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doi: 10.3390/biom12010043
described that GS is subject to feedback control by glutamine, which promotes its degradation (36, 37)
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Notably, NMDAR-dependent activity has been shown to directly regulate activity-dependent CCK release [55], and NL3 dysfunction disrupts postsynaptic NMDAR localization and NMDAR-dependent synaptic activity [56], potentially perturbing this developmental regulatory process
Misra, K., Banerjee, A
