Hormones do not regulate every function in every cell type. Instead, a single hormone controls specific cellular functions in cells that express receptors for that hormone. The receptor expression determines which cells respond to a particular hormone. The response of a cell to a hormone depends on its differentiated state. The specificity of hormonal responses is determined by the structure of the hormone, the receptor, and the cell type in which the receptor is expressed. Hormone concentrations in the serum are typically very low, so receptors must have high affinity and specificity for their corresponding hormone.

Hormone-receptor binding induces conformational changes in the receptor, which collectively form a signal. This signal is then transduced into the activation of intracellular messengers. These messenger molecules bind to effector proteins, which in turn modify specific cellular functions. The combination of hormone-receptor binding, activation of messengers, and regulation of effector proteins is referred to as a signal transduction pathway, resulting in the cellular response.

Signaling pathways have the following properties:
1. They involve multiple hierarchical steps, where downstream effector proteins depend on and are driven by upstream receptors, transducers, and effector proteins. Loss or inactivation of components within the pathway leads to general resistance to the hormone, while constitutive activation or overexpression of components can drive unregulated pathway activation.
2. The initial hormone-receptor binding is amplified, often achieving maximal response even when a small percentage of receptors are bound by the hormone.
3. One hormone-receptor binding event can activate multiple pathways or regulate multiple cell functions. For example, insulin binding to its receptor activates three separate signaling pathways. Even in simpler pathways, divergent downstream events allow the regulation of multiple functions.
4. Constitutive and regulated negative feedback reactions antagonize signaling pathways. This means that opposing reactions dampen or terminate the signal, and changes in the function of opposing components can lead to hormone-independent pathway activation or hormone resistance.

Hormones signal to cells through membrane or intracellular receptors. Membrane receptors have rapid effects on cellular processes independent of new protein synthesis. They can also rapidly regulate gene expression through mobile kinases or mobile transcription factors. On the other hand, steroid hormones have slower and longer-term effects that involve chromatin remodeling and changes in gene expression. There is growing evidence of rapid, nongenomic effects of steroid hormones, but these pathways are still being studied.
Although hormones can exert coordinated, pleiotropic control on multiple aspects of cell function, any given hormone does not regulate every function in every cell type. Rather, a single hormone controls a subset of cellular functions in only the cell types that express receptors for that hormone. Thus selective receptor expression determines which cells respond to a given hormone. Moreover, the differentiated state of a cell determines how it responds to a hormone. Thus the specificity of hormonal responses resides in the structure of the hormone itself, the receptor for the hormone, and the cell type in which the receptor is expressed. Serum hormone concentrations are typically extremely low (10−11 to 10−9 mol/L). Therefore, a receptor must have high affinity, as well as specificity, for its cognate hormone.
How does hormone-receptor binding get transduced into a cellular response? Hormone binding to a receptor induces conformational changes in the receptor. These changes are collectively referred to as a signal. The signal is transduced into the activation of one or more intracellular messengers. Messenger molecules then bind to effector proteins, which in turn modify specific cellular functions. The combination of hormone-receptor binding (signal), activation of messengers (transduction), and regulation of one or more effector proteins is referred to as a signal transduction pathway (also called simply a signaling pathway), and the final outcome is referred to as the cellular response.
Signaling pathways are usually characterized by the following properties: 1.
Multiple, hierarchical steps in which “downstream” effector proteins are dependent on and driven by “upstream” receptors, transducers, and effector proteins. This means that loss or inactivation of one or more components within the pathway leads to general resistance to the hormone, whereas constitutive activation or overexpression of components can drive a pathway in an unregulated manner.
2.
Amplification of the initial hormone-receptor binding. Amplification can be so great that maximal response to a hormone is achieved when the hormone binds to a small percentage of receptors.
3.
Activation of multiple pathways, or at least regulation of multiple cell functions, from one hormone-receptor binding event. For example, binding of insulin to its receptor activates three separate signaling pathways. Even in fairly simple pathways (e.g., glucagon activation of adenylate cyclase), divergent downstream events allow the regulation of multiple functions (e.g., post-translational activation of glycogen phosphorylase and increased phosphoenolpyruvate carboxykinase gene transcription).
4.
Antagonism by constitutive and regulated negative feedback reactions. This means that a signal is dampened or terminated (or both) by opposing reactions and that loss or gain of function of opposing components can cause hormone-independent activation of a specific pathway or hormone resistance. As discussed in , hormones signal to cells through membrane or intracellular receptors. Membrane receptors have rapid effects on cellular processes (e.g., enzyme activity, cytoskeletal arrangement) that are independent of the synthesis of new protein. Membrane receptors can also rapidly regulate gene expression through either mobile kinases (e.g., cyclic adenosine monophosphate–dependent protein kinase [PKA], mitogen-activated protein kinases [MAPKs]) or mobile transcription factors (e.g., signal transducer and activator of transcription proteins [STATs], Mothers against decapentaplegic homologs [Smads]). Steroid hormones have slower, longer term effects that involve chromatin remodeling and changes in gene expression. Increasing evidence indicates that steroid hormones have rapid, nongenomic effects as well, but these pathways are still being elucidated.