my teacher Late Hon. Prof. Dr. Iwao Kusaka (The Institute of Applied Microbiology, University of Tokyo, Yayoi-machi, Bunkyo-ku, Tokyo, Japan) (please see file; Dr. Kusaka Membrane).
Lipoamidase of pig brain has surely protease activity, and brain membrane lipoamisase is very labile as compared to brain soluble biotinidase. Therefore, I am now considering that membrane proteins have protease activity as has been shown in the case of the brain Lipoamidase (please see file; Multiple hydrolase LIP).
By the way, I have not found delta opioid receptors and mu opioid receptors in my human protein database (please see file; The Fascio effect). Then, I am now considering that true enkephalin receptor in the human brain seems to be thiol-type membrane-type biotinidase/enkephalin-amino-exo-peptidase (please see files; Brain BIN Pig and Enk serumBIN).
Further, I have recently found that half-life of membrane proteins are shorter in old persons than young persons and/or turnover of membrane proteins is faster in old persons. The excretion of membrane proteins into serum is higher in old persons as compared to young persons (my unpublished observation). Therefore, old persons unexpectedly should take more meat than young persons; i.e., aged tissues have shorter half-lifes of membrane proteins than young tissues.
This may be the cause of differences in effect of biotin deficiency; i.e., biotin deficiency in children induces Alopecia, but biotin deficiency in adult does not induce Alopecia (please see file again; JMBT Alopecia).
I am grateful to Dr. Charles Fisher (Department of Biological Sciences, Lehigh University, Bethlehem, PA, USA) for leading me to this important finding. in Human serum