Complex intracellular network interactions regulate gene expression and cellular behavior. Whether at the site of inflammation or within a tumor, individual cells are exposed to a plethora of signals. The transcription factor nuclear factor-kappaB (NF-kappaB) regulates genes that control key cellular activities involved in inflammatory diseases and cancer. NF-kappaB is regulated by several distinct signaling pathways that may be activated individually or simultaneously. Multiple ligands and heterologous cell-cell interactions have an impact on NF-kappaB activity. The G protein-coupled receptor (GPCR) superfamily makes up the largest class of transmembrane receptors in the human genome and has multiple molecularly distinct natural ligands. GPCRs regulate proliferation, differentiation, and chemotaxis and play a major role in inflammatory diseases and cancer. Both GPCRs and NF-kappaB have been, and continue to be, major targets for drug discovery. A clear understanding of network interactions between GPCR signaling pathways and those that control NF-kB may be valuable for the development of better drugs and drug combinations.

中文翻译：

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G蛋白偶联受体与炎症和癌症中NF-κB的连通性。

复杂的细胞内网络相互作用调节基因表达和细胞行为。无论是在炎症部位还是在肿瘤内，单个细胞都暴露于多种信号中。转录因子核因子-κB（NF-kappaB）调节控制与炎症性疾病和癌症有关的关键细胞活动的基因。NF-κB受几个不同的信号通路调节，这些信号通路可以单独或同时激活。多个配体和异源细胞间相互作用对NF-κB活性有影响。G蛋白偶联受体（GPCR）超家族构成了人类基因组中最大的跨膜受体，并具有多个分子上不同的天然配体。GPCR调节增殖，分化，和趋化性，在炎症性疾病和癌症中起主要作用。GPCR和NF-kappaB一直是并将继续成为药物发现的主要目标。清楚了解GPCR信号通路与控制NF-kB通路之间的网络相互作用对于开发更好的药物和药物组合可能有价值。