G protein signalling pathways are crucial for transmitting signals from many cell surface receptors to the intracellular machinery, regulating various cellular processes. Several key players participate in G protein signalling, and their dysregulation can contribute to the development and progression of cancer. These include: 1) G Protein-Coupled Receptors (GPCRs): GPCRs are a large family of cell surface receptors that sense a wide range of external signals, including hormones, neurotransmitters, and growth factors. They transmit signals by interacting with G proteins. GPCR dysregulation is commonly observed in cancer promoting tumour growth, metastasis, and angiogenesis; 2) Heterotrimeric G Proteins. Heterotrimeric G proteins consist of three subunits: α, β, and γ. Upon activation by GPCRs, the α subunit dissociates from the βγ subunit and regulates downstream signalling cascades. Mutations or alterations in G protein subunits have been implicated in various cancers, including lung, breast, and colorectal cancer. Gαs mutations found in adrenocortical tumours lead to constitutive activation of Gαs, resulting in increased production of cyclic AMP (cAMP) and aberrant stimulation of downstream signalling pathways, including protein kinase A (PKA). This dysregulated signalling promotes cell proliferation and hormone production, contributing to the development and progression of adrenocortical tumours; 3) Regulators of G Protein signalling (RGS). RGS proteins act as negative regulators of G protein signalling by accelerating the hydrolysis of GTP bound to the α subunit of G proteins, thereby inactivating them. Dysregulation of RGS proteins has been observed in several cancers and can lead to sustained G protein signalling; 4) G Protein-Coupled Receptor Kinases (GRKs). GRKs phosphorylate and desensitize activated GPCRs, preventing further G protein signalling. Alterations in GRK expression or function have been implicated in cancer progression. Aberrant GRK activity can contribute to enhanced GPCR signalling promoting tumour growth; 5) G Protein-Regulated Effectors. G protein signalling pathways regulate various downstream effectors, including enzymes and ion channels, which mediate cellular responses. Examples of effectors include adenylyl cyclases, phospholipase C, phosphoinositide 3-kinase (PI3K), and mitogen-activated protein kinases (MAPKs). Dysregulation of these effectors can lead to uncontrolled cell proliferation, survival, and migration, contributing to cancer development and progression. We provide a comprehensive product catalogue of research tools for investigating G protein signaling, including CCR5 antibodies, TIMP1 antibodies, SHP1 antibodies, CCR5 ELISA Kits, and TIMP1 ELISA Kits. Explore our full G protein signaling product range below and discover more, for less. Alternatively, you can explore our Small G Proteins and GPCR product ranges.