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No clear phenotype has been associated with CAV2 deficiency in humans, while Cav2 knockout mice demonstrate severe pulmonary dysfunction along with little or no change in caveolin-1 expression and caveolae formation [46]
Chaperones attempt to remedy the unfolded protein first and, if unsuccessful, activate cellular programs, including the UPR, heat shock response (HSR), and ER-associated degradation (ERAD), to induce processes to either fix the problem or destroy the unfolded proteins (324, 325)
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Therefore, dysregulation in kinase signaling might contribute to the synaptic impairment and is often associated with neurological and neuropsychiatric disorders [7, 26]
