Mutations of the regulatory subunit (PRKAR1A) of the cAMP-dependent protein kinase (PKA), leading to activation of the PKA pathway, are the genetic cause of Carney complex which is frequently accompanied by somatotroph tumors. Aryl hydrocarbon receptor-interacting protein (AIP) mutations lead to somatotroph tumorigenesis in mice and humans. The mechanisms of AIP-dependent pituitary tumorigenesis are still under investigation and evidence points to a connection between the AIP and PKA pathways. In this study, we explore the combined effects of Aip and Prkar1a deficiency on mouse phenotype and, specifically, pituitary histopathology.

中文翻译：

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Prkar1a 单倍体不足改善了 Aip 缺陷小鼠的生长激素过量表型。

cAMP 依赖性蛋白激酶 (PKA)的调节亚基 ( PRKAR1A ) 的突变导致 PKA 通路的激活，是 Carney 复合体的遗传原因，该复合体经常伴有生长激素肿瘤。芳基烃受体相互作用蛋白 ( AIP)突变导致小鼠和人类的生长激素肿瘤发生。AIP依赖性垂体肿瘤发生的机制仍在调查中，有证据表明 AIP 和 PKA 通路之间存在联系。在这项研究中，我们探讨了Aip和Prkar1a缺乏对小鼠表型，特别是垂体组织病理学的综合影响。