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ATM naturally exists as a resting inactive dimer which is auto-phosphorylated into an active monomeric form that interacts with the MRE11/RAD50/NBS1 (MRN) complex at the site of strand breaks, co-ordinating DNA repair 45,46
In rats, GCLC has a Km for glutamate that is about 10-fold higher than that of the GCL holoenzyme, which is higher than the cellular glutamate concentration in most tissues GCL is specific for the glutamyl moiety and is regulated physiologically by: (a) non-allosteric feedback competitive inhibition by glutathione (GSH) (Ki = 2.3 mM) which involves binding of GSH to the glutamate and another site on the enzyme [8, 9] and (b) availability of its precursor, cysteine [1]
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For certain patient populations, overeating is not the primary driver of excess adiposity
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