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Access to peer advocates is increasingly available to youth and their caregivers who are receiving services in the public mental health system. This study examines associations between reported access to a youth or family advocate and perceptions of satisfaction with mental health services. A cross-sectional survey of youth (N = 768) and caregivers (N = 1,231) who utilized public mental health services in New York State in 2012 was conducted. The survey includes items on access to youth or family advocates and degree of satisfaction with mental health services. A greater proportion of youth or caregivers with access to peer advocates compared to those without access responded positively on the satisfaction domains of access to services, appropriateness of services, participation in services and overall/global satisfaction. Access to peer advocates was also positively associated with agreement on the psychotropic medication comprehension domain for youth and on perceptions of child functioning and social connectedness for caregivers compared to those without access. This study adds to the growing understanding of the important role peer advocates play in engaging youth with mental health needs and their caregivers in mental health services.

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The tumor suppressor p53 (p53) is regulated by murine double minute 2 (Mdm2) and its homologous MdmX in maintaining the p53 basal level. The overexpressed Mdm2/MdmX inhibit the cellular p53 activity, highly relevant to cancer occurrence. The coiled-coil domain-containing protein 106 (CCDC106) has been identified as a p53-interacting partner. However, its molecular mechanism is still elusive. Here we show that CCDC106 functions as a signaling regulator of the p53-Mdm2/MdmX axis mediated by cellular p53. We identified that CCDC106 directly interacts with the p53 transactivation domain by competing with Mdm2 and MdmX. The CCDC106 overexpression downregulates the cellular level of p53 and Mdm2/MdmX, and the decreased p53 reversibly downregulates the cellular level of CCDC106. Our work not only provides a molecular mechanism of CCDC106 regulating the cellular levels of p53 and Mdm2/MdmX, but also suggests that the CCDC106-p53 interaction as a novel target for cancer therapy.