Loss of function of LH receptors can cause male pseudohermaphroditism.

With the rise in estrogens, LH receptors are also expressed on the maturing follicle, which causes it to produce more estradiol.

Small luteal cells have LH receptors that regulate PKA activity within the cell.

A mutation that cause a gain of function for LH receptor can result in a condition known as testotoxicosis, which cause puberty to occur between ages 2-3 years.

In addition, as more estrogen is secreted, more LH receptors are made by the theca cells, inciting theca cells to create more androgen that will become estrogen downstream.

Prolactin (PRL) increases the response of Leydig cells to LH by increasing the number of LH receptors expressed on Leydig cells.

LH induces androgen synthesis by thecal cells, stimulates proliferation, differentiation, and secretion of follicular thecal cells and increases LH receptor expression on granulosa cells.

LH has a beta subunit of 120 amino acids (LHB) that confers its specific biologic action and is responsible for the specificity of the interaction with the LH receptor.

They were co-expressed with the luteinizing hormone (LH) receptor in HEK 293 cells and cAMP accumulation was measured in both the presence and absence of the LH receptor agonist, human chorionic gonadotropin (hCG).

They contain a heptahelical transmembrane domain and a large glycosylated ectodomain, distantly related to the receptors for the glycoproteohormones, such as the LH-receptor or FSH-receptor.